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Biochem Year 1 > Final > Flashcards

Final Flashcards

1
Q

Fed: Absorptive State: efect on metabolism

A

•Anabolic (but not gluconeogenesis):

  • Synthesis:
    • glycogen
    • TG
    • protein
  • •Urea cycle (if high protein ingested)
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2
Q

liver metab: 2 hours after eating

A

insulin drops = gng increase

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3
Q

Xeropthalmia

A

dry eye syndrome

night blindness

xerosis: sclera = wrinkles, less shiny

  • Bitot’s spots - Patches of little gray bubbles on the sclera
  • Keratomalacia - Soft or bulging cornea. Opacities (keratin deposits)
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4
Q

Genetics of Obesity

A

30-40% = heredity

Familial aggregation: clustering of obesity in families

identical twins > non-identical twins

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5
Q

stress and insulin

A

stress —> + epi —> - insulin –> - dietary fuel

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6
Q

cobalt

A

fx: vit b12

defic sympt: anemia

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7
Q

•Korsakoff’s psychosis

A
  • hallucinations
  • Loss of memory
  • Confabulation (making up stories)

B1

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8
Q

•During initial fasting what fuel does the brain use for aerobic metabolism?

A

•Glucose.

prefers glucose

under prolonged fasting will use Ketone Bodies as the prefered state

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9
Q

Islets of Langerhans

A
  • α-cells (20%) produce glucagon
  • β-cells (60-80%) produce insulin
  • δ-cells (about 5%) produce somatostatin
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10
Q

allosteric regulation during fasting stages

A
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11
Q

initiator:of Insulin Secretion

A
  • Glucose = most important
  • aa
  • GI hormones (Secretin)
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12
Q

What causes Wernicke-Korsakoff Syndrome

A

•Most common B1 deficiency in developed countries

chronic alcoholics

Impaired intestinal absorption

poor diets

increased demand with carb, etoh

mg2+ deficiency

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13
Q

Deficiency of Niacin

A

pellagra: 4 D’s

dirrhea, dermatitis, dementia, death

  • derm: esp areas exposed to sunlight - thicken, scales, hyperkeratin
    glossitis: swollen tongue
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14
Q

Vitamin D

A

synth from inactive precursors from diet:

  • ergocalciferol: D2 - plant
  • cholecalciferol: D3 - animal

•Can also be synthesized from 7-dehydrocholesterol in the skin of persons exposed to sunlight

RDA: 5mg cholecalciferol, 200 IU/day vit d

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15
Q

Insulin Also Signals via ______ Pathway

A

PI 3-Kinase

  1. insulin binds to tyr receptors
  2. irs
  3. PI-3 kinase
  4. PDK 1
  5. activated and disassociated from membrane
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16
Q

Sources and Functional Forms

of Water Soluble Vitamins

chart

A
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17
Q

HH type 1

A

HFE

recessive

parenchymal iron overload, cirrh

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18
Q

Pro-Oxidant

A

Fe2+

Cu2+

Cr3+

Vitamin K3

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19
Q
  1. insulin –> carboxyl-terminal tyr residues
  2. irs-1
  3. SH2 domain of Grb2 of irs, sos binds RAS: GDP –> GTP = bind to Ras
  4. raf-1
  5. mek
  6. erk = map kinase
A
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20
Q

Vitamin D Toxicity

A
  • Most toxic of fat soluble vitamins
  • Excess calcitriol –> hypercalcemia and hypercalciuria
  • Dazed appearance
  • Loss of appetite
  • Nausea, thirst and stupor
  • May present with sarcoidosis
  • •Inflammation of tissues marked by clusters of immune cells (granulomas)
  • •Affects lungs, skin and lymph nodes
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21
Q

Brain: Fed State: uses what as fuel?

A

glucose

Consumes 120g glucose/day

70% of the energy is used to maintain the Na+/ K+ membrane potentials

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22
Q

fluoride

A

bone and tooth strength

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23
Q

HbA1c

A

covalent bonded gluc on NH2 group of N-terminal val of beta-globin chain

slow glycation of HbA: dep on plasma [gluc]

  • < 6.1 indicates good glycemic control
  • reflects level of 6 wks prior to measurement
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24
Q

Melanocortin

A

•(α-MSH) is an anorexigenic (appetite-suppressing) signal

stim: leptin, insulin

overprod in Addison’s and CAH

decreased production in Cushings

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25
Q

Anemia caused by…

A

deficiency in iron

sideropenia, hypoferremia

hypochromic, microcystic

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26
Q

_________ are fuel of last resort

A

protein

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27
Q

Enzymatic Changes:
Fed State

A

glycogen storage

  • glycogen synthase

glycolysis

  • pfk-2 –(+)–> F(2,6)BP –(+)–> PFK-1
  • PK
  • PDH

fat synth

  • ACC
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28
Q

molybdenum

A

fx:Xanthine oxidase, aldehyde oxidation

defic sympt: joint pain

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29
Q

when adipocytes reach max size, how does furthur wt gain happen?

A

recrutment and prolif of new adipocytes

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30
Q

27-year-old paramedical lady with no known comorbidities, who presented with rapid-onset coma with hypoglycemia (plasma glucose at admission was 35 mg/dL).

Clinical alertness suspected and confirmed the diagnosis of exogenous insulin administration probably with suicidal intent. A total of 470 g of dextrose was infused until she regained consciousness. No other complications of insulin overdose were observed during her stay in the hospital. Recovery was complete without any residual neurological deficits.

A
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31
Q

Folic Acid Deficiency

A

Megaloblastic anemia

  • Macrocytic (Large Cells)
  • Caused by diminished synthesis of purines and thymidine leading to an inability of cells to make DNA and to divide
  • Cell growth without division

high homocysteine (pre for cys & met) = CVD

  • May also be caused by a lack of vitamin B12

neural tube defects: anenecephaly, spina bifida

  • must occur @ conception: crit folic acid for neural tube dev @ first wks of life when women unaware preg
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32
Q

Adipose: GLUT _____

A

4

glycolysis

fat synth

accepts VLDL

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33
Q

”dipstick” measurement from urine for ketones

A

Ømeasures acetoacetate but ketones are 78%

β-hydroxybutyric acid, 20% acetoacetic acid and

2% acetone.

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34
Q

nutrients enter liver via

A

portal vein

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35
Q

thiazoladinediones

A

troglitazone, rosiglitazone, pioglitazone

target: PPAR-gamma

stim insulin genes in liver, M, adipose

  • increase gluc uptake
  • decrease gluc synth in liver
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36
Q

Vitamins

A

metab essential Ocmpds cannot by synth by body –> supply by diet or gut bacteria

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37
Q

Non-heme iron proteins

A

iron-sulfur proteins

Succ DH(Complex II)

NADH DH (Complex I)

Lipoxygenases

Phe (OH)ase

Ribonucleotide reductase

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38
Q

Brain: GLUT ____

A

1

glucose for aerobic metabolism

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39
Q

deficiency of insulin leads to

A

DM

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40
Q

Creatine

A

synthesized from:

  • met
  • arg
  • gly

E reserve in muscle

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41
Q

Vitamin B1

A

thiamine

TPP: cofac for ox-decarbox rxns: PDH, alpha-KGDH, BCKD

transketolase: PPP

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42
Q

Metabolic Changes in Obesity

A

insulin resistance –> increased HSL (horm. sens lipase) –> enhanced lipolysis –> increase free FA –> increase liver TAGs/choles –> increase VLDL/decreased HDL

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43
Q

induction of what enz in fasting state?

A

gng enz increase: G6Ptase, F(1,6)BPtase, PEP carboxykinase

increase in N-metab enz: urea cycle, glutaminase

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44
Q

Regulation of Metabolism & times

A
  • Substrate availability - min
  • Allosteric activation or inhibition - min
  • Covalent modification(e.g. Phosphate) - min to hours
  • Induction/repression of enzyme synthesis - days
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45
Q

Deficiency of Vitamin B12

A

usually due too lack of intestinal absorp

  • Autoimmune destruction of gastric parietal cells leads to a loss of intrinsic factor which is needed for absorption of B12
  • B12 deficiency causes megaloblastic anemia (called pernicious anemia if due to lack of B12 absorption)
  • Accumulation of both homocysteine and methylmalonic acid in B12 deficiency (only homocysteine accumulation in folate deficiency)
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46
Q

•Under the fed state, the liver would stimulate which of the following metabolic reactions :

A.Hormone-Sensitive Lipase

B.Chylomicron production

C.Carnitine palmitoyl transferase1

D. Glycogen Synthase

E.Glycogen Phosphorylase

●

A

A.Glycogen Synthase

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47
Q

Common forms of obesity are most likely due to

A

complex interactions between genes and the environment

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48
Q

Ketone Body Synthesis in Liver

A
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49
Q

Repression of Hepcidin synthesis

A
  • Hypoxia (HIF2a),
  • Iron deficiency (EPO)
  • Ineffective erythropoiesis (Thalassemias)
  • Leads to increased iron absorption and release via FPN
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50
Q

Glycosuria

A

>180 mg/dL (10 mM) = > threshold

diabetics: 54-300 mg/dL

reducing sugar

  • free oxygen on anomeric carbon
  • Benedict’s reagent (alkaline copper sulfate)
    • Cu2+ –> Cu+ = blue –> reddish brown
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51
Q

Basal/Resting Metabolic Rate

(BMR/RMR)

A

basic physiologic functions

  • heart, lungs, kid, ionic gradients, rxns

when:

  • @ rest
  • post-absorptive
  • warm environ
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52
Q

liver in fasting state using what as fuel?

A

fats

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53
Q

Orlistat

A

(Xenical)

inhib: pancreatic & gastric lipases - reduce absorption

Adverse effects

  • GI: loose stools, oily spotting
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54
Q

Dyslipidemia in Diabetes

A

Hypertriglyceridemia - Inactive Lipoprotein Lipase

High VLDL → High LDL

Hypercholesterolemia(High LDL) -Cardiovascular Risk/Stroke

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55
Q

Metabolism in Fasting State =

A
  • Decrease in Nutrient absorption
  • Decrease in plasma glucose
  • Decrease in Insulin/Glucagon ratio

(Increase in Glucagon)

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56
Q

Brain During
Fasting

A

metab rate of brain = constant: other tissues reduce metab req

undergoes metab changes to adapt to decreased avail of gluc

  • increased amts of enz necc to metab ketone bodies

GLUT -1: BBB

GLUT -3: neurons

Ketone Bodies: main fuel in prolonged fast: b-OHbutyrate (4.69Cal/g; 21.5ATPs)

Glucose: still 25% of fuel

Amino acids: Phe, Tyr, Ile, Leu, Val, Trp, Met, His: specific transporter: brain uptake of neurotransmitter precursors

  • high concentration of any one in the blood can compete with uptake of others
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57
Q

marasmus

A

inadequate intake of both protein and energy - fat and carb

general stavation

prominent bones, loose skin, decrease subQ fat

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58
Q

defic Vitamin B6

A

microcytic anemia (smaller RBC) and sideroblastic anemia (ringed sideroblasts – abnormal RBC)

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59
Q

Absorption of Dietary Iron steps:

A
  • Iron absorbed as Fe2+ via the apical surface of mucosal cells in duodenum via (DMT1) after reduction by feri-reductase (Dcytb)
  • Heme iron is absorbed via (HCP1) and Fe2+ is released by heme oxygenase
  • Some of the absorbed iron is stored as ferritin (Fe3+)
  • Rest of the iron (Fe2+) is transported to the bloodstream via ferroportin (FPN)
  • Hephaestin (ferroxidase) converts Fe2+ to Fe3+ for transport by transferrin (TF) in the blood
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60
Q

HH type 4

A

ferroportin

dominant

hepatocyte, mmacrophage iron loading

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61
Q

Acute Promyelocytic Leukemia

(APL)

A

cancer of the blood: accumulation of immature white blood cells (Promyelocytes)

presence of PML-RARα, a product of the fusion between the promyelocytic leukemia (PML) gene and the retinoic acid receptor (RARα) gene

•PML-RARα represses certain genes and prevents the differentiation of promyelocytes

tx: all-trans-retinoic acid (ATRA) relieves the repression –> differentiation of promyelocytes into mature leukocytes

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62
Q

Liver:Fasting State: Activates/Upregulates

A

Activates/Upregulates:

ØGlycogenolysis: lasts 18-24 hrs

•Phosphorylase and Phosphorylase Kinase

(active in phosphorylated state)

ØGluconeogenesis

•F1,6BPtase, PEPCK, G6Ptase

ØFatty Acid Oxidation:

  • •CPT-1 transport of F.A.
  • •Acetyl-CoA –>
    • Activates Pyruvate Carboxylase –> Glucose
    • Inhibits PDH so pyruvate –> glucose

ketone body synth

aa breakdown: ALT/AST, GluDH: glucogenic aa –> glucose

Urea cycle: CPS-1 N-acetyleglu synth: removes NH3 from glucogenic aa

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63
Q

BMR is proportional to

A

lean body mass: adipose less metab active

SA: rate of heat loss = greater with increasing SA

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64
Q

provitamin A

A

beta-carotene - plants

lowers: CAD, lung and skin ca, cataracts, mac-degen

beta-carotene —(15,15’-Dioxygenase)—> retinal

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65
Q

Menke’s Disease

A

x-linked - cu metab

•Mutation in ATP7A gene - widely distrubuted

  • •Cu accumulation in intestinal mucosa, muscle, spleen, kidney
  • •Low Cu levels in brain, plasma and other tissues

kinky hair

onset usually during infancy: males

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66
Q

Dicoumarol And Warfarin

A

inhibit reductases: form & recyc K

  • block vit-k-dep Glutamyl residue precursors for clotting fac:
    • II, VII, IX and X

tx: anti-coag: thrombosis and pulmonary embolism

Warfarin = rat poison

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67
Q

exercise and glucose and M

A

Stimulates Glucose Uptake By The Muscle

•AMPK also promotes translocation of GLUT4 to plasma membrane

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68
Q

Mediterranean Diet

A

fish (ω-3 fatty acids)

nuts (ω-6 fatty acids)

olive oil (monounsaturated fatty acids)

red wine (polyphenols - anti-inflam)

  • resveretrol
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69
Q

Most vitamins and minerals are needed in _________ amounts

A

μg or mg

exceptions: : calcium, phosphorus and magnesium

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70
Q

Muscle: GLUT _____

A

4

glycolysis

glycogen storage

protein synth

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71
Q

Thermic Effect Of Food

A

•Equal to about 10% of kcal ingested

usually ignored since amts less than roudning errors of daily energy expenditure

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72
Q

Definition of Obesity

  • Waist circumference
  • Waist/Hip ratio
A
  • Waist circumference
  • > 35 in. in women or > 40 in. in men
  • Waist/Hip ratio
  • > 0.8
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73
Q

Iron Metabolism Review

absorption

txp, storage

recycling

regulation

A
  • Absorption
  • DcytB, DMT1, HCP1 (HFG1), FPN, Hephaestin, HOX1

•

  • Transport, Storage
  • TF, Ceruloplasmin, TFR, Ferritin, Hemosiderin, Heme

•

  • Recycling
  • HOX1, FPN

•

  • Regulation
  • Hepcidin, BMP6, TFR2, HFE, HJV, IL-6, IRP1/IRP2
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74
Q

•Saturated fats

sources?

A

high choles and LDL –> increased risk CHD

meat, dairy, coconut/palm oil

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75
Q

Insulinoma

A

Neuroendocrine tumor of pancreas

Unregulated secretion of insulin

Hypoglycemia

Elevated C-peptide levels

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76
Q

rough estimate BMR

A

24 x weight (kg)

kcal/day

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77
Q

Hemosiderin

A

fe inactive storage

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78
Q

•Adipose tissue TAG stores

A
  • Efficient storage of energy reserves
  • Adipose contains about 15% water
  • Muscle contains about 80% water
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79
Q

magnesium

A

cofac: ATP rxns

CNS depressant

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80
Q

Muscle:Fed State: inhibits

A

glycogenolysis

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81
Q

whats the mechanism to store excess protein?

A

none! –> excess = metabolized

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82
Q

osteoclasts are stim by….

A

vit d

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83
Q

Vitamin C and Collagen

A

hydrox pro and lys

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84
Q

Metabolism in Fasting State: catabolic or anabolic?

A

catabolic

  • Glycogen degradation
  • Lipolysis
  • Protein Degradation –> Urea
  • Ketone Body Synthesis
  • Glucose used by glucose dependent tissues
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85
Q

processes for Glycerol-P for TAG

A
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86
Q

Macroelements and

Microelements

A

Macro (g)

  • calcium
  • P
  • Mg
  • Na
  • K
  • Cl

micro (µg to mg)

  • iron
  • copper
  • zinc
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87
Q

Liver
Metabolism in Prolonged Fast

A

Glycogen Stores depleted –> Gluconeogenesis decreases:

Glucose-Alanine cycle decreases: spares muscle protein

A fraction of a.a. used for biosynthetic functions: e.g. neurotransmitters

Urea synthesis decreases

Ketone Body synthesis increases: Brain uses Ketones as fuel

Spares glucose for dependent tissues: RBC

Liver uses Fatty acids as Fuel via beta-oxidation

  • Cannot use Ketone bodies as fuel (lacks thiophorase)
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88
Q

Diabetes Insipidus

A

freq urination: unrelated to DM but with sim signs and symp

usually controlled by vasspressin (ADH)

  • central: storage/release
  • nephrongenic: kid’s response to ADH
  • dispogenic: decreased ADH = abnorm thirst
  • gestational: degrad of ADH by placental enz
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89
Q

kwashiorkor

A

Insufficienct protein - adequate calories

usu: increased protein demands by infection

plump appearance = edema - lose of oncotic P (low albumin lvls)

prominent belly, xerosis (itchy rash)

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90
Q

LIVER acts as the ______________ center in the fed state

A

Distribution Center for Nutrients

Fuel = glucose (from portal vein)

Venous drainage: Gut –> pancreas—> portal vein–> periportal zone

Liver receives all the dietary nutrients first

No Lipoprotein Lipase in adult liver

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91
Q

Soluble fiber

A

gums/pectin: legumes and fruit

slows rate of dig and absorp of carbs

delays postprandial rise in blood sugar

–> buyrate: fuel for colonocytes

decreases absorption of toxins

excessive = affects absorption fat-sol vit

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92
Q

Vitamin K And Blood Clotting

A
  • hepatic synthesis of prothrombin (factor II)
  • blood clotting factors (VII, IX and X).
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93
Q

Skeletal Muscle: Fasting State

A

ØNo Glucose uptake

ØFatty Acids carried by Albumin and Ketone Bodies from Liver are used as Fuels

ØIncrease Beta-oxidation of fats and Ketone Body metabolismàATP for contraction

ØAmino Acids degraded for gluconeogenesis

ØProlonged Fast: Glucose-Alanine cycle decreases: spares muscle protein

ØLong-term Starvation: eventually Muscle protein degraded

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94
Q

Insulin Structure

A
  • 51 amino acids; 2 polypeptide chains linked by 2 disulfide bonds; disulfide bond in A chain
  • C-peptide needed for proper folding
  • Inactive hexamer formed for greater stability
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95
Q

RDA

EAR/AI/UL

A

Defined as the nutrient requirement 2 SD above EAR

  • EAR: Average daily intake estimated to meet the requirement of 50% of a population.
  • RDA: Average daily intake estimated to meet the requirements of 98% of a population.
  • AI: Used if there is insufficient data to calculate an RDA. Estimated to be adequate for almost all of a population.
  • UL: The maximum amount of a nutrient that can be taken by almost all individuals without adverse effects.
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96
Q

acute complications of DM 1

A

ketoacidosis

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97
Q

all tissues use ____ as preferred E source except for…

A

gluocose

Heart prefers FA

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98
Q

How We Counter Hypoglycemia (chart)

A
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99
Q

Transferrin Cycle

A
  • Ferrotransferrin (Fe3+-TF) binds to Transferrin receptor (TFR, Chr 3)
  • The (Fe3+-TF)-TFR complex is endocytosed from clathrin-coated pits
  • The vesicles fuse with endosomes
  • The low pH in the late endosome causes iron to release while TF remains bound to TFR
  • TF-TFR recycled back to plasma membrane where apotransferrin (TF) dissociates
  • Released iron is stored as Fe3+ bound to Ferritin
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100
Q

Metabolic Syndrome - Criteria

A

3 or more of:

Elevated

  • waist circumference:
    • Men — ≥ 40 inches (102 cm)
    • Women — ≥ 35 inches (88 cm)
  • TAG:
    • ≥ 150 mg/dL
  • BP:
    • ≥130/85 mm Hg
  • fasting glucose:
    • ≥100 mg/dL

Reduced

  • HDL (“good”) cholesterol:
    • Men — < 40 mg/dL
    • Women — < 50 mg/dL
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101
Q

Repression: Fed-State : enz and pathways

A

GNG

  • PEP Carboxykinase
  • F1,6BPtase
  • G6-Ptase

Cholesterol synthesis:

  • HMG-CoA Reductase: under high cholesterol via SREBP
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102
Q

Liver: Long-term Starvation (weeks)

A

ØGluconeogenesis continues to deliver glucose to dependent tissues

ØKetone Body synthesis Main synthetic pathway

ØFatty acid degradation is main source of fuel

ØEventually, muscle protein will begin to breakdown for glucose and protein synthesis and urea synthesis will increase

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103
Q

Vitamin B2

A

riboflavin

precursor: FMN, FAD

cofac in redox rxns - non-dissociable prosthetic group

light sens

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104
Q

Trans Fats

sources:

A

high LDL & risk of CHD

no effect on HDL

•Sources: primarily artificial – industrial hydrogenation of vegetable oils

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105
Q

Glucose Tolerance Test

A

definitive test for the diagnosis of Diabetes Mellitus

2 hr GTT (mg/dL)

≤ 140 Normal

141-199 Prediabetic

≥ 200 Diabetic

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106
Q

Forms of Vitamin A

A

retinol: primary etoh
retinal: aldehyde

retinoic acid: Ts fac

11-cis-retinal: Rhodopsin

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107
Q

Transferrin

A

Fe Transport in blood

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108
Q

Haptoglobin

A

immunoglobulin-like plasma protein that binds hemoglobin

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109
Q

Mature Onset Diabetes of the Young

(MODY)

A

autosomal, dominantly inherited monogenic - @ least 1 fam memb before 25 y/o

Defects in either the transcription factors involved in insulin gene transcription or in energy production (GCK - glucokinase)

  • hepatic nuclear factor 1a (most common) - MODY 3: TCF1
  • glucokinase (common) - MODY 2: GCK

non-obese, mild asymp hyperglycemia

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110
Q

Retinoic Acid

A

nuc horm

binds to RAR: RA-RAR complex = heterodimer to RARE

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111
Q

Which of the following proteins regulates the entry of iron into the bloodstream from the enterocytes as well as from liver and the macrophages of the reticuloendothelial system?

A.Ferroportin (FPN)

B.DMT1

C.Ferritin

D.Hepcidin

E.Transferrin Receptor (TFR)

A

Ferroportin

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112
Q

•Heme Iron : examples

A
  • Hemoglobin
  • Myoglobin
  • Cytochrome P450 enzymes, other cytochromes
  • Cytochrome c oxidase
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113
Q

Metabolic syndrome / X syndrome

A

A cluster of conditions occurring together:

  • increased blood pressure
  • high blood sugar
  • abdominal obesity
  • abnormal cholesterol levels

Increasing the risk of heart disease, stroke and diabetes

Metabolic abnormalities

  • Glucose intolerance
  • Insulin resistance
  • Hyperinsulinemia
  • Dyslipidemia (Low HDL and elevated VLDL)
  • Hypertension
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114
Q

Fed: Absorptive State: effect on glycolysis

A

increase: E from ingested glucose and TCA

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115
Q

BMR increases by with each celcius increase in body temp

A

12%

increases slightly in colder climate due to shiving thermogenesis

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116
Q

In diabetics, the rate of hepatic gluconeogenesis is

A

3-times the normal

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117
Q

Anti-Oxidant

A

Vitamin C

Riboflavin

Vitamin E

β-Carotene

Selenium

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118
Q

Adipose:Fed State:
activiates

A

Uptake of Glucose via GLUT-4(Insulin sensitive)

Glycolysis –> Glycerol-P –> TAG

HMPS –> NADPH

Fatty acid synthesis occurs under high glucose or refeeding after starvation

ØLipoprotein lipase (upregulated by insulin) degrades TAG from chylo and VLDL

  • FA stored as TAG in adipocytes
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119
Q

Brain: Fed State: activates

A

glut-1 (insulin insensitive)

aerobic glycolysis

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120
Q

thiophorase

A

b-ketoacyl-CoA transferase

succinyl-CoA as the CoA donor –> succinate, acetoacetyl-CoA

bypasses the succinyl-CoA synthetase step of the TCA cycle

  • TCA cycle must be running to allow ketone body utilization –> aerobic metabolism –> ATP from acetyl CoA
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121
Q

regulation of metabolism: Substrate Supply

A

(within minutes)
Fed-State

glucose, FA, aa

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122
Q

Liver: GLUT ____

A

2

  • Glycolysis –> PDH –> TCA
  • Glycogen Storage
  • HMPS(PPP) and Malic Enzyme –> NADPH
  • Lipid synthesis –> VLDL –> peripheral tissues
  • Accepts Chylomicron remnants
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123
Q

Regulation of Translation of TFR and Ferritin Synthesis

A

5’-Untranslated region (UTR) of ferritin mRNA and 3’-UTR of TFR mRNA contain stem-loop structures with an Iron Response Element (IRE) sequence which binds IRP

Low cellular iron:

•Binding of IRP to IRE stabilizes TFR mRNA (increased synthesis of TFR) but inhibits ribosomal reading of ferritin mRNA (reduced synthesis of ferritin)

High cellular iron:

•Iron binds to IRP which prevents it from binding to IRE (reduced synthesis of TFR and increased synthesis of ferritin)

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124
Q

Iron Homeostasis

A

body = lots of iron, but very small amts are either absorbed or excreted

liver = maj storage organ for non-heme iron - mainly bound to ferritin

iron lost via intestinal sloughing of muc & skin cells during hemorrhage and sweat

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125
Q

Iron Storage - Ferritin

A

Active form of storage

Apoferritin (iron-free): 24 polypeptide units in raspberry-like cluster

Can contain up to 4500 Fe atoms as Fe3+

Iron enters and leaves as Fe2+

Liver contains ~60% of ferritin in the body

Two isoforms

  • H subunit: 22 kDa, 182 AA (Chr 11, predominant in heart)
  • L subunit: 20 kDa, 174 AA (Chr 19, predominant in liver)
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126
Q

Sibutramine

A

(Meridia)

Serotonin-NE Reuptake Inhibitor

Significant adverse effects:

  • htn and tachycardia: contra for card-condition pt
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127
Q

Anemia-Iron Deficiency

presentation?

causes? (5)

A

Hypochromic, microcytic RBC

Causes

  1. Blood loss - menses, GI patho (colon ca)
  2. Inadeq diet
  3. Malabsorption
  4. preg - increased need
  5. high hepcidin
    • Inflammation - Anemia of chronic disease
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128
Q

Iron Absorption Disorders Related to Hepcidin

A

anemia = iron accum in duodenal enterocyte (ferroportin internalization and degrad)

hemochromatosis: overloaded iron in plasma

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129
Q

Glutamine

A

the major metabolic fuel of the small intestine and immune cells

130
Q

Sources vit A

A

liver

kidney

butter

egg yolk

yellow and dark green veg

131
Q

Diabetes – Complications

A

Heart disease and stroke

Blindness (retinopathy)

Kidney disease (nephropathy)

Nervous system dysfunction (neuropathy)

Susceptibility to infections

Limb amputations

Pregnancy complications

Sexual dysfunction

132
Q

phosphorus

A

phosphate esters of organic intermediates in metabolism, bone mineralization

133
Q

chloride

A

main anion of extracellular and intracellular fluids

134
Q

normal human insulin and manmade insulin

A
  • Normal human insulin has a Pro at position 28 and a Lys at 29 of B-chain
  • Lispro
  • Lys at 28 and Pro at 29
  • •Faster acting, more readily absorbed

•Aspart

  • Asp at 28 instead of Pro
  • •Similar to Lispro

•Glargine

  • Gly instead of Asn at position 21 of A-chain and 2 Arg added to C-terminus of B-chain
  • •Longer acting
135
Q

Regulation of Ketone Body Synthesis

A
  1. Increased supply of fatty acids from adipose triacylglycerols due to H.S. Lipase
  2. Decreased insulin/glucagon ratio –> inhibition ACC –> decreased malonyl-CoA
  3. activates CPTI –> fatty acyl-CoA –> β-oxidation
  4. When enough NADH/FADH2 are generated from β-oxidation for liver ATP needs, acetyl-CoA –> ketogenesis: Acetoacetate, β-Hydroxybutyrate**, (Acetone)
  5. NADH/NAD+ ratio increases :β-Hydroxybutyrate> Acetoacetate
136
Q

Vitamin C

A

ascorbic acid

functions:

  • •Hydroxylation of Pro and Lys in collagen
  • dopamine –> NE
  • trimethyllysine –> carnitine
  • Absorb iron
  • Antiox
137
Q

Importance of Iron in Metabolism

A

cofactor - oxygen and E metabolism

138
Q

Graves disease

A

autoantibodies bind TSM –> activate –> hyperthyriod

  • Increased BMR
  • Enlarged thyroid gland (Goiter), weight loss, fatigue, heat intolerance, increased bowel movement
139
Q

Iron Storage - Hemosiderin

A
  • Inactive storage
  • ~50% Liver iron stores
  • Reacts to ferritin antibodies - likely a degradation product
  • Insoluble, ~30% iron by weight
  • Less available for mobilization (slower release than ferritin)
  • Hemosiderin deposits in interstitial macrophages of the lung are indicative of chronic bleeding
140
Q

Metabolic state of organs: brain: well-fed and starvation

A

ØWell-fed: uses glucose, glycolysis etc,

ØStarvation: uses glucose, ketone bodies, glycolysis and aerobic metabolism

141
Q

a TAG can occupy how much of an adipocyte?

A

entire volume

142
Q

5 phases of glucose homeostatis

A
143
Q

calcium (4)

A

bone and tooth

membrane signal

nerve and muscle excite

coagulation

144
Q

•Fuel composition of the average 70 Kg man after an overnight fast

A

M glycogen: 0.4%

liver glycogen: 0.2%

fat: 85%
protein: 14.5%

145
Q

iron status markers: iron excess

A
  • High serum iron
  • Low or normal TIBC (why?)
  • High % saturation of TF (>50%)
  • High serum ferritin (>250 ng/mL)
  • Liver Fe >2 mg/g
146
Q

Vitamin K sources

A

Cabbage, cauliflower, spinach, egg yolk and liver. Vitamin K is also synthesized in the gut by bacteria

147
Q

Glucose-Alanine Cycle

A
148
Q

Intertissue relationships during fasting/starvation

A

Liver:

  • Out; Glucose/Ketone Bodies,
  • Urea
  • In: Fats from adipose(fuel)
  • gluconeogenic precursors

Muscle:

  • Out:A.A. to liver
  • In: Fats /Ketone Bodies (Fuel)

Adipose:

  • Out:fats/glycerol
  • Fats as fuel

Brain:

  • In:Glucose/Ketone Bodies

Kidney:

  1. In: Fats/Ketone Bodies(fuel)
  2. Out: Glucose/NH4
    3.
149
Q

deficient vit b5

A

fatigue, sleep disturbances, impaired coordination, nausea

150
Q

Deficiencyof Vitamin D can be due to…

A

Inadequate dietary

Malabsorption of lipids

Liver or kidney dysfunction

Hypoparathyroidism

•Lack sunlight

  • Northern latitudes (winter)
  • Excessive sunscreen
151
Q

Synthesis of Vitamin D

A
152
Q

does brain have glycogen stores?

A

no

153
Q

wt reduction and adipocytes

A

adipocytes are not lost, weight loss requires cells to decrease in size

•Adipocytes, that are too small, stop secreting hormones that control appetite

154
Q

Dyslipidemia in Obesity

A
  • The liver releases excess cholesterol and TAGs as VLDLs
  • Elevated serum TAGs
  • HDL levels decrease
155
Q

Alcoholic Hypoglycemia

A

Alcohol - ↑ NADH levels

Gluconeogenesis intermediates diverted to other pathways, leading to

  • ↓ gluconeogenesis
  • ↓ glucose
156
Q

Fed state is the _________ state

A
  • 2-4 hours during and after a meal
  • Nutrients are being absorbed
  • Increase in plasma glucose, a.a. and TAG
  • Increase in Insulin/Glucagon ratio
157
Q

Diabetes may also be suspected by:

A

Random glucose (non-fasting) ≥ 200 mg/dL & symptoms such as

Polyuria (increased urination)

Polydipsia (increased thirst)

Polyphagia (increased hunger)

158
Q

Insulin is degraded by

A

Insulinase

Mostly in the liver

Minimally in the kidneys

Insulin T½ = 4-6 minutes

159
Q

Fats/Lipids functions

A
  • Act as the vehicle for fat-soluble vitamins
  • Supply essential fatty acids
  • Linoleic acid (18:2, N-6/ω-6)
  • α-Linolenic acid (18:3, N-3/ω-3)
160
Q

gluc prod in starvation

A

Renal > hepatic

  • mainly from aa: gln –> glu via gln-ase and GluDH
  • kidneys do not make urea (in LIVER)
  • excrete NH4+ –> to urine as couterion for acids

reachs max as hepatic gng stab

161
Q

Deficiency of Vitamin B2

A
  • Angular stomatitis: Fissures at the corner of mouth
  • Cheilosis: vertical fissuring later complicated by redness and swelling of the lips

Glossitis: •Tongue is smooth, swollen and has purplish/magenta color

•Corneal Vascularization: 2 C’s: Cheilosis and Corneal Vascularization

162
Q

Fenton Reaction

A

Iron is toxic to liver, heart and pancreas

no mech to detox OH radical

163
Q

Type 1 M fibers

A

• slow oxidative fibers(red fibers)

–slow contraction speed (great for marathons)

–specialized for steady, continuous activity

–rich in mitochondria and myoglobin which gives them a red color: aerobic metabolism

Prefers fat as a source of energy

164
Q

Energy Expenditure

A

70% - Resting Metabolic rate

15% - Thermogenesis

  • Food intake
  • Cold
  • Stress

15% - Physical activity

165
Q

Kidney:Fasting State: bufferring

A
  • NH4+ buffers H+ in urine, decreasing the acid load .
  • Long term starvation: this is important function of kidney
166
Q

Metabolic state of organs: adipose: well-fed and starvation

A

ØWell-fed: uses all fuels, stores fat

ØStarvation: uses ketones, degrades fat storage

167
Q

Insulin

A
  • β cells of pancreas
  • Promotes transport of glucose from the blood into cells (Glut4)
  • Inhibits lipolysis of TAG
  • Induces expression of glucokinase, PFK-1 and PK (glycolysis)
  • Stimulates glycogen synthesis in liver and muscle
168
Q

Transferrin

A

iron txp in blood as Fe3+

Chr 3 - iron binding

─Binds 2 Fe3+ and 2 HCO3─

─Normally 25-50% saturated with iron

169
Q

Arginine

A

nitric oxide production

immunostim

170
Q

Insulin Secretion

A

•Pancreatic β-cells express Glut2 transporters

high [glucose] = txp into β-cells —> ATP

•ATP: closes K+ channels = open Ca2+ channels

high [Ca2+] = exocyto insulin

171
Q

calorie

A
  • Amount of energy needed to raise the temperature of 1 g of water by 1°C
  • 1 calorie = 4.185 joules (J)
  • Kilocalorie (Kcal or Cal) = 1000 calories
  • The Calories listed in nutritional tables refer to Kcal!
172
Q

Functions of Vitamin D

A

maint adeq plamsa lvls calcium, phosphate - reabsorption from kid

resorption of bone - maintain proper bone density

173
Q

g-carboxyglutamates

A

prothrombin

good chelators (bonders) of calcium.

prothrombin-calcium complex binds phospholipids = blood clotting on the surface of platelets

174
Q

selenium

A

fx:Glutathione peroxidase

defic sympt: Cardiomyopathy

175
Q

•Under the Fed state, how is glucose transported into the different tissues?

A
  • Liver: GLUT-2
  • Muscle: GLUT-4* Insulin- sensitive
  • Adipose: GLUT-4* Insulin sensitive
  • Brain: GLUT-1
176
Q

zinc

A

fx: muc acid metab

defic sympt: skin lesions, poor wound healing

177
Q

Regulation of Hepcidin Synthesis

A
  • Bone morphogenic protein 6 (BMP6) signaling induces hepcidin synthesis from HAMP gene
  • Involves BMP6 receptor (a serine kinase), HFE, Transferrin receptor 2 (TFR2), Hemojuvelin (HJV), and SMAD complex
  • Mutations in HAMP (Chr 19), HFE (Chr 6), TFR2 (Chr 7), or HJV (Chr 1) decrease the synthesis of hepcidin
  • Excessive iron absorption and release via FPN
  • Hereditary Hemochromatosis
178
Q

Macronutrients: Carbohydrates

A

not essential nutrient: C of most aa –> converted to glucose

absense = ketone bodies, degrad body protein

179
Q

liver metab: 12 hour fasting: basal state

A

maintains gluc 80-100 mg/dL

•Glucagon High —> gng increases

  • •Lactate from Muscle and RBC: Cori cycle
  • •Amino acids from Muscle: Glucose–Alanine cycle
  • •Glycerol from adipose lipolysis –> can be used in gluconeogenesis (Glycerol-Pà Glyceraldehyde 3-P)

•Glycogenolysis is getting limited (~80 g remain~25%)

180
Q

induction of fed state results in….

A

Signal Transduction via MAP Kinase (ERK)

Fatty Acid Synthesis:

  • ATP/Citrate Lyase
  • ACC
  • FAS

Glycolysis:

  • GK
  • PK

NADPH producing Enzymes:

  • G6PDH (HMPS)
  • Malic Enzyme
181
Q

Cardiac Muscle fibers primary use what as a fuel source?

A

Fatty Acids preferred fuel

  • Strictly Aerobic
  • Fats : Beta-oxidation
  • Glucoseàglycolysis (aerobic)àPDHàTCA/ETC
  • Creatine-P stored as energy
182
Q

Complementary Protein Sources

A

two incomplete proteins with complementary amino acids = higher biologic value

183
Q

Defective transport of Trp

A

(Hartnup syndrome) leads to impaired synthesis of niacin

184
Q

Biotin

A

cofac bicarb-dep carboxylations: carries CO2

  • pyr –> OAA
  • propionyl CoA –> methylmalonyl CoA: Odd chain FA

deficiency usually duie to dec util, not diet

  • raw eggs (avidin) - tightly binds biotin & prevents absorption
185
Q

insulin effects are mostly: anabolic/catabolic

A

Major effects are anabolic

−Carbohydrates

−↑ Glucose uptake & glycogen synthesis

−Fat

−↑ fatty acid & triacylglycerol synthesis

−Protein

−↑ Amino acid uptake & protein synthesis

186
Q

does brain do FA metabolism?

A

no: FA cannot cross BBB

187
Q

glycemic index

A

change in blood sugar due to a substance

normalized to glucose (GI = 100), measured for 2-3 hours @ 30min intervals

high = > 70

low = < 55

188
Q

Folic Acid

A

precursor THF

forms of THF synth: gly, ser, met, purines, TMP

189
Q

•Dry Beriberi

A

symmetrical lower peripheral neuropathy

confusion

speech difficulties

vomiting

190
Q

•N-6 fatty acids (ω-6)

A

low LDL and HDL

Sources: Linoleic acid - nuts

191
Q

Glucagon: generally promotes ________ of enzymes

what type of enz have high activity?

A

•phosphorylation

(Signal Transduction via Gs –>cAMP –>PKA)

  • Protein Kinase
  • Glycogen Phosphorylase
  • Phe hydroxylase
  • H.S. Lipase
192
Q

Hypervitaminosis A

A

polar bear liver

Signs & Symptoms:

  • dry and itchy skin, cheilitis (inflammation of the lips), hair loss, nail fragility
  • blurred vision, dizziness, change in consciousness, loss of appetite, headache, irritability, nausea, vomiting
  • enlarged liver, ascites (peritoneal fluid)
  • increased intracranial pressure that may mimic a brain tumor

congenital malformations - in fetus

193
Q

Insoluble fiber

A

cellulose and lignin

lowers blood choles: bind BA and diet choles

increase motility, softens stool: draws h2o

decreased intracolonic P

may reduce risk of colon ca

194
Q

•Holocarboxylase synthase deficiency

A

Biotin

auto-recessive

attaches biotin to lys of biotin carrier protein

•Causes multiple carboxylase deficiency

HADED

hallucinations, alopecia, dermatitis, enteritis, depression

195
Q

Diabetes, Type 1

A

onset in childhood/puberty - sympt dev rapidly

freq undernourished

beta cells of pancreas destroyed

unresponsive to hypoglymeic drugs

insulin is always necessary

196
Q

Regulation of Blood [Glucose]

A

Hormones

  • Insulin
  • Glucagon
  • Epinephrine
  • Cortisol
  • Growth hormone

Nervous System

  • Norepinephrine

Glucose

197
Q

•Liver glycogen

A
  • Used to maintain blood glucose levels between meals
  • Amount fluctuates during the day
  • ~200 g after a meal
  • ~80 g in between meals
198
Q

pancreas: endocrine secretions

A

Insulin

Glucagon

Somatostatin

199
Q

Incretins

A

horm that increase insulin secretion

glucose in GI –>​ oral gluc stim insulin release sooner than IV glucose

incretins

  • GIP - gluc-dep insulinotropic peptide
    • also known as gastric inhib peptide
  • GLP-1: glucagon-like peptide-1

secr by endocrine cells in small intestines

200
Q

Deficiency of Vitamin E

A

premature infants

only in adults with defective lipid absorption/txp

Signs:

  • RBC peroxide Sensitivity
  • abnormal cellular membranes
  • RBC death (hemolysis & hemolytic anemia)

Neurological deficit – loss of deep tendon reflexes, muscle weakness, impaired balance, visual impairment

201
Q

Hypoglycemia

A

Glucose ≤ 40 mg/dL

Resolution of symptoms with glucose administration

•Central nervous system symptoms (due to major dependence of brain on glucose as a fuel source)

  • Confusion
  • Altered mental status
  • Coma
202
Q

Vitamin B12

A

Cobalamin

  • Not in plants, therefore vegans need B12 supplements
  • Methylcobalamin is a cofactor in the conversion of homocysteine to Met
  • Deoxyadenosylcobalamin is a cofactor in the isomerization of methylmalonyl CoA into succinyl CoA
203
Q

During low-intensity submaximal exercise, what is the main source of E?

A

blood glucose and fatty acids

204
Q

•Diabetic Ketoacidosis: complications and tx

A

•Treatment

§Hyperglycemia - Insulin

§Intravenous fluid - Replace lost water

§Monitor electrolyte levels in the body

§Acidosis -Bicarbonate solution intravenously

205
Q

HH type 2

A

HFE2 (HJV)

recessive

parenchymal iron overload, cardiomyopathy

206
Q

biguanides

A

meformin

target: activates AMPK

increase gluc uptake by M, decreases gluc prod in liver

207
Q

Cori Cycle

A
208
Q

Glucagon

A

Produced by α cells of Islets of Langerhans in the pancreas

Contains 29 amino acids

Single polypeptide chain

Conserved sequence in all mammals

Synthesized similar to insulin: requires proteolytic cleavage of a prohormone

209
Q

Regulation of Glucagon Release

A

Stimulation of Release

  • Low Blood Glucose
  • Amino Acids
  • Epinephrine / Norepinephrine

Inhibition of Release

  • Glucose
  • Insulin
210
Q

DM 1 tx

A

An effective insulin regimen

Monitoring of glucose

Appropriate diet and physical activity

211
Q

Vitamin B6

A

pyridoxine

PLP = cofac

  • •Transaminases: Aminotransferases
  • Decarboxylases
  • Glycogen phosphorylase
  • ALA synthase (Heme)
212
Q

Symptoms of Hypoglycemia

A

Adrenergic

  • Anxiety, palpitations, tremor, diaphoresis
  • Usually occur with abrupt onset of hypoglycemia

Neuroglycopenia

  • Decreased glucose delivery to the brain
  • Headache, confusion, seizures, generalized weakness, focal neurological deficits, coma
  • Usually occur with gradual onset of hypoglycemia
213
Q

Wilson’s Disease

A

Mutations in ATP7B gene

  • hepatocytes: Cu –> golgi –> ceruloplasmin –> secr-vesc –> bile cap
    • defective = accumulaties in liver & excess txp to other organs through blood

accumulation Cu in tissues

Liver Disease - onset: late childhood-adoles

  • hepatomeg, acute liver failure

Neuropsychiatric: onset - 20-30 yo

  • Movement disorders, drooling, dysarthria, rigid dystonia, migraines, insomnia, seizures

Others

  • Cardiomyopathy,
  • pancreatitis,
  • Kayser-Fleischer rings,
  • aminoaciduria
214
Q

blood sugar levels:

normal, prolonged fasst, post-meal (postprandial), hyperglycemic

A

normal pre-meal: (70-100mg/dl) 83 mg/dl (4.6 mM)

Prolonged fasting: 65-70mg/dL (3.3-3.9mM)

Post-Meal Blood Sugar (Postprandial)

  • –Under 120 mg/dl (6.6 mmol/L) 1-2 hours after a meal.
  • –Normal metabolism: under 100 mg/dl (5.5 mmol/L) 2 hours after eating

•Hyperglycemic fasting blood sugar >126mg/dl

215
Q

SGLT-2 Inhibitors

A

tx DM2

wt loss, decrease BP, increase HDL

second-line or third-line diabetes therapy

•Canagliflozin, Dapagliflozin

216
Q

Absorption, Transport & Storage of Vitamin A

A
217
Q

manganese

A

fx:Mucopolysaccharide metabolism

defic sympt: Growth retardation

218
Q

Transferrin Receptor

A

fe cellular uptake

219
Q

Simple carbohydrates

A

monosacc, rapidly hydrolyzed oligo/poly

•Digestible: most are polymers of glucose, galactose and fructose with α-glycosidic linkage

220
Q

Adult RDA for protein is higher is whom?

A

Pregnant women

hospitalized patients

221
Q

Central Role of G 6-P is in what organ?

A

liver

222
Q

Vitamin K Deficiency

A

causes Hypoprothrombinemia

  • Deficiency in prothrombin (factor II)
  • Increased coagulation times, bleeding tendency

second-generation cephalosporins (antibiotics) by a warfarin-like mechanism

  • Examples: cefoperazone, cefmandole, and moxalactam

newborn

  • sterile intestines
  • no synth (hemorrhagic disease of the newborn)
223
Q

Diabetes, Type 2

A

insulin resistance high - able to be reduced but not completely reversed

  • key pathophysio fac

beta cells of pancrease unable to produce appropirate quant of insulin

obesity usually present

224
Q

Minerals

A

inorg mol

struc & fx: enz and proteins

225
Q

insulin MoA

A
226
Q

A 50-year old male presents with memory problems, depression, joint pain and fatigue. Skin shows dark spots on ankles and elbows. Serum ammonia, % saturation of TF, serum ferritin, AST and ALT are all elevated. Screening reveals C282Y mutation in HFE. The most likely diagnosis is:

A.Iron deficiency anemia

B.Urea cycle enzyme disorder

C.Hereditary hemochromatosis

D.Transfusion overload

E.Anemia of chronic disease

A

A.Hereditary hemochromatosis

227
Q

General Aspects of Water Soluble Vitamins

A

energy-releasing - usually with coenq fx

no toxic from excess

deficiency symptoms:

  • peripheral neuropathies
  • depression
  • mental confusion
  • loss of coordination
  • malaise

rapid turn over tiss = most at risk of deficiency –> show first symp:

  • Skin
  • GI
  • Immune
228
Q

Definition of Obesity: BMI

A
229
Q

Effects of Glucagon

A

Liver glycogen degradation

Liver gluconeogenesis

Glucogenic amino acid uptake: increase blood glucose

Adipose lipolysis

↑ Free fatty acids

↑ Ketone bodies

230
Q

Signaling by Glucagon

A
231
Q

Gestational Diabetes

A

most = 24-28 weeks of gestaion

results in bigger babies

uncontrolled –> fetal beta-cell hyperglasia –> increased insulin secr –> postnatal hypoglycemia

232
Q

diets high in _________ have low levels trp and absorbable niacin

A

untreated corn

233
Q

pancrease: exocrine secretions

A

Dig Enz:

  • Proteases
  • Lipase
  • Amylase

HCO3-

234
Q

Types of Hypoglycemia

A

Insulin-Induced

  • missed a meal & took insulin or insulin overdose

Post-Prandial: exaggerated insulin release

  • Insulinoma

Fasting

  • Decreased glucose production
  • liver disease, alcohol

Increased glucose metabolism

  • sepsis
235
Q

Deficiency of Vitamin B1

A

2 manifestations:

  • •Cardiovascular disease (Wet Beriberi)
  • •Nervous system disease (Dry Beriberi and Wernicke–Korsakoff syndrome)
236
Q

Priorities of Metabolism
during Fasting State

A
  • Maintaining blood [glucose]
  • Mobilizing f.a. from adipose
  • Synthesizing ketone bodies
  • Minimizing protein catabolism
237
Q

rough est BMR

A

24 x wt in kg (kcal/day)

Harrist-Benedict eq = most used by overest by about 5% - less accurate for: young, old, obese

238
Q

Fed: Absorptive State: effect on enz

A

•Most enzymes are dephosphorylated

239
Q

Benefits of Dietary Fiber

A

metab to butyrate: major fuel of colonocytes

dec:

  • constipation
  • hemorrhoids
  • absorption diet fat/choles
  • prostprandial blood gluc concentration

increase:

  • bowel motility –> decreases gut to ca
  • fecal loss of choles

delays:

  • gastric empty –> sense of fullness
240
Q

NAD+ controls ….

A

respiration

e-carrier

  • NADH/NADPH act as reducing agents
  • NADPH protects against ROS
241
Q

Iron storage

A
  • Iron is stored bound as Fe3+ to Ferritin or Hemosiderin in liver, spleen, bone marrow, duodenum and skeletal muscle
  • Iron is readily released as Fe2+ from ferritin when needed
  • Iron release from hemosiderin is very slow
  • Ferritin is slight in excess of hemosiderin when body iron levels or normal or low
  • The amount of hemosiderin relative to ferritin increases in iron overload
242
Q

•Bone disorders: vit D

A
  • Rickets in children
  • Poor growth
  • Skeletal deformities
  • Osteomalacia in adults
  • Pathological fractures
243
Q

Vitamin E

A
  • α-Tocopherol = most active
  • γ-Tocopherol = major form: diet and in supplements

anti-ox

least tox of all fat-sol vit

244
Q

iron

A

txp: O2, e-

redox

245
Q

Weight should be lost at a rate of

A

1 to 2 pounds per week, based on a caloric deficit between 500 and 1,000 kcal/day

246
Q

In healthy patient, kidney reabsorbes how much glucose

A

180

247
Q

Fat Soluble Vitamins

A

efficient absorption = bile salt micelles in small intestine

can toxicity lipid rich areas: N, adipose, liver

  • Vitamin A (Retinal, Retinol)
  • Vitamin D (Calcitriol)
  • Vitamin E (α/γ-Tocopherol)
  • Vitamin K (Phyllo/Menaquinones)
248
Q

•Muscle glycogen

A
  • Supplies energy for muscle contraction
  • 400 g of muscle glycogen at rest
249
Q

Early Refed State

A

Ø Liver remains gluconeogenic for a few hours after refeeding –>G6P–> replenish Glycogen

Ø A.A. also used to replenish glycogen stores

ØGluconeogenesis then decreases

ØGlycolysis then increases

ØGlycogen stores maintained by blood glucose

250
Q

Therapeutic Actions of Vitamin A

A
251
Q

Hashimoto thyroiditis

A

autoantibodies attach thryoid –> destroy ability to synth throid horm

  • Decreased BMR
  • Fatigue, modest weight gain, cold sensitivity, constipation
252
Q

Diminished synthesis of purines and TMP =

A

•erythropoietic differentiation and causes megaloblastic anemia

253
Q

Absorption of Dietary Iron

A

Heme Iron

  • •Constitutes 15% of iron in a mixed diet
  • Fe2+
  • •5-25% absorbed

Non-heme iron

  • 85% of iron in a mixed diet
  • Fe3+
  • •2-5% absorbed
    • enhanced by acsorbate (Vitamin C)
    • inhibited by phytate (myo-inositol hexakisphosphate), polyphenols, and calcium
254
Q

Glucagon

A

α cells of pancreas

  • Promotes lipolysis of TAG to deliver fatty acids to the liver
  • Promotes gng in the liver
  • inducing expression of PEP carboxykinase
  • activation of F1,6-BPase
  • inactivation of PFK-1 and pyruvate kinase (PK)
255
Q

Metabolic state of organs: liver

well-fed and starvation

A

ØWell-fed: stores glycogen, glycolysis, uses all fuels

ØStarvation: degrades glycogen, gluconeogenesis, ketogenesis, uses fats

256
Q

Zn Deficiencies

A

1st signs

  • Dermatitis
  • poor wound heal
  • periorificial lesions

Affects:

  • immune
    • cytokines(IL-2) - reg T lymphocytesL Cd4 helper, NK
  • Heme synth:
    • lead poisoning: lead replaces Zn in ALAD (heme synth) –> buildup ALA
  • taste (children)
    • gustin - taste bud dev
  • tx Wilson’s disease
    • penicillamine chelation
257
Q

Cysteine

A

detoxification (GSH)

taurine production - bile salt synth, osmotic reg

258
Q

Neuropeptide Y

A

•(NPY) is an orexigenic (appetite-stimulating) signal

stim by ghrelin: gastric horm

inhib by:

  • leptin - adip
  • cck - sml intes
  • peptide YY (pyy) - colon
  • insulin - pancreas
259
Q

HH type 3

A

TFR2 (HFE3)

recessive

parenchymal iron overlaod, cirrhosis

260
Q

Muscle:Fed State: activates

A

GLUT-4

  • reduce blood glucose after a meal

Glycolysis

Glycogen Synthesis

Uptake of fats from Chylo and VLDL

  • Fatty acids are secondary to glucose in feeding

Uptake of amino acids

  • especially branched chain a.a. (Leu, Val Ile) via branched chain transaminase (Vit B6)

Protein synthesis to replace any degraded proteins since previous meal

Synthesizes Creatine-P as a phosphagen

261
Q

Factors That Affect BMR (5)

A
  1. gender: men > women (women = fatter)
  2. body temp: higher > lower
  3. ambient temp: lower temp > higher (due to shivering)
  4. age: children > adults
  5. hormones: thyroid, GH, epi, cortisol
262
Q

Complex carbohydrates

A

slowly hydrolyzed oligo/poly: composition or non-dig structures

263
Q

Metabolic state of organs: M: well-fed and starvation

A

ØWell-fed: stores muscle glycogen, glycolysis, uses all fuels

ØStarvation: degrades glycogen, can degrade protein, uses fats and ketone bodies

264
Q

regulator of ferroportin

A

HAMP (chr 19) –> Hepcidin – (-) –> FPN –> lyso –> degrad

enterocytes, macrophages and liver

excess = low serum [iron] by inhib release

deficiency = increases iron uptake = high serum [iron]

265
Q

Vitamin D active form

A

•1, 25-Dihydroxycholecalciferol - calcitriol

266
Q

Hereditary Hemochromatosis

A

abnorm high absorption over many years - iron overload

auto-recess in mut of HRE, HJV, HAMP, TFR2 (reduced synth of hepcidin)

auto-dom in mut of FPN (prevent interaction with hepcidin)

Iron accumulation and failure of liver, heart, pancreas (ROS)

  • hemosiderosis: accum hemosiderin

Treatment – phlebotomy, chelation

267
Q

•Wernicke’s encephalopathy

A
  • severe acute deficiency
  • neurological damage
  • horizontal nystagmus, ptosis, ataxia, confusion

B1

268
Q

Under Activation of the MAP Kinase pathway via Insulin, which of the following enzymes would be induced?

A.Glucose 6-Ptase

B.Phosphoenolpyruvate carboxykinase

C.Pyruvate carboxylase

D.Glucokinase

E.Fructose 1,6-bisPtase

A
  • Glucokinase:
  • Insulin induces the synthesis of glucokinase in glycolysis during higher [glucose] concentrations and represses enzymes in gluconeogenesis
269
Q

sulfonylureas

A

glipizide, glyburide, glimepiride

–> panc beta-cells –> blocks K+ channels –> stim insulin secetion

270
Q

•Which of the following enzymes would be induced/activated under low insulin/glucagon ratio?

A.Glucokinase

B.PFK-1

C.PEP carboxykinase

D.Acetyl-CoA carboxylase

E.Lipoprotein lipase

●

•

A

A.PEP carboxykinase

271
Q

Fat Soluble vs Water Soluble Vitamins Chart

A
272
Q

Leptin and Obesity

A

adipocyte-derived hormone

  • Total leptin deficiency causes obesity
  • Treatment with leptin normalizes the body weight of such patients
273
Q

Adipose:Fasting State

A
  • No Glucose uptake(GLUT-4 Insulin sensitive)
  • No TAG synthesis from Glucose
  • Increase Lipolysis
  • HSL activatedà degradation of TAG
  • Elevated norepinephrine and epinephrine activates HSL
  • Fatty acids released into blood bound to Albumin –> tissues(not used as main fuel)
  • Glycerol from TAG –> sent to liver for gluconeogenesis
  • Ketone Bodies serve as main fuel during fasting
  • TAG can last as a fuel source 2-3 months during starvation
274
Q

Hyperinsulinemia

how to tell if due to exo or endo insulin?

A

hypoglycemia

C-peptide levels in blood

−Correspond to those of insulin if all of the insulin is of endogenous origin

−Insulin levels much higher than those of C-peptide if the insulin is of exogenous origin

275
Q

Lactoferrin

A

fe Transport in milk, tears

276
Q

synth insulin

A

1/2. genes Ts, TL

  1. elong directs polypeptide chain into lumen of RER –> forms preproinsulin
  2. cleavage: proinsulin formed in cisternal space (lumen)
  3. txp to golgi: cleaved –> insulin + c-peptide

6/7. secretory granules –> exocytosis

277
Q

t(1/2) vit d =

A

2-4 hours

278
Q

Signs and Symptoms of Diabetes

A

Frequent urination (polyuria)

Excessive thirst (polydipsia)

Extreme hunger (polyphagia) - Cells are starved for energy

Unexplained weight loss - Insulin can not trigger the storage of fat

Fatigue

Delayed wound healing

279
Q

Ferritin

A

fe active storage

280
Q

Type 2B

A

•fast glycolytic fibres:White

– fast contraction speed

–Used for brief maximal efforts: weight lifting; sprinting

–have few mitochondria and little myoglobin: white

–anaerobic metabolism of glucose –> lactic acid

–Cori Cycle: lactate –> liver

281
Q

Allosteric Regulation: Fed-State

A

(Short-Term Regulation-minutes)

282
Q

•Insulin resistance can develop as a result of

A
  • Inflammation
  • Lipid overload
  • Interference with insulin signaling
  • increase in Ser/Thr phosphorylation of IRS and a decrease in Tyr phosphorylation
283
Q

Diabetic Cataract

A

gluose –(aldose reductase)–> sorbitol = increased P

no sorbitol DH = DM complications

284
Q

copper

A

fx: ox enz

defic sympt: anemia, skel defects

285
Q

Ketoacidosis can appear …

max severity @

A

overnight fast; reaches maximum severity in 3 to 14 days of starvation

286
Q

Maternally inherited diabetes with deafness

A

a defect in the mitochondrial tRNAleu gene that causes decreased ATP production in pancreatic β-cells

287
Q

Bariatric Surgery - Bypass

A

large portion of stomach and duodenum bypassed

No “cheating” possible because of side effects of introducing undigested food into jejunum

288
Q

iron status markers: Iron Deficiency

A
  • Low serum iron
  • High TIBC
  • Low % saturation of TF (<25%)
  • Low serum ferritin
  • Bone marrow aspiration and staining of macrophages for Fe is negative
  • Low Hb
289
Q

Adipose:Fed State: inhibits

A

ØLipolysis (TAG breakdown) by Hormone-Sensitive Lipase: (inhibited by Insulin due to àdephosphorylated form of the enzyme)

290
Q

•Wet Beriberi

A

peripheral edema:

  • tachycardia
  • cardiomegaly/myopathy
  • CHF

infantile

  • •During breastfeeding by thiamine deficient mothers
  • Rapid onset of tachycardia, vomiting, convulsions
  • High fatality rate
291
Q

Renal Glucose Reabsorption:

A

•Kidney: SGLT-2, SGLT-1: Glucose reabsorption

ØSGLT-2:

  • • In Proximal Convoluted Tubule (PCT)
  • • Reabsorbs ~90% of filtered glucose

ØSGLT-1:

  • •In Proximal Straight Tubule (PST)
  • •Reabsorbs ~10% of filtered glucose

Ø20 active transport:Na/K ATPase

292
Q

Glucose-Alanine Cycle

A
293
Q

•Monounsaturated Fats

A

lower choles/LDL

higher HDL

decreased risk CHD

mediterranean diet: olive & fish oil - low LDL

294
Q

Hemopexin

A

plasma protein with high affinity for Heme

295
Q

GLUT-1:

A

BBB

296
Q

Fasting blood glucose levels:

A
  • Normal < 100 mg/dL (< 5.6 mM)
  • Prediabetic 100-125 mg/dL (5.6-6.9 mM)
  • Diabetic > 126 mg/dL (> 6.9 mM)
297
Q

Induction of Hepcidin synthesis

A
  • Increased iron stores and also by inflammation (mediated by IL-6)
  • Leads to decreased iron absorption and release via FPN
  • Anemia of chronic disease
298
Q

iodine

A

thyroid hormones

299
Q

what happens to acetyl-coa during fasting states?

A

acetyl-coa –> ketone bodies

instead of going into TCA

not used in liver since deficient in thiophorase

300
Q

Deficiency of Vitamin C

A

smokers require more vit C than non-smokers

deficiency:

  • scurvy
    • sore,spongy gums
    • petechaie (purple hemorr spots)
    • bruising, poor wound healing
301
Q

chromium

A

fx: gluc metab

defic symptom: impaired gluc metab

302
Q

Type 2A M fibers

A

• fast oxidative-glycolytic fibres (mixed 1 and 2:red fiber)

–fast contraction speed

–rich in mitochondria and myoglobin

aerobic metabolism:use either glucose/fats

303
Q

Kidney:Fasting State

A

gng:

  • prolonged fasting –> kid = 50% blood gluc production
  • BCAA from muscle picked up by kidney
  • Alpha-KG = skeleton
  • Some of this glucose can be used as a fuel by kidney
304
Q

Transfusion overload - iron

A

Frequent transfusions secondary to chronic hemolytic anemia (e.g., Sickle cell disease)

Treatment: IV administration of iron-chelator (e.g., deferroxamine, deferasirox)

305
Q

Use of Ketone Bodies by Skeletal Muscle

A
306
Q

Ceruloplasmin

A

serum also acts as ferroxidase to oxidize Fe2+ to Fe3

307
Q

BMI

A
  • BMI is defined as body weight/(height)2
  • Kg/m2
  • (703 x lb)/in2

•

  • Underweight < 18.5
  • Normal range 18.5-24.9
  • Overweight 25.0-29.9

Obese ≥ 30.0

308
Q

During high-intensity isometric exercise, what provides E?

A

phosphocreatine and anaerobic glycolysis

309
Q

Definition of Fasting States

A

Early Fasting: ~4hours after eating

Basal or post-absorptive : ~12 hr (overnight fast)

Brief Fast: 1-2 days

Short term starvation:3-14 days

Long-term starvation:14-60 days

310
Q

most enz in the fasting state are….

A

phosphorylated

311
Q

GLP-1 modulators

A

exenatide, stiagliptin

target: glucagon-like peptide -1 (GLP-1), dipeptide protease IV

increase insulin secr by panc

312
Q

tx •Wernicke-Korsakoff Syndrome

A

admin thiamine

complete recovery unlikely form Korsa

313
Q

Fuel Sources used by Brain
During Starvation:

A

Glucose reduce to less than 1/3 consumption
Ketone Bodies almost 2/3 of fuel consumption

314
Q

Covalent Modification: Fed State

A

(Short-Term Regulation-min/hrs)

•Insulin: generally promotes dephosphorylation

liver:

  • •Low activity of protein kinase
  • •High activity of phosphoprotein phosphatase
  • •Low activity of glycogen phosphorylase a
  • •High activity of Branched-chain a-Keto acid DH
315
Q

•N-3 fatty acids (ω-3)

sources?

A

low:

  • TAG
  • thrombosis
  • BP
  • CHD

Little effect on LDL or HDL

•Sources: α-linolenic in plants; (DHA), (EPA) in fish oils

316
Q

Vitamin B5

A

pantothenic acid

precursor: CoA
* from pantothenic acid, cysteamine, atp

activated carrer acetyl (C2) units: acetyl CoA

317
Q

sulfur

A

bile acid conjugation, connective tissue biopolymers

318
Q

vit k toxicity

A

giving too much to newborn

hemolytic anemia and jaundice

319
Q

Vitamin B3

A

niacin

synth from trp

precursor: NAD, NADP

320
Q

Non-digestible carbs

A
  • Polymers with linkages for which no hydrolytic enzyme is present.
  • Often major components of fiber
321
Q

Regulation of Body Weight

A

“set point” - behaviour & environmental changes

  • Sedentary + increased caloric –> obesity

polygenic

  • obese parents = higher chance to be obese

Biochem Year 1 (3 decks)

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