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DEMS > Metabolism Pathways > Flashcards

Metabolism Pathways Flashcards

1
Q

effect of niacin

A

best HDL increase, but no evidence of use in treatment.

would rather use exercise, sustained weight loss, alcohol,, stop smoking

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2
Q

Tendinous Xanthomas

A

Lipid deposits in achilles and extensor tendon of hands

seen with high cholesterol.

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3
Q

Glucocerebroside

A

sphingolipid

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4
Q

Glycerol P dehydrogenase

A

converts Dihydroxyacetone phosphate into glycerol Phospate in liver and adipose

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5
Q

Colestipol

A

bile acid sequestran

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6
Q

Steps in Glycogen synthesis

A

G6P -(phosphoglucomutase)-> G1P–> UDP Glucose - (glycogen synthase-> Glycogen

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7
Q

Polyolpathway

A

Aldolase reductase enzyme that converts glucose to sortitol and fructose to muck up the cell
found in lens of eye, periocytes, nerves, kidney
Tx: aldose reductase Inhibitor

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8
Q

Fatty Acid alpha hydroxylase

A

hydroxylates phytnic acid at alpha C before entering intoo Beta oxidation

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9
Q

SREBP

A

Steroid Regulatory element binding protein
sequestered in the ER when cholesterol levels are high to inhibit transcription of HMG CoA Reductase in Cholesterol synthesis.
Released from ER when cholesterol levels are low.

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10
Q

Risks of Recombinant insulin

A

variable absoprtion, does not mimics insulins release into portal vein as from pancreas

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11
Q

polyols

A

alcohol sugars
sorbitol, mannitol, hydrogenated starches.
don’t get absorbed.

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12
Q

Short acting insulin onset, peak, duration

A 
onset: 30-60 minutes (0 for IV)
peak 2 hours
duration: 6-8 hours
must take 30 minutes prior to eating
Route: SQ or IV
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13
Q

Growth hormones

A

released from anterior pituitary and is reelased by hypoglycemia and stress.
increase lipolysis, and favors using lipids over proteins.

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14
Q

does lowering TG reduce CV death/events?

A

not yet! still not shown in scientific study

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15
Q

Ratio of TG to cholesterol in lipoproteins

A

Chylomicrons 10:1
VLDL 5:1
Remnants 1:1
LDL TG

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16
Q

when does glycogenolysis occurs

A

4 hours after meal

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17
Q

3- Hydroxybutyrate dehydrogenase

A

form 3-hydrozybutyrate from acetoacetate.

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18
Q

FDA approved use of Omega 3 FA

A

TG >500

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19
Q

What energy source is used for Cholesterol synthesis

A

NADPH and ATP

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20
Q

Detemir (levemir)

A

long acting insulin - extra FA chain so binds to albumin to have slower peripheral distribtuion
12-20 hours duration

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21
Q

How does a small H+ gradient play out?

A

Increase respiration due to increased Oxygen consumption

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22
Q

HIgh intesnsity statins

A

Atorvostatin, Resuvastatin

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23
Q

Mixed Function oxidase

A

adds double bonds to Palmitic acid to make unsaturated

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24
Q

what is produced from TCA cycle

A

3 NADH, 1 FADH2, GTP

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25
Q

pathogenesis of high TAGs

A

lipolytic toxic hypothesis: increased LPL action to release lipolysis productions and increase adhesion, inflammation and coagulation.

2) remnant entry into subendothelial space to cause foam cell foramtion

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26
Q

Cholesterol Ester transfer protein

A

CETP

transfers CE to and from Triglyceride rich VLDL, IDL aand LDL.

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27
Q

PCSK -9

A

protein kinase that binds to LDL receptor that decrease recycling and promotes lysosomal degradation.
GOF mutation causes increase LDL
LOF causes decreases LDL

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28
Q

Fructose

A

does not increase glucose levels, but has affect on liver to cause insulin resistance., increase TG in blood, increase visceral adipose.
Fructose enters glycolysis after phosphofructokinase so it is not subject o regulation.

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29
Q

Thiolase

A

4th step in beta oxidation - cleavage
Releases Acetyl CoA
Transferes short FA chain for more Beta Oxidation

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30
Q

SE of bile sequestrants

A

GI symptoms - N, V, blaoting, constipation
Contraindicated with high TG >300
DDI: binds to warfarin and thyroid hormones, BB thaizides

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31
Q

ADRs of GLP1 agonist?

A

Nausea, pancreatitis? Pnacreatic CA?

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32
Q

Fructose 1 phosphate

A

made via fructokinase

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33
Q

Insulin actions - liver

A

Glygcogen synthesis and fat synthesis, does not increase uptake

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34
Q

what decrease risk of diabetes

A

High carb, low calorie diet
lifestyle changes (weight loss)
Mediterranean diet

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35
Q

Statins

A

Inhibitors of HMG CoA reducase in cholesterol synthesis to increase LDL receptor and catabolism of LDL.

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36
Q

Loss of CETP

A

increased HDL

protective against atherosclerosis.

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37
Q

Adenosine binding casette prtoein A1

A

ABC A1

facilitates uptake of cholesterol from plaques into HDL

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38
Q

Beta hydroxy-CoA dehydrognase

A

Rx3 in beta oxidation - dehydrognation

creates double bond with oxygen (instead of alcohol)

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39
Q

Lomitapine

A

MTP inhibition to decrease liver TG incorporation in VLDL and blocks apoB48 in gut
ADRS: steatorrhea

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40
Q

Aldolase

A

converts Fructose 1 phosphate to glyceraldehyde3 phosphate and dihydroxyacetate.

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41
Q

Lipemia Retinalis

A

chylomicrons in vessesl of eye

associated with high TG

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42
Q

Undiagnosed T2D

A

28%

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43
Q

Secondary prevention of T1D

A

No difference with parenteral insulin

Oral insulin delays the progression of autoantibodies to create protective T cells

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44
Q

ADRs of Ezetimibe

A

None!

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45
Q

Branching enzyme

A

works alongside glycogen synthase to increase branching.

More branching increases solubility and increases sites of synthesis

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46
Q

Ganglioside

A

sphingolipid

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47
Q

duration of insulin: Glargine, detemir, degludec

A

Detemir (12-20) < Glargine 24 hr < Degludec 42 hrs

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48
Q

Pathogenesis of T1D

A

genetic predisposition
environmental trigger that causes autimmune attack (t cell) to Beta islet cells
Develppnent of AutoAntibodies with loss of phase 1 insulin release
progresses to clinical onset of diabetes

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49
Q

Short acting Insulin

A

Humulin R, Novulin R

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50
Q

Aldolase

A

Converts Fructose 1 phosphate into Glyceraldehydate and dihydrozyacetone P

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51
Q

Glycemic Index

A

representative of the amount of glucose excursion in response to the ingestion of starch.
small - small glucose release
large - large glucose release, and more insulin release - potenial for more health affects
determined by area under the cruve of blood glucse vs. time - compared to a standardized sample.

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52
Q

Hexokinase vs Glucokinase

A

Hexokinase is present in all tissues, while glucokinase is only present in liver and beta cell
Hexokinase has a low Km (low affinity), while glucokinase has a high Km (so high affinity
Hexokinase has low VMax and Glucokinase has high VMax
These variations make it so, at high glucose concentrations, glocokinase can be active and liver can take up the most glucose.

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53
Q

acquired low HDL

A

diet - increased carb, obesity
Drugs: BB, diuretics, sex steroids
hyper TG, lifestye, sedentary, smoking

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54
Q

Basic outline of TCA cycle

A

Acetyl coA –> Citrate –> alpha-ketoglutarate –> SuccinylcoA –> Succinate –> Fumarate –> malate –> Oxaloacetate

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55
Q

SGLT1 and 2/ Na/Glucose transporter Inhibitors

A

GLIFLOZIN endings
blocks SCLG1 and 2 in proximal tubule of kidney to lower threshold for glucose reabsorption. causes glucosuria.
loss of 100g or 400 cal of glucose per day.

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56
Q

Where does Fatty acid oxidation take place

A

Mostly in the mitochonrial matrix

some in the peroxisome (LCFA and Branched FA)

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57
Q

Inhibitiors of insulin release

A

diazoxide, somatostatin,

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58
Q

Methylmalonyl CoA Mutase

A

rearrangment of methylmaonyl CoA L to succinyl coA.

Requires VB12 as coenzyme.

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59
Q

cheap DM meds

A

Metformin, Sulfonyluria, Insulin

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60
Q

Types of phospholipids

A

Glycerophospholipids and sphingolipids

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61
Q

PKC pathway in T2D

A

due to IRS phosphorylation of Serine, to increase DAG, Advanced glycogenic end products, oxidative stress.
to increase collagen formation, adhesion molecules, clotting factors, VEGF, and decrease NO

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62
Q

Pathogenesis of atherosclerosis

A

LDL gets into subendoethlial space to produces oxidized LDL, macrophage release of cytokines and chemokines, the development of FOAM cells.

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63
Q

Fate of OAA in cytoplasm

A

must be converte back to malate and pyruate to enetery back into the mitochondria.

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64
Q

Arachidonic Acid

A

formed from elongation of Linoleic acid (dietary intakeO to form prostaglandins, thromboxanes, leukotriens.
by COX enxymes

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65
Q

what lowers TG?

A

Fibrates, Omega 3 FAs, Niacin, high dose statins (no low)

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66
Q

how much does diabetes increase risk of CV disease

A

2-4x - increased to equivalent of normal person with one MI

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67
Q

what drugs promote weight loss for DM?

A

GLP1 agonists, SGLT1 Inhibitors

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68
Q

Glucagon secretion

A

regulated with hypoglycemia

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69
Q

Peroxisome oxidation

A

Long chain FA and Branched FA underge same reactions with beta oxidation with unique enzymes until they are medium size and are exported for beta oxidation.

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70
Q

Humalog

A

rapid acting insulin
Lispro
28th lysine switched with 29th amino acid proline

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71
Q

LDL purpose

A

delivers hepatic cholesterol to peripheral tissues.
form from modification of VLDL by lipoprotein lipase
Taken up by LDL R via endocytosis.
contains B100

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72
Q

Effects of bile acid sequestrant

A

decrease LDL by 10-30%, increase HDL by 3-5%, increase TG by 5-30%

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73
Q

Ceremide

A

springosine + FA

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74
Q

Ezetimibe mechanism

A

Selective inhibition of cholesterol absorption by binding to NPC1L1 at brush border to decrease liver cholesterol and increase LDL R

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75
Q

Where is ATP or GTP required in gluconeogenesis

A 
Pyruvate carboxylate (2 ATP)
Phosphoenolpyruvate carboxykinase (2GTP)
Conversion of PEP to F16BP (2 ATP and 2 NADH)
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76
Q

Risks of Statins

A 
Biggest is myopathy 
1) Myalgia muscle pain 10-20%
2) Myositis (increase creatinine kinase 2.5%)
3) rhabdo very high CK, less than .1%
New onset T2D (10%)
elevated AST/ALT small risk
rare cognitive impariment
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77
Q

Retinopathy

A

1 cause of blindness

in 10years 90% will have retinopathy
high glucose decreases pericytes blood flow regulation to cuase thickeneing of BM, leakage of soft and hard exudates, hypoxia, and Growth in middle of eye.
Neovascularzation and proliferative retinopathy.

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78
Q

Goals of T1D treatmetn

A

1) Increase glucose transport
2) decrease glucose production - glycogenolysis or gluconeogensis)
Decrease hormone senstive lipase that promotes FFA metabolism and ketone generation
Done via Insulin!

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79
Q

other LDL lowering drugs

A

Bile acid sequestrant/Resins
Exetimibe
Plant sterol
PCSK9 inhibitors

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80
Q

Nephropathy

A

primary cause of kidney failure
35% of those with DM develop this
associated with long preclinical phase with normal GFR, but proteinuria is marker for serious renal disease.
5-10% require dialysis, 20% on dialysis will be alive within 5 years

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81
Q

Pyruvate dehydrogenase

A

converts pyruvate into acetyl co-A
Produces NADH
Activated by Insulin, Ca, ADP
Inhibited by ATP, NADH, Fatty Acids

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82
Q

Use of rapid acting insulin

A

used for prandial therapy and correctional - when pre meal hyperglycemia occurs

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83
Q

Degludec (tresiba)

A

longa acting insulin

42 hours duration

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84
Q

LDL source

A

VLDL metabolism

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85
Q

Fenofibrate ADRs

A

Rash, myopathy, increase liver fxn tests, increase Cr (reversible)

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86
Q

Effect of ezetimibe

A

15-20% reduction in LDL

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87
Q

ADRs of DPP4 I?

A

URI, pharyngitis, allergic rxn

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88
Q

ADRS of niacin

A 
Severe skin rash
moderate/severe liver disease
Hyperuremia
PUD, or IBD
impaired glucose tolerance
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89
Q

second step of fat biosyntehsis

A

Conversion of acetyl coA to malonyl coA by actyl coA carboxylase in cytoplasm

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90
Q

NPH Novulin N

A

Int. Acting insulin

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91
Q

diabetic fasting glucose

A

> 125

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92
Q

What regulates phosphofructokinase 1?

A

Activated by: Fructose-2,6, bisphosphate and AMP (insulin)

Deactivated by: ATP and citrate (from TCA cycle)

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93
Q

Glucose lowering ability - highest to lowest

A

metformin and insulin> Sulfonylura > SGLT1/2I> TZD, GLP1A, DPP4

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94
Q

GLP1

A

an incretin
produced from L cells in the intestine.
Stimulated by contents in the gut lumen to potentiate insulin release
Acts on Membrane associated receptrs on beta cells to decrease glucagon, potentiate insulin, decrease apetite, increase Beta cell proliferation, increase gastric emptying.

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95
Q

phosphatidylcholine

A

glycerophospholipid

found in surfactant

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96
Q

how often should LDL be measured

A

> 20 years fasting lipid panel every 4-6 years

measure Choelsterol, HDL, TG and calcualte LDL

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97
Q

Apo C2

A

Lipoprotein Lipase Cofactor

Found on chylomicrons, VLDL and HDL

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98
Q

Genetic causes of high TG

A

familial chylomicronemia -due to mutations in LPL, APoC2, GP1HBP

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99
Q

phosphoglucomutase

A

regulates conversion of Glucose 6 phosphate into glucose 1 phosphate and in reverse in glycogen synthesis and metabolism.

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100
Q

Glycogen phosphorylase

A

enzyme the converts glycogen into G1P
Activated by Ca, AMP, Glucagon and Epinephrine
Inhibited by ATP, Insulin and protein phosphatase 1

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101
Q

how do you calculate LDL

A

LDL = Total cholesterol - (HDL + TG/5)

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102
Q

Oligomycin

A

prevents ATP synthesis so NADH and FADH2 build up

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103
Q

Fructokinase

A

converts Fructose into Fructose 1 phosphate

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104
Q

NPH Humulin N

A

Int. Acting insulin

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105
Q

Lipoprotein lipases

A

on endothelium that degrades TAGs into 2 fatty acids and monoacylglycerol and remnant.
involved in both chylomicron and VLDL pathway.

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106
Q

Glucose-6 phosphotase

A

Enzyme that converts G6P to glucose.

Only found in liver and kidney ER

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107
Q

Glycolipids

A

also glycosphingolipids
spingosine + FA + Mono or oligosacchardies
found in CNS

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108
Q

Hexosamine Pathway

A

from Fructose 6 Phosphate in glycolysis.

Leads to O-glycosylated glucose to muck up cell

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109
Q

what is average value of LDL

A

116

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110
Q

how is the ETC linked to the TCA cycel

A

via the Succinate to Fumerate linkage in complex 2

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111
Q

Potentiators of insulin release

A

increase insulin in presence of glucose (GLP1, ACh)

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112
Q

Diabetic OGTT

A

> 200

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113
Q

Glut 4 vs Glut 2

A

Glut 4 is the glucose transporter for insulin sensitive tissue like muscles and adipose
Glut 2 is the glucose transporter for insulin insensitive tissue like liver and pancreatic beta cell

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114
Q

Zellweger syndrome

A

defect in peroxisomal biogenesis which leads to accumulation of pytantic acid and ether linked glycerol lipids

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115
Q

pathogenesis of T2D

A

Genes, Obesity, inactivity and age all lead to insulin resistance to decrease tissue response to insulin to decrease glucose uptake and cause hyperglycemia.
Hyerglycemia - signals for more insulin so hyperinsulinemia and decrease glucose transport - both of which potentiate Insulin resistance.
Hyperglycemia also overwhelms Beta cells and impairs their function
hyperinsulinemia and impaired Beta cells leads to post-receptor defects that poteniates insulin resistance.
Impaired beta cells occurs due to genetic predisposition, glucotoxicity, and lipotoxicty that potentiate decreased insulin release and hyperglycemia.

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116
Q

who is cholesterol formed

A

acetyl coA into Acetoacetyl CoA into HMGCoA by HMG CoA Synthase (like ketogenesis). Except HGM CoA is then made into Mevalonic acid by HMG coA Reductase. This goes through Geranyl pyrophosphate and farnesly pyrophosphate to form cholesterol

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117
Q

structural changes in insulin (rapid acting)

A

formation of monomers faster to decrease hexamer formation and promote fast absorption in the blood.

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118
Q

DPP4 Inhibitors

A

GLIPTIN endings

increase the T1/2 of endogenous GLP1 and GIP

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119
Q

ATP citrate lyase

A

converts Citrate to oxaloaceteate and acetyl coA in the cyto.
Requires ATP and CO-A

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120
Q

Thiophorase

A

converts acetoacetate into acetoactyl-CoA in ketogenesis.

only found outside liver!

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121
Q

Fenofibrate

A

fibrate, TG lower agent

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122
Q

Chylomicron purpose

A

deliver dietary TG to peripheral tissue
deliver Cholesterol to liver in chylomicron remnants
Secreted by intestinal epithelial cells.
Contains: B48, ApoE, and Apo C2

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123
Q

NADH and activation or inhibition of TCA

A

Inhibits Pyruvate dehydrogenease and downstream (isocitrate dehydrogenase)

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124
Q

Guidlines for statin use for T2D

A

40-75 regardless of lipid levels

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125
Q

Insulin Receptor

A

heterotetramer with 2 extracllular alpha and 2 beta chains.

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126
Q

Route of rapid acting insulin

A

SQ injection prior to meal, or pump

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127
Q

Methylmalonyl CoA Racemase

A

2 step in odd chain FA

D to L

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128
Q

Where is glycogen?

A

liver and skeletal muscle
In liver - glycogen can be converted into blood glucose and sent elsewhere
In skeletal muscle - glycogen must be used for own muscle metabolsim

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129
Q

How are TAG broken down?

A

TAG – (Hormone sensitive Lipase) –> Fatty acids + glycerol.
Glycerol is used in liver for Glycerol phosphate production
FAtty acids are transfered to mitochoria for breakdown

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130
Q

Eruptive Xanthomata

A

pimple like painless bumps associated with hyper TG

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131
Q

Tangeir’s Disease

A

loss of ABC A1

no formation of HDL and orange tonsils

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132
Q

what is the rate limiting step in FA synthesis

A

Acetyl CoA Carboxylase (Acetyl CoA into malonyl CoA)

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133
Q

Mipomersen

A

antisense RNA to block transcrption of ApoB

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134
Q

Gemfibrozil

A

fibrate - lowering TG agent

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135
Q

Omega 3 FA as TG lowering agent

A

mechanism to decrease VLDL TG production and secretion by blocking formation with long chains
no evidence for reduction of CV events

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136
Q

Pyruvate Kinase

A

Converts Posphoenolpyruvate into pyruvate in glycolysis.
Produces ATP
Activated by: Insulin and Fructose 1,6 bisphosphate
Inhibited by glucagon, ATP, alanine

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137
Q

ADRs of SGLT1/2 I?

A

risk of GU and GI infection

Hypokalemia

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138
Q

Pancreatic Diabetes

A

due to chronic pancreatitis and decreased exocrine fxn

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139
Q

Sphingomyelin

A

Sphingolipid

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140
Q

Pathogenesis of nephropathy

A

high glucose leads to osmotic diuresis, intrarenal and peripheral hypertension, BM thickening, mesangial prolifeartion, glomerular obliteration

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141
Q

Fish eye disease

A

LCAT deficiency

decrease HDL that leads to kidney disease

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142
Q

Tertiary prevention of T1D

A

Intensive glucose control
Ab against T lymphocytes (anti CD3) - delays the slowing of phase 1
Abatacept - blocks T cell activation to delay onset.

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143
Q

sucrose

A

is glucose and galactose

144
Q

Autoantibodies in T1D

A

ZnT8 - zink transporter used in zinc hexamer foramtion
IA-2 potentiates insulin release
GAD65 - protntiates granule relsease
mIAA - anti insulin Ab.

145
Q

Amylose

A

starch, non branched that is slow absorption.

Found in basmati and bananas

146
Q

Long acting insulin

A

Glargine, Detemir, Degludec

cant mix with other insulins!

147
Q

Drugs in LDL lower capability?

A

Statin> Bile Acid sequesterant >Exetimibe >Plant sterol

?? PCSK9

148
Q

ADR of metformin?

A

N, bloating, Diarrhea that decrease with slow titration up.

Risk of lactic acidosis

149
Q

Phosphadtidylserine

A

glycerophospholipid

150
Q

Types of diabetic neuropathy

A

Mononeuritis multiplex
Distal symmetric polyneuropathy*
Autonomic neuropathy
Diabetic amyotrophy

151
Q

Screening for T2D

A

1) BMI >25 of >23 for asians.
2) inactivity, large for gestation age baby, PCOS
3) older than 45 yo, or kids with risk factors (obestiy, Family or maternal Hx)

152
Q

Xantheiasmus

A

lipid depoits on eyelids seen with hypercholesterol.

decrease with treatment of LDL

153
Q

Acetyl Co-A –?–> Citrate

A

Citrate synthase

154
Q

Cholystyramine

A

bile acid sequestrant

155
Q

Hygiene hypothesis

A

decreased immune stimulation that suppresses our natural immune system and leads ot increase autoimmuniety and allergies.

156
Q

Plant sterols ADRs

A

NOne!, but require 2-3 g per day!

157
Q

Glycerophospholipid vs. Sphingolipids

A

Glycerophospholipid: phospholipid with glycerol backbone + 2 FA + Phosphate and alcohol
Sphingolipid: phospholipid, with sphingosine + FA + Phosphate + Choline

158
Q

Apo B 100

A

Structural protein that binds to LDL receptor

found in VLDL, LDL, and IDL

159
Q

Glycemic Load

A

Glycemic Index X grams of starch

160
Q

Malate Dehydrogenase

A

Converts malate to oxaloacetate in cytoplasm.
required because only malate can cross mitochondrial membrane
Produces one NADH

161
Q

Metformin Mechanism

A

Supresses hepatic glucose production, so no effect on insulin
only used for insulin resistance

162
Q

pathogenesis of CV disease in DM

A

HTN, Hyperlipidemia, hyperglycemia –> damage endothelial, decreased NO, attractive to WBC, platelets, accumulation of lipids in subendothelial space to lead to procoagulation and proatherogenic.

163
Q

Insulin action Adipose

A

stimulates GLUT4 uptake, increase fat synthesis

164
Q

What is the rate limiting step of Ketone body formation

A

HMG CoA Synthase

165
Q

Steps for odd chain FA

A

1) Propionyl CoA convertion to D methylmalonl coA by Pripionyl CoA Carboxylase
2) conversion to L methylmalonyl CoA by Methylmalonyl coA racemase
3) conversion to succinyl coA by Methylmalonyl CoA mutase.

166
Q

Triolase

A

enzyme the aids inthe formaiton of acetoacetyl-CoA in ketogenesis

167
Q

Evolocumab

A

PCSK9 Inhiitor

168
Q

what common med promotes high TGs?

A

oral contraceptives

169
Q

Plant sterols mechanism

A

Prevent micelle formation in intestine to decrease cholesterol absorption by preventing micelle formation.

170
Q

Cell types in pancrease islet

A

60% beta - release isnulin
25% alpha release glucagon
delta - release somatostatin

171
Q

HMG CoA Synthase

A

Acetoactyle CoA into HMG CoA

rate limiting step in ketone formation. and also in cholesterol synthesis

172
Q

Impaired OGTT

A

140-199

173
Q

Guidelines for Aspirin use in T2D

A

only for high risk patients.

174
Q

how to treat low HDL

A

manage LDL
intensify weight loss and physical activity
Tx TGs
not indiated to increase HDL

175
Q

MODY

A

maturity onset diabetes of the young

glucokinase defect in glycolysis, so you don’t get insulin release or production.

176
Q

HDL purpose

A

mediates reverse cholesterol transport from peripehery to liver
Repository for apolipoproteins C and E (needed for chylomicrons and VLDL).
scretes from both liver and intestine.
Forms from ApoA1 with accumulation of cholesterol from plaques

177
Q

Gemfibrozil ADRs

A

cholelithiasis, myopathy, GI

178
Q

Insulin Receptor binding

A

Insulin binds and leads to autophosphorylation.

Which leads to tyrosine phosphorylation of IRS to activate the PI3Kinase pathway or the MAPK pathway

179
Q

Glycogen phosphorylase vs Glycogen Phosphrylase kinase

A

GPK potenitates the action of GP

180
Q

why does the body want to increase Acetoacetate or 3- hydroxybutyrate in starvation

A

Acetoacetate or 3HB can diffuse int he blood and entery peripheral tissues.
3HB is converted to Acetoacetate in the tissues (releases NADH).
Acetoacetate can be converted to Acetoacctyle- COA in mitties (an enzyme not found in liver) by Thiophorase which can be made into acetyl coA.

181
Q

Fructose metabolism

A

Enters below the Posphofructose kinase - so it is less regulated!

182
Q

Corticosteroids

A

counterregulatory hormones.
Promote protein breakdown for gluconeogenesis and decrease insulin ation.
Potentiates the action of glucagon and catecholamines.

183
Q

what is the change in insulin resistance

A

most due to signaling problems downstream - change from tyrosine to serine or threonine phosphorylation.

184
Q

autonomic neuropathy

A

increased HR, or MI risk,

can affect colon and stomacha s well

185
Q

GLP1 agonists

A

TIDE endings
stimulates glucose dependent insulin secretion to decrease hepatic glucose output, glucagon output.
also decreases gastric emptying and intake.
used for insulin resistance and decreased production

186
Q

What do you do for high LDL?

A

Mipomersen
omitapine
LDL aphoresis

187
Q

what are the outside actions of insulin

A

Decrease food intake, regulate blood flow, regulate salt/water balance, growth stimulation

188
Q

alpha cell role in T2D

A

increased alpha stimulation to cause increased glucagon levels. Glucagon promotes hepatic glucose output.

189
Q

Alirocumab

A

PCSK9 inhibitor to decrease LDL

190
Q

what drug to give in Renal Dz for DM?

A

insulin

191
Q

what happens with odd chain FA oxidation?

A

last round of beta oxidation you are left with a FA acteyl coA with 3 Carbonds - Propionyl -CoA

192
Q

Carnitine Palmitoyl Transferase 1

A

converts fatty acid CoA into Acetyl CoA for diffusion of LCFA through mito membrane (inner).
the rate limiting step in Beta oxidation.
Inhibited by large amounts of malonyl coA.

193
Q

what drug is only avaliable SQ for DM?

A

GLP1 agonists

194
Q

two major emergencies of diabets

A

DKA - too little insulin and too much glucagon and epinerphine to promote lipolysis and ketone formation.
unknown hypoglycemia - due to mismatched insulin and food intake. overtime you get sensitized, so when you get hypoglycemia, you don’t feel any changes and are seizure risk.

195
Q

how does a large H+ gradient play out?

A

decreased respiration due to lower oxygen consuption

196
Q

apidra

A

glulisine

rapid acting insulin

197
Q

Novolog

A

Asprat
rapid acting insulin
29th AA change to asparate

198
Q

how do we prevent macrovascular complications of T2D?

A

Statin, lower HTN, aspiring?

199
Q

HBA1C imparied

A

5.7-6.4%

200
Q

Fatty acid synthase

A

converts malonyl coA into Palmitic acid in cytoplasm of FA synthesis
Multifunctional enzyme with 7 activiites
Completes 4 step process in formation of Palmitic acid.

201
Q

when is insulin used for T2D?

A

when lifestyle modification and drugs fail to meet target A1C
contraindications to meds
Signs of insulin deficiency (WL, fasting >250, random >300, A1C > 10%)
DKA, or HHS

202
Q

Wipples triad

A

BG <50, symptoms of hypoglycemia, symptoms improve with glucose administration

203
Q

VLDL purpose

A

delivers hepatic TG to peripheral tisses. Gets degraded into LDL
Secreted by liver
contains Apo B100, Apo C2 and Apo E

204
Q

LADA

A

latent autoimmune diabetes of adulthood.
30-70 YO
>6 months of non insulin requiring Diabetes
+ AutoAb

205
Q

PI3Kinase pathway

A

activation of AKT to elad to GLUT4 translocation, and glycogen synthesis
THis is the metabolic pathway

206
Q

PCSK9 inhbitors mechanism

A

mAB that binds to PCSK9 to allow LDLR to recycle

207
Q

low intensity statin

A

pravastatin, lovastatin

208
Q

Prevalence of T2D

A

9.3%

209
Q

Effect of Omega 3 FA

A

lower TG by 15-35% increase HDL, and no effect on LDL

210
Q

what are the steps of beta oxidation in the mitochondria

A

1) dehydrogenation/oxidation by acyl co dehydrogenases
2) Hydration by enoyl CoA Hydratase
3) Oxidation (dehydrogenationase) by Beta hydrozy-CoA dehydrogenase
4) cleavage by Thiolase

211
Q

How do glucagon and epinephrine signal?

A

they both increase cAMP to activate PKA to phosphorylate enzymes

212
Q

Phosphoenolpyruvate carboxylase

A

Converts oxaloacetate in cytoplasm to Phosphenolpyruvate

Requires 2 GTP

213
Q

Novulin R

A

Short acting insulin

214
Q

Pripionyl CoA Carboxylase

A

converts propionyl CoA into Methylmalonyl CoA D - by adding carboxyl group to FA.
Requires CO2 and ATP

215
Q

what is required for the ETC

A

O2, NADH, FADH2, ADP

216
Q

What are the steps in Triglyceride synthesis

A

1) Acteyl transferase - adding on FA to 3-Glycerol phosphate backbone.
2) Acteyl transferase - adding 2nd FA to 3-Glycerol phosphate backbone.
3) Phosphatase - removal of phospate to create an alcohol.
4) Acteyl transferase - adding 3rd FA to 3-Glycerol phosphate backbone.

217
Q

Actyl CoA carboxylase

A

Acetyl CoA –> Malonyl CoA (synthesis of FA)
Cytoplasm
Requires ATP, CO2, Biotin.
Activated by high citrate concentrations and insulin (to increase Vmax)
Inhibited by Long chain Fattay acids and glucagon

218
Q

what is the marker for decreased GFR in nephropathy?

A

proteinuria

219
Q

Uses of Short acting insulin

A

DKA, HHG, perioperative, critical hyperglycemia.

220
Q

Niacin

A

no major benefit in decrease CV events
Decreases synthesis of VLDL by decreasing catabolism of Apo A1
Liver: binds to AMP kinase to increase FA oxidation, and decrease TG synthesis
Adipose : activation Gi to decrease lipolysis

221
Q

Bile Acid sequesterant

A

high molecular weight qauternary amines that bind to bile acid to prevent reabsoprtion to decrease entrahepatic circulation and promote synthesis of bile.
Ultiamtely decreases liver cholesterol and increase LDL Receptor

222
Q

Clinical features of severe hypertriglyceridemia

A 
Eruptive xanthomata
Lipemia retinalis
hepatosplenomegaly
ab pain and acute pancreatitis
lipemic serum
223
Q

How do Fatty acids get into the mitochonria

A

Short and medium <12 C diffuse
LCFA can diffuse through outer membrane, but use Carnitine Palmitoyl Transferse 1 to bind with carnitine to make CoA + Acteyl Carnitine.
This can diffuse through the inner membrane.
CPT2 converts acteyl carnitine back to FA-CoA and carnitine.

224
Q

Accelerator hypothesis

A

obesity causes increased beta cell stress to lead to increased beta cell antigens in T1D

225
Q

ADRS of PCSK1 I

A

injection rejection 5%
Drug antibodies <5%
Allergy
Neurocognitive?

226
Q

Apo E

A

Ligand for Remnant Receptor
Mediates remnant reuptake
found on chylomicron, chylomicron remnant, VLDL, IDL, HDL (NOT LDL)

227
Q

Hormone sensitive lipase

A

in cytosol - breakdown of TAG into FAT
Activated by Epinephrine
Inhibited by insulin and glucose

228
Q

Apo B48

A

Mediates chylomicron secretion, structural protein

Found on Chylomicron and chylomicron remnants

229
Q

Incretin

A

a signal that increases insulin release in the presence of glucose.

230
Q

what DM drug can cause lactic acidosis

A

metformin

231
Q

DPP4

A

degrades GLP1

232
Q

what is produced for each beta oxidation round

A

1 acetyl coA
1 NADH
1 FADH2

233
Q

Glucose –?–> Glucose-6-phosphate

A

Hexokinase, glucokinase

234
Q

Advanced Glycolytic End products

A

producs that get stuck on protein, DNA, cholesterol to disrupt basement membrane, sequester NO, activated deleterious pathways (collagen), cross link DNA to decrease repair.

235
Q

risks of early insulin (animal)

A

allergy, resistance, lipoatrophy of SQ fat.

236
Q

guidlines for HTN treatment in T2D

A

<140/90 (lower for those in renal dz)

237
Q

What converts Glucose to Glucose-6 phosphate

A

Hexokinase and Glucokinase

Requires ATP

238
Q

alpha oxidation

A

occurs in the perisoxisome.
Phytanic acid - branched FA is hydroxylated at alpha C by Fatty Acid alpha hydroxylase.
2) Decarboxylated
3) activation for beta oxidation

239
Q

Long acting insulin - onset, peak, duration

A

onset: 1-1.5 hours
Peak - not pronounced
duration: 12-42 hours depending on type

240
Q

PAI-1

A

increased in DM to promote coagulation

241
Q

ADRs of Sulfonyluria?

A

weight gain, hypoglycemia, resistance with long term use

242
Q

what drugs promote weight gain for DM?

A

Sulonylurea

243
Q

Acyl Co A Dehydrogenase

A

first step in beta oxidation that creates a TRANS double bond (enoyl CoA)
there are 4 forms of these
short, medium, long, and very long. producess FADH2

244
Q

Rapid acting insulins

A

Humalog, Novolog, Glulisine, Afrezza

245
Q

when does ketogenesis occur

A

2 days after meal

246
Q

Gestation Diabetes

A 
weight gain during pregnancy to cause insulin resistance
Increased risk of T2D in the future
Fasting >95
1 Hr >180
2 Hr >155
3 Hr >140
more at risk for baby than mother
247
Q

Glulisine

A

apidra
rapid acting insulin
33 Lysine switched with 29th glutamate

248
Q

Pathogenesis of insulin release

A

Glucose travels through GLUT2 into beta cell
Glucose undergoes Gycolysis and TCA to generate ATP
ATP acts on close K Channel (dependent on ATP) to cause cell depolarization
Depolarization opens Ca (VSCC)
TO cause exocytosis

249
Q

how do we slow the progression of nephropathy

A

ACEI, glucose control, protein restriction, Bp control

250
Q

Adrenoluekodystrophy

A

defect in peroxisomal biogenesis.

251
Q

Amylopectin

A

starch, branched for faster absorption

found in white bread, potato, pasta

252
Q

effectivness of fibrates

A

lower TG by 20-40%

increase HDL by 5-15%

253
Q

How does exercise improve diabetes

A

depletion of glycogen to increase muscle Insulin sensitivity.

254
Q

Arcus Cornealis

A

Hypercholesterolesmia
lipid deposits in cornea (gray band around cornea) that starts at 12 and 6, but becomes circumferential.
Can be seen in African americans without high cholesterol.

255
Q

Refsum

A

back of alpha hydroxylase that leads to accumulation of phyantic acid in liver and kidney.
pigmented retina, poly neuropathy.

256
Q

HDL roles

A

cholesterol transport, antioxidant, antiinflammatory

257
Q

Sulonylurea

A

IDE endings
closes ATP sensitive K channels in Beta cells to increase Insulin release.
used for insulin production problems.

258
Q

Phosphofructokinase 1

A

Enzyme that converts Fructose-6-phosphate into fructose 1-6, bisphosphate
Requires ATP
rate limiting step of glycolysis

259
Q

Fructose biphosphatase -2

A

enzyme that converts Fructose 2,6 biphosphate back to fructose-6-phosphate.
Activated in fasting state by glucagon
Inhibited in fed state by insulin

260
Q

Fibrates mechanism

A

induction of PPAR alpha expression to increase intrahepatic oxidation and decreases VLDL TG synthesis
also, decrease APoC3

261
Q

Steps in Glycogen metabolsim

A

Glycogen – (glycogen phosphorylase) –> Glucose 1 phosphate – (phosphoglucomutase)–> Glucose - 6 Phosphate that goes either into glycolysis or Gluccose via Glucose 6 phosphatase.

262
Q

What genes promotes high TG?

A

Increase in LPL and ApoA5 and a number of others

each is additive and leads to increasing TG accumulation

263
Q

HMG CoA Lyase

A

HMG coA into Acetoacetetate

264
Q

Citrate

A

part of TCA cycle
Activates Fructose 1,6 bisphosphatase in gluconeogenesis
Inhibits Glycolysis by inhibiting Phosphofructokinase 1

265
Q

Mononeuritis multiplex

A

tiny n. infarctions in nerve root - looks like ptosis, but has good prognosis

266
Q

tests to run when evaluating cause of CAD

A

Glucose, A1C, TSh, Liver Fx, Creatinine, Urine Protein

267
Q

when does glycogen metabolism occurs

A

In tissues lacking mitocondria (sperm, RBCs), Brain, in vigorous exercise

268
Q

Colesevelam

A

bile acid sequestrant used clinically

269
Q

Phosphatidylethanolamine

A

glycerophospholipid

270
Q

What drugs are weight neutral for DM?

A

Metformin, DPP4 inhibitors

271
Q

Structure of Triglycerides

A

GLycerol backbone with 3FA
C1 = saturation
C2 - unsaturated
c3 - either

272
Q

undiagnosed Prediabetes

A

90%

273
Q

Fructose 1,6 biphosphatase

A

Converts F1,6 BiP to F6P
Activated by ATP, Acetyl CoA, and Citrate
Inhibited by Fructose 2,6 biphosphatase

274
Q

Basal metabolic rate =

A

due to the generation of head due to the Hydrogen leak without ATP being made

275
Q

Stages of retinopathy

A

early, mild, severe, preprolifeative (severe preproliferative is where we try to intervene)
Early proliferative
neovacularization
macular edema

276
Q

Phosphoenolpyruvate -?–> Pyruvate

A

Pyruvate Kinase

277
Q

When do I use fibrates?

A

when TG >200 with low HDL

to decrease TG when not on a statin

278
Q

Impaired fasting glucose

A

100-125

279
Q

symptoms of hypoglycemia

A

ANS - increase epinephrine and catecholamines

Neurologic - head ache, confusion, looks drunk due to not enough glucose in brain

280
Q

Effect of Fatty liver disease

A

1) ethonol oxidizes acetone into acetate, which is a precursor to Acetyl CoA to increase FA synthesis
2) NADH lows TCA and promotes Glycerol Phosphate production
3) secretion of VLDL is impaired via decreased ApoB100 synthesis in liver –> liver fat accumulation

281
Q

IRS1 normally

A

is phosphorylated on tyrosine, but when the body is stressed increased TNFalpha, phosphorylation occurs on serine to potentate lipolysis and FFA, so cause insulin resistant and hyperglycemia for healing.
This rxn is normally beneficial, but when you get constant hyperglycemia, it leads to diabetes.

282
Q

Enzymatic differences in Glycolysis and gluconeogenesis-

Fructose 6 phosphate - Fructose 1,6 Bisphosphate

A

Glycolysis: phosphofructokinase 1
Gluconeo: Fructose 1,6 bisphosphatase

283
Q

Pyruvate–?–>Oxaloacetate

A

Pyruvate carboxylase

284
Q

energy expenditure

A

30 cal/kg

285
Q

Pyruvate carboxylase

A

converts pyruvate into oxaloacetate
requires Biotin, ATP and CO2
Activated by Acetyl CoA

286
Q

what drugs have CV protective effects?

A

GLP1 agonist, SGLT1/2 inhibitors

287
Q

Int. Acting Insulin

A

Neutral protamine hagedorn (NPH)
NPH Humulin N
NPH Novulin N
This one is cloudy!

288
Q

what carries electrons from complex 1 to complex 3 in ETC

A

Coenzyme Q

289
Q

Galactoscerebroside

A

sphingolipid

290
Q

lactose

A

is fructose and glucose

291
Q

what does high TG levels lead to atherosclerosis

A

with diseases
Metabolic disease (especially in women)
pancreatitis

292
Q

When is FA synthesis promoted

A

when ATP levels are high and they inhibit isocitrate dehydrogenase to allow citrate to accumulate in to the mito

293
Q

when does gluconeogenesis occur

A

12 hour after meal

294
Q

Sphingosine

A

built from palmitoyl Coa and serine

resembles glycerol but has a nitrogen due to protein component

295
Q

Insulin actions Muscle

A

Stimualtes GLUT4, increase glycogen synthesis

296
Q

TG levels

A 
Normal <150
Borderline 150-199
High 200-499
very high >500
level is qualitative, not an accurate risk assessment
297
Q

Targets of insulin therapy

A

fasting 80-130
2hr post bolus <180
A1C <7% adults, <7.5% kids

298
Q

Glycogen Synthase

A

enzyme - converts UDP glucose into Glycogen
Adds glucose onto glycogen chain >4 with Glycogenin (starter of chain)
Activated by Glucose 6 phosphate, Insulin, Protein phosphatase 1, and cortisol
Inhibited by: Epinephrine and glucagon

299
Q

Purpose of Glycerophospholipids

A

Cell membrane component, signaling

300
Q

what DM are expensive

A

GLP1 agonists, DPP4 I, SGLT1/2, Insulin analogs

301
Q

Int. Acting insulin onset, duration, peak

A

onset: 1-3 hours
peak 6-8 hours
duration: 12-16 hours
Route SQ only, 2x per day

302
Q

Phosphoenolpyruvate (PEP)

A

produced through a series of steps from fructose 1.6 bisphosphate in glycolysis

303
Q

Propionyl-CoA

A

end product of regular Beta oxidation with odd chain FA

304
Q

Rule of 6?

A

for each 2x dose of statin, expect to decrease LDL by 6%

305
Q

Lispro

A

Humagloc Rapid acting insulin

306
Q

Phase 1 vs phase 2 insulin release

A

phase 1 lasts 5 minutes and is quick release of insulin (predocked)
phase 2 starts 8-10 minutes after food ingestions to increase insulin synthesis.

307
Q

Glucose-6-phosphate –?–> Glucose 1 phosphate

A

Phosphoglucomutase

308
Q

what generates the H+ gradient in ETC

A

I, III, IV into intermembrane spane

309
Q

MAPKinase pathway

A

leads to ERK activation ot cause vasoconstriction and growth and mitogenesis. The mitogenic pathway.

310
Q

Glycerol Kinase

A

converts glycerol into Glycerol Phsophate in liver only

311
Q

Hypertriglyceridemia

A

Promotes thrombosis, endothelial dysfunction, and less commonly cholesterol in vessel wall

312
Q

Genetic causes of higher LDL

A

Familial Hypercholesterolemia
AD disease with defect in LDL receptor
Heterozygotes 1:500 have 200-300 LDL levels
Homozygoates (rare) have cholsterol >500
Causes accelerated atheroscelerosis (before 20 yo), Arcus Cornealis, Zantheiasmus, tendinous xanthomas**

313
Q

Fructose 2,6 bisphosphate

A

produced from fructose6 phosphate in glycolysis by phosphofructokinase -2.
Promoted by insulin in fed state and inhibited by glucagon in fasting state

314
Q

how do we slow the progression of retinopathy

A

survelliance
Panphotocoagulation
antiVEGF

315
Q

who do we treat with statins

A

1) those with CVD (high intensity)
2) LDL >190 (high intensity)
3) primary prevention: DM, 40-75 yo, LDL 70-189 (high/mod)
4) primary prevention: no DM, 40-75, LDL 70-189 + >7.5% risk/10 years

316
Q

Malonyl coA –?–> Palmitic Acid

A

Fatty acid synthase

317
Q

UDP Glucose –?–> Glycogen

A

Glycogen Synthase

318
Q

First step in Biosynthesis of FA

A

Citrate from TCA cycle diffuses out of mitochondria and is converted to OAA or Acteyl Co-A by ATP Citrate Lyase.

319
Q

initiators of insulin release

A

direct stimulation - glucose, AA, drugs

320
Q

Formation of Palmitic acid process

A

1) condensation to form 3 Ketoacyl ACP
2) Reduction - converts keto to alcohol using NADPH
3) Dehydration - induces double bond
4) reduction - removes double done (NADPH)
Firs 2 Cs are made from actyle coA, the rest are from malonyl Co-A
Palmitic acid is released from FAS by palmitoyl tioesterase

321
Q

Affrezza Onset, peak, duration

A

onset: 5 min
Peak 1 hour
Duation: 2 hr
dosage cartridges only

322
Q

Enzymatic differences in Glycolysis and gluconeogenesis-

Glucose Glucose 6 phosphate

A

Glycolysis: hexokinase and glucokinase
Gluconeogenesis: glucose 6 phosphatase

323
Q

How does Insulin signal?

A

activates protein phosphatase 1

324
Q

Lecitin Cholesterol Aminotransferase

A

LCAT makes it so Cholesterol turns into CE of HDL to promote it staying in the lipoprotein center

325
Q

naming glycerophospholipids

A

Phosph….

326
Q

Debranching enzyme

A

works alongside glycogen phosphorylase to decrease branching and convert to linear structure

327
Q

Where does Glycerol phosphate come from for Triglyceride synthesis?

A

Glycolysis in the liver or adipose: produeces Dihydroxyacetone phosphate – (Glycerol P dehydrogenase) –> Glycerol P - this is the indirect method.
This requires NADH
Direct: in liver only: Glycerol – (glycerol kinase) –> Glycerol P.
This requires ATP

328
Q

how much insulin does pancreas usually release

A

30 U/day

329
Q

What is the fate of palmitic acid?

A

1) elongation in ER or Mito into LCFA
2) remains as is as a FA
3) desaturation (adding double bonds) in ER by Mixed Function Oxidase

330
Q

Phosphatidylinostiol

A

glycerophospholipid

signaling molecle

331
Q

what drugs can be combined with metformin in one pill?

A

DDP4 I, SGLT1/2, Sulfyuria

332
Q

Rapid acting Insulin Onset, peak, and duraiton

A

onset: 5-15 minutes
Peak: 1-1.5 hours
Duration: 3-5 hours

333
Q

when does FA breakdown occur?

A

18 hours after meal

334
Q

Treatment goals of lowering TG

A

prevent pancreatitis, lower below 500 for severe cases

Lifestyle/statin recommendations`

335
Q

Distal symmetric polyneuropathy

A

more common in tall epoeple
nerves bathe in high glucose to cause tingling, numb, hyperalgesia that progresses to complete numbness, abnormal structures, hammer toe and ulcers.

336
Q

HbA1C Diabetic

A

> 6.4

337
Q

Enoyl CoA Hydratase

A

Rxn2 in beta oxidation - hydration

adds H20 to the double bond

338
Q

Risk factors of Atheroscelrosis

A 
Male, AA, Current smoker (risk decreases within 6-12 months of quiting), HTN >140 systolic, High Total cholesterol, decreased HDL, DM
Family Hx (male <55 and female <65)
339
Q

protocol for treatment if diabetes in hosptial

A

stop non insulin meds and use IV insulin with monitoring.

or scheduled insulin SQ

340
Q

HMG CoA Reductase

A

converts HMG CoA into mevalonic acid
Rate limiting step for Cholesterol syntehsis
Activated by insulin, and SREBP release from ER
Inhibited by, AMP, Glucagon, and SREBO being sequestered in the ER by high levels of cholesterol.

341
Q

How are ketone bodies formed

A

Acetyl coA and Fatty Acyl COA combine via triolase to form acetoacetyl-CoA.
HMG CoA Synthase (RL) adds acetyl COA to form HMG CoA.
HMG CoA Lysase cleaves into acetoacetate, which is unsable and usually forms acetone or 3-hydroxybutyrate.

342
Q

Catecholamines

A

counterregulatory hormones NE and Epi to increase blood glucose
Act on Beta receptor on liver to increase cAMP

343
Q

Glargine (lantus)

A

long acting insulin - extra arginines added so it forms preciptiate at body’s pH for slow release
24 hours duration

344
Q

Glucagon Actiosn

A

acts with GPCR to increase cAMP and lead to phosphorylation.

345
Q

Fructokinase

A

converts fructose to Fructose 1 phosphate

uses ATP

346
Q

How do we prevent microvascular complications of T2D?

A

lower A1C

347
Q

Afrezza

A

rapid acting inhaled insulin

348
Q

Humulin R

A

Short acting insulin

349
Q

Plant sterols effectivity

A

lowers LDL by 5-10%

350
Q

Uncoupling protein

A

dissipation of H+ gradient without generation of ATP - as seen in brown fat.

351
Q

Asprat

A

novolog

rapid acting insulin

352
Q

Basic pathway of gluconeogenesis

A

Pyruvate – (payruvate carboxylase–> Oxaloacetate –> malate – (malate dehydrogenase) –> oxaloacetate – (phsophoenolpyruvate carboxykinase) –> Phosphoenolpyruvate –> Fructose 1,6 biphosphate – (fructose 1.6 biphsophotase) –> F6P –> G6P – (G6PDehydrogenase) –> glucose

353
Q

when is stimulate insulin released

A

when >100 serum glucose( Glucose stimulated insulin release)

354
Q

BG for newborns

A

<12 hours hypoglycemia <30
after 12 hours hypoglycemia <45
after 48 hours hypoglycemia <50

355
Q

Somatostatin

A

release from hypothalamus and inhibits GH release.
Inhibitor of glucagon and insulin -
Decrease GI motility, splanchnic flow, digestive enxymes and absorption in intestines.

356
Q

what carries electrons form complex 3 to 4 in ETC

A

Cytochrome C

DEMS (5 decks)

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