Week 4 Flashcards

Question 1

Q

Outline 3 major differences between fat and water soluble vitamins

Answer

A

They have different absorption processes
They are transported differently
They’re stored differently

Question 2

Q

Absorption of fat vs water soluble vitamins

Answer

A

○ Water soluble are absorbed through neutral specialized carriers
○ Fat soluble are absorbed with the dietary fats - they’re factored into chylomicrons, which are lipoproteins, and then they are released into blood close to where they have to go

Question 3

Q

Transportation of fat vs water soluble vitamins

Answer

A

○ Water soluble are transported directly in the blood

○ Fat soluble require some kind of lipoprotein to be packaged in with the dietary fats

Question 4

Q

Storage of fat vs water soluble vitamins

Answer

A

○ Fat soluble stays in the body for a longer amount of time; We store a lot of the fat soluble vitamins in the liver and some in the adipose tissue, On a day when somebody did not take an adequate amount of fat soluble vitamins, the liver can actually send some amount of the stored form out and then the person should be okay
○ Water soluble have to be taken everyday because they won’t be stored anywhere; Most of them are not stored, but some are stored but at much lesser quantities, For instance, vitamin B12 does store in the liver, which is still a water soluble vitamin

Question 5

Q

Vitamins produce energy directly: true or false?

how do they help?
Can we oxidize a vitamin to make ATP?

Answer

A

False
They act as coenzymes of some of the enzymes involved in production of energy,
No

Question 6

Q

in the US, which vitamins and minerals are not adequate for the majority of the population

Answer

A

Vitamin E is the most deficient
Vitamin A (over 50%)
Folate
Vitamin D
Calcium
Magnesium
Potassium

Question 7

Q

What is the recommended dietary allowance (RDA)?

For that value, what percentage of the population is it going to be sufficient for?
How does this differ from the estimated average requirement (EAR)?

Answer

A

The needed recommendation for one day
97%
It covers 50% of the population

Question 8

Q

adequate intake

Answer

A

researched from a few trials but not major epidemiologic surveys
used when there is not an RDA

Question 9

Q

particular vitamins or minerals are helpful in particular populations

infants
Women of child-bearing age
older people
colored people
diabetes
heart disease

Answer

A

Vitamin D, K, A, Zinc
Iron,
Vitamin D, Calcium, Vitamin B12
Vitamin D
Vitamins B6, C, D, E, A, thiamine, biotin, folate, B12
Vitamins B6, C, D, E, Niacin

Question 10

Q

multivitamins and minerals for the general population

who needs it? who doesnt?
synthetic

Answer

A

people that are eating well-balanced diets, you probably don’t need the vitamins and minerals
use multivitamin for patients who do not eat well because some of these vitamins and minerals are found only in certain foods
vitamins and minerals, especially vitamins, are synthetic vitamins, so our bodies may not recognize them quite the same way as if we were getting them from food sources

Question 11

Q

benefits of vitamins

Answer

A

reduction in minor psychiatric symptoms with multivitamins and minerals
People had a little less perceived stress, a little less anxiety, fatigue, and confusion

Question 12

Q

How could you connect the 7-year history of alcohol abuse with these neurological symptoms?
- absorption

Answer

A

Alcohol use can lead to thiamine deficiency (vitamin B1) because it affects the absorption.
The active form of thiamine in the body is TPP (thiamine pyrophosphate) and Alcohol interferes with the conversion of thiamine to thiamine pyrophosphate, the transporting or the absorption of thiamine at the intestinal level, and also depletes some of the thiamine that is stored

Question 13

Q

Wernicke’s Korsakoff Syndrome

symptoms
consequence if not treated
why is this happening?
treatment

Answer

A

It starts with odd eye movements, Change in gait, Leads to slight memory loss
might lead to loss of working memory and become very serious
If you’re thiamine deficient, then you’re not being able to oxidize glucose as efficiently as a normal individual
Supplement with thiamine; 500mg, IV at beginning (48 hrs, 3x a day) and then IM injections the rest of the week, and then switch to oral supplementation

Question 14

Q

Beriberi

- symptoms

Answer

A

dry: neuropathy; wet: neuropathy and cardiac symptoms

- does not have to be alcoholic, could just have bad diet

Question 15

Q

PDH

what is it?
what is it made of?
E1 and B1
E2 and lipoamide

Answer

A

mitochondrial enzyme complex made of E1, E2, and E3
E1 decarboxylates pyruvate and uses TPP as its coenzyme - Pyruvate is a 3-carbon molecule that’s converted to a 2-carbon molecule intermediate called hydroxyethyl, that’s attached to the TPP
E2 uses lipoamide as a coenzyme and takes the intermediate that is formed from pyruvate and extracts the acetyl group and then attaches it to coenzyme A forming acetyl-CoA

Question 16

Q

Thiamine and Alpha-ketoglutarate dehydrogenase

Answer

A

works just like PDH and uses the same mechanism

Question 17

Q

Cells most affected by thiamine deficiency

Answer

A

Neurons are dependent on glucose on a normal day and only during extreme starvation can they use ketones which leads to issues of the functions of neurons and shows up as neurological symptoms
The cardiac issues build up later on

Question 18

Q

Pellagra

pertinent findings
3 D’s
underlying cause
treatment

Answer

A

Dermatitis ,Diarrhea, Scaling of skin,
dermatitis (sun exposed hyper-pigmentation), diarrhea, and dementia
Niacin deficiency (Vitamin B3)
B3 supplementation

Question 19

Q

Hartenup disease

Answer

A

Genetic deficiency in the amino acid transporter that’s going to transport tryptophan which is used to make niacin is broken

Question 20

Q

Niacin

existence in body
participate in
ultimate use
PPP; where?
deficiency?
where are they used with glucose and fat?
LDL; reactions
short vs long

Answer

A

exists as NAD and NADP in the body
participate in redox reactions and therefore carry electrons from one substrate and then take it to another
become NADH and transfer electron to ETC to make ATP
produces NADPH in RBC to reduce the oxidized glutathione
Glucose and fat utilization will be compromised because they’re both dependent on vitamin B3
make NADHs when glucose is being oxidized which is then used acetyl-CoA in TCA where 3 more NADH are made
When we oxidize fat we produce NADHs and FADH2 and acetyl CoA
causes decrease in LDL but side effects are flushing
short has more flushing but long has greater effect on liver and increase LFTs

Question 21

Q

Riboflavin (Vitamin B2)

functional form
deficiency causes? common?

Answer

A

FAD and FMN
will affect glucose and fat oxidation
no because most food sources have riboflavin such as milk

Question 22

Q

coenzyme A

used in
Structure

Answer

A

TCA (formation of acetyl CoA), cholesterol biosynthesis (HmG CoA), and required for activation of fats before they get into mitochondria for oxidation
ADP, mercaptoethylamine, and pantothenic acid

Question 23

Q

Pantothenic acid

what is it?
deficiency would cause?
made from?

Answer

A

Vitamin B5
we wouldn’t have coenzyme A, and therefore utilization of glucose and fats at cellular levels would be compromised
Alanine

Question 24

Q

Vitamin B6

name
involved in?
enzymes it helps? function? ex?
deficiency will cause

Answer

A

PLP (pyridoxal phosphate)
glycogen and AA metabolism
Aminotransferases (ALT and AST) which transfer AA; amine groups are toxic so aminotransferase will grab the amine group and dumps it onto an alpha ketoglutarate
from TCA forming gluterate which will travel to liver and dump off the amine to make urea
for glucose it helps glycogen phosphorylase breaks glyosidic bone and releases a glucose molecule out of the glycogen
sideroblastic anemia (because B6 is a coenzyme for ALA synthase which makes heme from succinate and glycine), issues maintaining blood glucose homeostasis (bc liver glycogen is now not breaking down into glucose to release glucose into the blood during fasting conditions), and problems metabolizing AA from proteins

Question 25

Q

Vitamin B7

what does it do?
co-factor for what enzymes?
deficiency
what can it help with anatomically?

Answer

A

promotes carboxylation reactions at cellular levels
Pyruvate carboxylase (Carboxylates pyruvate, reduces oxaloacetate from TCA– Conversion of pyruvate to oxaloacetate is the first step of gluconeogenesis) and
Acetyl CoA carboxylase (Carboxylates Acetyl CoA to produce Malonyl CoA which goes into fatty acid synthesis
yes, raw egg whites has anti microbial agent called Avidin which binds to Biotin and prevents its absorption. If 2 or more raw eggs a day eaten, overtime they become Biotin deficient. However, We don’t normally get biotin deficient bc intestinal bacteria make it
adequate level helps with skin, nails, hair, etc.

Question 26

Q

B12

role with B9
deficiency
why bigger cells?
Cause of neurologic symptoms?

Answer

A

catalyzes reaction of methyl group from MTHF to homocysteine which converts it to methionine; if not enough then MTHF builds up and THF cant be recylced
macrocytic anemia with hypersegmentation of neutrophils
B12 and folate are needed for DNA synthesis.
Demyelination from B12 deficiency

Question 27

Q

Pernicious anemia

symptoms
what happens
why?
what do we see?
Blood test to detect pernicious anemia?
treatment

Answer

A

Loss of memory, Disorientation, Mild chest pain. Macrocytic anemia, Folate levels low
there will be autoimmune attack against parietal cells within stomach;
parietal cells make intrinsic factor and acid production
GI disturbances (difficulty digesting bc not enough acid in stomach)
Antibody against intrinsic factor and Anti parietal cell antibodies (more specific to autoimmune gastritis)
B12 (cobalamin) and folic acid supplementation
give a dose of 1000 micrograms of B12 IM once a week for about a month, then recheck levels, If levels come up then do maintenance dose of once a month injections

Question 28

Q

What is it called it there are autoimmune cells against ALL parietal cells in stomach

Answer

A

pan gastritis

Question 29

Q

B 12 supplementation

Answer

A

use cyanocobalamin (synthetic form) because it is easiest and cheapest to produce; however, Vast majority of people can probably convert cyanocobalamin into Vitamin B12, but there may be some people with single nucleotide polymorphisms that can’t make the conversion quite as well
Methylcobalamin and Adenosyl cobalamin are the bioactive forms within the body, so for some people that may be more helpful for them

Question 30

Q

B9 (folic acid)

how is it made?
folate cycle
what happens to RBC?

Answer

A

comes into body as dihydrofolate, which is then reduced to tetrahydrofolate by DHFR because THF is the biologically active form of folic acid
THF, in folate cycle, picks up methylene group and become methylene tetrahydrofolate (MTHF)which will then donate methyl group to dUMP (deoxyuridine) converting it into dTMP making thiamine and Formyl Tetrahydrofolate (FTHF). FTHF then donates single carbon groups to help in synthesis of purines.
folate deficiency, you have enlarged erythroblasts without well developed nucleus. Large in size bc cytoplasmic activities happening ok in blast cells but bc the low levels DNA and RNA, division not happening well. Cell uses all energy to grow big and they appear as megaloblasts in the peripheral blood smear.

Question 31

Q

What happens with deficiency in Methylene Tetrahydrofolate reductase?

occurence?
how to fix?

Answer

A

Increase in homocysteine and affects rest of cycle as well.
super common, heterozygous mutations in this gene occur in up to 2/3 of population.
Important to have good sources of folate in diet. For homozygous mutations, may want to go straight to bioactive form of 5 MTHFR supplement.

Question 32

Q

Folate trap

Answer

A

give more folic acid to patient, everything gets stuck as MTHR and at one point there’s no THF recycling

Question 33

Q

cause of neuro symptoms with B12 deficiency?

Answer

A

B12 helps add methyl group to homocysteine making methionine which then picks up adenine group from ATP to form SAM (S Adenosyl Methionine) which will donate its methyl group for different Methylation reactions

With B12 deficiency, once SAM gives off methyl group, recycles back to homocysteine and build up of homocysteine results in neuro toxicity
In order to prevent Homocysteine build up, supplement with B6 bc it helps converts excess homocysteine to cysteine

Question 34

Q

Vitamin A

- different forms

Answer

A

Retinol: transport form; has OH group
Retinal: important for visual cycle; used by rods and cones
Retinoid acid: modifies gene expression so important for cellular growth; in skin creams; has COOH
Retinaldehyde: storage form in liver of animals; has aldehyde
Beta carotene: precursor of vitamin A, will make 2 molecules of retinol, broken down by Beta carotene dioxygenase

Question 35

Q

Vitamin A sources

salmon vs carrot
what happens after eating?
how can it be used?

Answer

A

get retinal ester (storage form) vs getting beta carotene
absorbed and converted to retinol for transport, bind to retinol binding protein, transported to different cells for use
interconvertible: Retinol can be converted to retinal in the RPE (retinal pigmented epithelium), can get converted to retinoic acid in different cells

Question 36

Q

Dosage of Vit A

- synthetic vs food

Answer

A

High doses of synthetic retinol are toxic (50,000 IU/day or more) but if getting carotenoids from diet, you can control how much of the carotenoid is converted
Basically impossible to have Vitamin A toxicity from food sources

Question 37

Q

Synthesis of Vitamin D

Answer

A

Vitamin D3 to 25-hydroxyvitamin D3 to 1alpha25-dihydroxy vitamin D3

Question 38

Q

What is metabolic homeostasis?

Answer

A

Balance of catabolic and anabolic reactions w/in the body

- balance btwn food nutrient availability, nutrient utilization, and nutrient storage

Question 39

Q

How would you categorize tissue needs? (In terms of anabolic or catabolic)

Answer

A

It can be both
If the cell has too much glucose then it will store it if it is a hepatocyte and then prob will utilize some of it for oxidation

Question 40

Q

ATP

what is it?
Where does it come from?

Answer

A

chemical form of a fuel

- fats, carbs, and proteins (indirectly) help in prod of chemical fuel (ATP),

Question 41

Q

What helps in maintenance of metabolics? What are some of the most imp factors that would contribute to metabolic homeostasis?

Answer

A

Hormonal signals from the endocrine pancreas (insulin & glucagon)
Other hormones that help maintain metabolic homeostasis: epinephrine (comes from adrenal medulla), incretins (to some extent. Through insulin and glucagon will link the insulin glucagon pathway), cortisol (from the cortex)

Question 42

Q

What do these hormones actually do, how do they help in metabolic homeostasis, what kind of messages do they carry?

Answer

A

How much nutrient is present in blood

- Insulin and glucagon signals the cells about the nutrient levels in blood

Question 43

Q

What do nerve impulses do in GI?

- what kind of nerves are used? and what do they do?

Answer

A

Stimulate
Parasympathetic - is highly activated during fed state (Vagus, rest and digest)
Sympathetic - is your fasting state, uses Epinephrine

Question 44

Q

Hepatocyte during fed state

Answer

A

○ It is an anabolic state and Glycogenesis (glucose to glycogen), protein synthesis (AA to protein), lipogenesis (glucose to FA, the excess glucose is converted and stored as fat) is occurring

Question 45

Q

Adipocytes during fed state

Answer

A

After liver makes fat it has store it in other areas so it mobilizes it out via VLDL
In order to maintain homeostasis, the triglycerides are broken down and the FA are put into VLDL which will dump the FA into the tissue which will then be formed back into triglycerides

Question 46

Q

Muscle in fed state

what is happening
hormone?

Answer

A

○ They are using up the blood glucose immediately also via oxidation and they are storing the excess into glycogen

Protein synthesis is happening, excess AA are used for protein synthesis
Insulin because it is an anabolic hormone. All anabolic cycles are on in the fed state so that makes sense

Question 47

Q

Effects of insulin

Answer

A

In the liver: glycogenesis & lipogenesis
In the muscles: glycogenesis, oxidation of glucose (glycolysis, TCA, ETC), and protein synthesis
Adipocyte - storage of FA into triglycerides

Question 48

Q

Fasting state

What is happening in liver? adipocyte? muscle?
Why?
What would you call all these cycles happening in the fasted state?
hormones involved

Answer

A

glycogen is being broken down and glucose is being released into the bloodstream by the Liver
FA are being released from adipocyte (Lipolysis-fat mobilization of stored fat into the blood in form of FA to be used)
The muscle is releasing AA into the blood to travel to the liver to make glucose through gluconeogenesis
To maintain an adequate level of nutrients in the blood so that all other cells can get the nutrients from the blood and produce energy for survival
Catabolic
glucagon: primary one released from pancreatic alpha cells

Question 49

Q

Glucagon effect on:

liver?
muscle?
adipose?

Answer

A

In the liver: glucagon stimulates gluconeogenesis and glycogenolysis
In the muscle: glucagon is doing nothing bc it doesn’t have glucagon receptors. There is no glucagon, but glycogenolysis does happen in the muscle. So what activates the glycogen phosphorylase there? High levels of AMP
Adipose is doing mobilization

Question 50

Q

proinsulin vs mature insulin

Answer

A

Mature insulin is 2 chains (alpha and beta chain or A or B chain)
Proinsulin are 3 peptides (a, b, & c chain)
Maturation removes the C chain

Question 51

Q

proinsulin

is it produced from insulin gene?
what converts it?
when does it mature?
What is the stimulus for insulin release?

Answer

A

No, before proinsulin there is a pre-proinsulin which undergoes post translational modifications btwn the ER and the golgi
It is released as a single peptide at the N terminal end and this happens in the ER so a pre-pro converts into the pro
in the storage vesicles, proinsulin gets packaged into vesicles and released from the golgi into the cytoplasm of the beta cells and the cells will store them and the secretory vesicles are packed w/ a protease enzyme, while in the vesicles the protease cleaves the C peptide out and converts proinsulin into mature insulin in the vesicles, so the vesicles are now storing C peptide and mature insulin.

Question 52

Q

Release of enzyme

Answer

A

High ratio of ATP caused by glucose coming in going through glycolysis, TCA, ETC to make a lot of ATP and so it leads to ATP build up –the ATP sensitive K+ channels close which leads to depolarization and that will open up the calcium channels and the calcium then helps the cell exocytose insulin and c peptide into the blood from the cell

Question 53

Q

significance of C peptide

Why do we measure insulin vs C peptide?
Can we say that C peptide is a marker of functionality of beta cells?

Answer

A

It is a marker/measure of the endogenous insulin that the pts pancreas is releasing
C peptide has a longer half life; Insulin is degraded very quickly so its very hard to catch endogenous insulin
Yes, if you have high C peptide we can say that a large amount of the pts beta cells are working in the pancreas

Question 54

Q

3 levels of insulin

1st level, when does it occur? why is it important?
2nd level

Answer

A

First phase - post prandial insulin so when you eat, the insulin spike is the first phase
Second phase: helps maintain normal glycemia; After the post prandial spike of the first phase, it doesn’t remain elevated forever, it will come down btwn the basal and first phase and that will help maintain the normal glycemia and keep everything balanced
Basal level: the sugar level. 5mmol/microliter is your homeostatic sugar level so at that 5mmol the basal level of insulin is always there. The basal level of insulin prevents too much mobilization of fats and glycogen. So prevents excess lipolysis & glycogenolysis in order to maintain the stores.

Question 55

Q

Glucagon synthesis and secretion

What is the difference between the prepro & mature
stimulus for glucagon secretion in terms of numbers

Answer

A

protein hormone so itll be a gene product.
Prepro is much longer (120 AA) vs the mature one which is 29 AA; The mature is folded one & prepro is the straight one
If you have a glucose level below 5 mmol/liter that is a stimulus for glucagon height
and when glucose is greater than 5 mmol that inhibits glucagon synthesis
greater than 5 mmol will stimulate insulin and inhibit glucagon and less than is going to increase glucagon and decrease insulin

Question 56

Q

insulin glucagon ratio

what happens when you eat high carb meal?
what happens when you eat high protein meal?
what happens if you only eat protein and no carbs?

Answer

A

there is always a ratio of glucagon to insulin; so even when sugar is above 5 mmol there will be some glucagon secretion
insulin to glucagon ratio will be increased bc high carb spike in insulin dip in glucagon
if there are high amounts of AA in the blood following a protein meal that is a stimulus for insulin to be released bc it is getting the cells ready for protein synthesis. So there will be a spike in insulin,
glucagon will increase bc you have less glucose in blood and that is a stimulus to the alpha cells to secrete more glucagon. So the insulin glucagon ratio will be low bc glucagon is prob higher and stays higher for a longer time than insulin. Insulin will spike a little and then dip; Insulin stimulates protein synthesis. So therefore high AA levels is a stimulation to the beta cells to release insulin, but if you compare the insulin release when the beta cells are stimulated by high glucose increase vs the AA increase, there is a difference, the level will be less than the glucose stimulation

Question 57

Q

Glucose release during fasting

which organ does this?
2 metabolic processes that lead to glucose release in the blood?

Answer

A

liver

- Glycogenolysis and gluconeogenesis

Question 58

Q

AA release during fasting

what releases it?
What is the fate

Answer

A

skeletal muscle

- Go into liver and make glucose via gluconeogenesis

Question 59

Q

Brain homeostasis

In a fasted state, which organ provides fuel to the brain?
brain fuels

Answer

A

Liver, when fasting there is still glucose in the blood bc the liver is working hard to keep glucose at the homeostasic level.
Glucose and Ketones (used in extreme starvation)

Question 60

Q

Ketones

Where do they come from?
Where are the fats coming from?
which organ produces the ketones?
If you have too much ketone production what will happen?

Answer

A

Fat.
Adipose: during extreme starvation, adipose tissue is doing a lot of mobilization of fats into FA and glycerol in the blood,
The liver: FA get into the liver, get oxidized, and the liver is taking up a lot of fats to make a lot of AcetylCoA. The liver is using some Acetyl CoA for its own TCA/ETC and the abundant ones are converted into ketones, released out in blood and gets to the brain.
Ketoacidosis: This is when someone who hasn’t eaten for a long time will faint

Question 61

Q

main hormone that regulates the fasting state?

Question 62

Q

How does glucagon work at the cellular level

- role of PKA

Answer

A

A glucagon binds to its GPCR (G alpha S) which is a plasma membrane bound receptor. Activates AC which breaks ATP to cAMP and that activates PKA which will recruit other kinases and those kinases are going to phosphorylate and activate diff rate limiting enzymes involved in the diff metabolic cycles that are turned up by glucagon
PKA: has transcriptional regulation and activates CREB which binds to CRE sections of the DNA and activates the transcription of PEPCK
also inhibits the transcription of PFK-1 (rate limiting enzyme of glycolysis) which leads to inhibition of transcription of pyruvate kinase so it stops glycolysis and increases gluconeogenesis

Question 63

Q

PEPCK

Answer

A

(phosphoenol pyruvate carboxykinase) this is a gluconeogenesis enzyme, it is one of those bypass steps of gluconeogenesis, so PEP cannot go back in the other way so it has to take this bypass step and this is the bypass enzyme.

Question 64

Q

rate limiting enzyme of glycogenolysis

Answer

A

Glycogen phosphorylase - this enzyme is phosphorylated and it is activated by a downstream kinase from PKA

Answer 64

A

Insulin binds the extracellular α domain of the insulin receptor tyrosine kinase–> receptor dimerizes–> transmembrane β domains auto-phosphorylate eachother–> IRS (insulin receptor substrate) is recruited to the β domains and are phosphorylated–> PI3K is phosphorylated/activated—> convers PIP2 to PIP3–> Increases PIP3 concentration activates PDK1–> Phosphorylates/activates AKT–> goes on to do a number of things

Answer 65

A

AKT recruits GLUT4 transporter-containing vessicles to the cellular membrane by inhibiting AS160 which allows for an increase in expression of GLUT4 on the cellular membrane so glucose can now enter the cytoplasm of muscle and adipose cells from the blood.
also phosphorylates/inhibits GSK3 which is always acting to inhibit glycogen synthase glycogen synthesis can now occur.
activates mTOR pathway which activates SREBP and releases it from the ER,it translocates to the nucleus, and acts as a transcription factor for the genes responsible for fatty acid synthesis.
Note that a lot of the actions that occur due to the binding of insulin will result in activation by DEPHOSPHORYLATION.

Answer 66

A

inhibit the transport of GLUT4 vessicles to the membrane

Answer 67

A

She would have increased insulin levels.
Poor diet and sedentary lifestyle result in low energy demands, low energy expenditure, and increased storage of glucose in adipose tissue.

Answer 68

A

stuck in a catabolic state and is in a state of starvation
He would have increased levels of glucagon by breaking down muscle to obtain protein for gluconeogenesis and ketone production and breaking down fat due to stress-induced epinephrine in blood circulation.

Answer 69

A

It can be disrupted by prolonged periods of anabolism/catabolism because any prolonged/chronic state causes stress on the body and can cause a sympathetic response to protect vital organs such as the brain and heart.
The fatty acids generated by this stress response used by the heart; breakdown of protein will contribute to ketone production which can be used by the brain as fuel.
If we subject our body to a prolonged/chronic state of one or the other metabolic states (either catabolic or anabolic), homeostasis will be disrupted resulting in starvation or obesity.

Answer 70

A

released by the hypothalamus,
inhibits orexigenic peptides (AgRP and NPY) and increases production of anorexigenic peptides (α-MSH and CART)–> turns down appetite so you don’t want to eat.
more adipose tissue you have, the more Leptin you produce –> more orexigenic peptide inhibition and more anorexigenic peptide stimulation–> will hopefully decrease appetite–> will hopefully make her eat less/lose some of her fat stores.
Less adipose/fat–> less leptin production–> less orexigenic peptide inhibition and less anorexigenic peptide stimulation–> will increase appetite–> will hopefully make him eat more/replace energy stores as a result.

Answer 71

A

She is becoming leptin resistant so the leptin receptors in the hypothalamus are not responding adequately and she is not having satiety occur in the food-inhibiting center.
Now she is more prone to over-eat which will feed into the vicious cycle of more fat deposition–> more leptin–> more desensitization of leptin receptors–> still hungry–> eat more–> more fat deposition—> repeat.

Answer 72

A

produced by the adipose tissue and functions to promote insulin sensitivity.
When adipose tissue is low, adiponectin is increased–> increases the body’s ability to respond to insulin levels–> increasing effectiveness of glucose intake–> increase glucose storage/fat deposition
When adipose tissue is high, adiponectin is decreased–> decreases the body’s ability to respond to insulin levels–> decreasing effectiveness of glucose intake–> decrease glucose storage/fat deposition

Answer 73

A

CCK: comes from I cells in the duodenum during the intestinal phase of digestion; It helps stimulate satiety by inhibiting orexigenic peptides (food-inducing) and increasing anorexigenic peptides (food-inhibiting), It does this because the meal has reached the intestines and there is no need to continue eating.
PYY: Does the same thing as CCK but is produced in the ilium and colon, Tells the hypothalamus that food is in the intestines and colon so there is no need to eat a meal while you are currently digesting a meal.
Ghrelin- is the opposite of lectin; increased during fasting to tell your brain that it is hungry and needs a meal decreased in patients with obesity and increased in patients consuming low calorie diets (also low in patients who are exercising)

Answer 74

A

The apple (central adipose tissue) is worse due to the increased risks that come along with abdominal fat.
Abdominal fat is in close proximity to the liver and fatty-acid breakdown products of the adipose tissue can easily enter the portal circulation. The free fatty acids will stimulate gluconeogenesis/glucose production at the level of the liver–> will stimulate the pancreas to produce more insulin–> chronically desensitizes insulin receptors–> insulin resistance
chronic metabolic imbalance induces a state of stress and epinephrine release which has more of a lipogenic effect on centralized fat than it does on peripheral fat so under stress, abdominal fat will break down a lot more. Additionally, its’ location will allow for easy entrance of free fatty acids into the portal circulation.

Answer 75

A

High glucose levels despite high C peptide levels (adequate insulin production by the pancreas) indicates insulin resistant Type 2 Diabetes.
AKT pathway including AS160 is likely not working which means that GLUT4-containing vessicles are not being released or expressed on the cellular membrane despite insulin binding. This decreases the amount of glucose being taken up into muscle and adipose cells. Hyperglycemia (increased glucose in the blood) is the result.
Even though AS160 pathway is not working the SREBP is still being activated by AKT due to bound insulin, causing increased fatty acid synthesis.
High insulin levels–> increased SREBP activity–> increased fatty acid synthesis–> hyperlipidemia
The protein synthesis pathway still works and is accelerated by insulin levels.
Type 1: There is no insulin produciton–> with no insulin signal, there is decreased fatty acid and protein synthesis–> these patients are thin; Type 2: There IS insulin produciton–> the fatty acid and protein synthesis pathways are still able to respond to insulin–> increased fat and muscle density
Gluconeogenesis is upregulated in diabetic patients despite high blood glucose levels due to metabolic dysregulation (one of the most important things that metformin does as a treatment is decrease gluconeogenesis)

Answer 76

A

® 2 pyruvtaes from 1 glucose because pyruvate is a 3 carbon structure and glucose is a 6 carbon structure
Insulin and glucagon
PFK 1: Insulin will activate PFK2; insulin with dephosphorylate PFK2 making it a kinase and PFK2 will make more Fructose-2,6-bisphophate. And if there is high amount of F-2,6-BP that will activate PFK1 to make more fructose-1,6-bisphopshate. ; indirect regulation but it is still regulation
High levels of glucagon will phosphorylate PFK2 which makes it a phosphatase and will take off the phosphate from 6th position of F-2,6-BP and then it will down regulate PFK1
pyruvate, ATP( 2), NADH (2)

Answer 77

A

Limits too much production of G6p, it prevents cells from absorbing too much glucose

Answer 78

A

regulated by insulin and glucagon

- Insulin will activate and glucagon will de-activate

Answer 79

A

PDH- pyruvate dehydrogenase
It is an enzyme complex: E1, E2, E3
Co enzymes: Vit B 1 (thymine)–most important because E1 is dependent on it; Vit B2–riboflavin, lives in form FAD+/FMN so it is needed to make FADH2; Vit B 3- niacin, because glycolysis produces NADPH and will require niacin because it lives in form of NAD+
Down regulate PDH because PDH is making acetyl CoA so if you already have it you wouldn’t want to make more
No, acetyl CoA cannot be made back into pyruvate–cannot go from fat to glucose directly

Answer 80

A

Dehydrogenases will be down regulated because they make NADH and you already have too much so you want to prevent making more
Will turn off a lot of TCA enzymes, PDH, and GAP-DH in glycolysis

Answer 81

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Iso citrate dehydrogenase, Citrate synthase, Alpha ketogluterate dehydrogenase
Producing 3 NADH and 1 FADH2 and a GTP that can be converted to ATP
Electron carriers for the ETC

Answer 82

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NADH dehydrogenase- it converts NADH to NAD+, this is redox reaction; NADH is giving up 2 electrons as hydride ions and oxidizes to NAD+
Called NADH co-enzyme Q oxidoreductase: because it is redox reaction occurring
FMN: Also known as vit B2–riboflavin; will grab the electrons and give it to Fe-S and then give the electrons to the main acceptor (Co-enzyme Q)
Lipid derivative that moves freely in the mitochondria and is not attached to membrane; Acts as electron carrier and will carry (2) electrons to complex III; it waits for another one, but if another one doesn’t come then it becomes semi-quinone which is a free radical

Answer 83

A

Succinate dehydrogenase is attached to FADH2 and FADH2 will pass electrons to the Iron-sulfur complex to Co-Q
Succinate dehydrogenase is also in TCA enzyme and is shared by ETC; succinate dehydrogenase is what turns FAD into FADH2 in the TCA then will immediately take the FADH2 to complex 2 of the ETC
Carrier between complex II and III is Co-Q

Answer 84

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○ Contributes to proton gradient like complex I (complex II does not)
○ Complex III has complex cytochrome b-C1
□ Similarity between cytochrome and hemoglobin is that they both have heme but the heme is different in that cytochrome heme is Fe+3 and hemoglobin heme is Fe+2

Answer 85

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Helps to recycle one electron from co-enzyme Q through cytochrome B and then back to co-enzyme Q
co enzyme Q from 1 is brining in 2 electrons and cytochrome C between complex 3 and 4 can carry only 1 electron, so the extra electron has to go through a cycle and come back again so that it can be loaded into cytochrome C. So Co-Q coming from complex 2 or 3 will donate 1 electron that will go through Fe-S and will keep going through cytochrome C1 and then cytochrome C which will bring it to complex 4; the other electron will go down to cytochrome b (there are two types of cytochrome b, bH and bL) and be held at the Q site by oxidized co-enzyme making it semi-Q (as known as co-Q H). When the next CoQ goes through the same cycle of donating 1 electron to go through cytochrome C and the other to the Q cite making the co-Q H into co-Q H2.
supplementation of Co-Q10 when on statins is important, because if you deplete the amount of cholesterol with long term use of a statin then you deplete co-Q10 and the effect will be most pronounced in muscles because of high energy demand

Answer 86

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takes electrons from cytochrome C and the electrons will go to Oxygen which will be reduced to water
AAC and has copper.

Answer 87

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there will be high NADH in the blood because NADH will not be able to donate its electron and will therefore stay in reduced form as NADH.
Everything beyond the complex will remain oxidized and everything before the complex will remain reduced; All CoQ will remain oxidized
No ATP will be produced; because there will not be any proton pumping
Lactate dehydrogenase will be activated; High NADH built up in mito which shuts down all dehydrogenases–this causes the TCA to shut down. To compensate for ATP production glycolysis will accelerate to make more ATP–this leads to an increase in pyruvate. In order to prevent a build up of pyruvate that would stop glycolysis and therefore ATP production the pyruvate will be converted to lactate. Over compensation will therefore lead to lactic acidosis.

Answer 88

A

Complex 5 with the ATP anythase
Build up of proton gradient on outside
there is proton build up in intermembrane space, so then the protons will flow down their gradient in complex 5 (proton channel). The proton channel is linked to an F1 portion and as the protons flow down their gradient it will combine ADP with Pi making ATP.

Answer 89

A

Oxidation of NADH ; every time two electrons moves from NADH to the next complex the energy that is released will pump out four protons from that complex
So at complex 1; from complex 1 to 3; from complex 3 to 4 only one electron is moved at a time so only 2 hydrogen will be pumped out at a time
FADH2 comes in at complex 2 and complex 2 does not do proton pumping.

Answer 90

A

It will uncouple ETC from ATP synthesis
The proton gradient is diffused by the un-coupler so there is no more proton gradient and therefore the protons wont come back through complex 5 so ATP will not be produced
It will speed up TCA in order to make more NADH and FADH2 to try and speed up ETC in an effort to make ATP. Electrons are going to oxygen fine but because of presence of un- coupler and absence of proton gradient we are no longer making ATP. Increase in TCA will increase amount of NADH which will transport more electrons to oxygen leading to an increase in oxygen consumption.
Increased basal metabolic rate because at resting state you will have increase in oxygen consumption but less ATP production
When the electrons are being transferred you are producing energy which is normally used to pump out protons, however, since there is not a proton gradient we are not pumping out the protons so the energy comes out as heat and presents as hyperthermia.

Answer 91

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Fructose and galactose

- sucrose comes naturally from fruits (fructose and glucose) lactose comes from milk (galactose and glucose)

Answer 92

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Fructose will be phosphorylated into fructose-1-phosphate by fructokinase (this happens in order to lock it in cell, if not it can just leave the cell through the glut 5 transporter) and then that gets cleaved into DHAP (di-hydroxy acetone phosphate) and glyceraldehyde by aldelase B (also called F1P aldelase). Then the glyceraldehyde gets phosphorylated to glyceraldehyde 3 phosphate (GAP) by triose kinase.
DHAP is also seen in glycolysis, and is a glycolysis intermediate so it will go back into glycolysis immediately, GAP is also an intermediate in glycolysi, Once GAP and DHAP are formed and put into glycolysis they will continue and make pyruvate
Can go to lactate or to acetyl CoA into the TCA to make more fats
There is no feedback inhibition with fructose. So basically, nothing gets blocked at point number one with fructose kinase. So when there is excess fructose you continue to go down same pathway in excess.
no way to inhibit the pathway like we can with glucose since hexokinase is inhibited with product inhibition.

Answer 93

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we will have a lot of pyruvate forming a lot of Acetyl CoA which will supply a lot of carbohydrate carbons to make fat from because we will form acetyl CoA it will go into the TCA, become citrate, and as citrate can get out of the mitochondria, it will get into cytoplasm become oxaloacetate and acetyl CoA and then Acetyl CoA can be used to make fatty acids and cholesterol. We will talk about this more on Monday when we get into lipids, but we can see some fat build up in the liver with excess fructose. Therefore, excess fructose is a risk factor for fatty liver.
lead to increase in lactate because if there is too much pyruvate it will start being shunted into lactate
if there is enough fructose then the liver cells will become exhausted and be unable to make ATP because they run out of phosphates, which will affect the functioning of the hepatocytes
Since pyruvate can also be turned back into glucose with gluconeogenesis then it will cause a higher amount of G6P which can go down pentose phosphate pathway which will form more NADPH and 5-carbon sugars and that will contribute to increase in uric acid
High fructose corn syrup– some experts have said that high fructose corn syrup may be one of the contributing factors to the obesity epidemic and fatty liver epidemic in western countries.

Answer 94

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F1P aldolase cleaves fructose to glyceraldehyde to GAP and then to DHAP so if this is deficient the large amount of fructose being taken in would not be able to be utilized in glycolysis

Answer 95

A

No, because then all peripheral cells will have difficulty keeping glucose in the so that cannot be the problem here. It will be a much bigger problem and probably not a viable mutation.

Answer 96

A

• Glycogen is made up of a lot glucose molecules. Glucose is a monosaccharide and glycogen is a polysaccharide

Answer 97

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Glycogen is stored in the liver and muscle but more in muscle.
Muscle glycogen is for energy and liver glycogen maintains blood glucose homeostasis.
It is highly Branched
alpha 1-6 (at the branch point ) and 1-4 glycosidic bonds (main growing chain)
one reducing end and it is where the anomeric carbon( carbon 1) binds to glycogenin the protein that starts glycogen synthesis.
branches or the ends of the branches are non-reducing ends so they don’t have the anomeric OH available which means the exposed end of the last glucose is the 4th carbon. Having non-reducing ends is good because the enzyme glycogen phosphorylase acts at the non-reducing ends and breaks the glycogen to glucose.

Answer 98

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Glucose is converted to G6P by glucokinase or hexose kinase then it is turned into G1P by phosphoglucomutase. UDP glucose phosphorylase then converts UTP to UDP and adds it to the G1P to give UDP glucose which is ready to form glycogen. We also have a glycogen primer, glycogenin which is already made by the cell. Glycogen synthase will add 4 UDG glucose to the non-reducing end of the glycogenin and facilitate the formation of alpha 1,4 bonds.
When we reach about 11 glucose units in our growing glycogen chain, then the debranching enzyme comes in and cuts out 6-8 units and attach it as a branch forming an alpha 1,6 bond. The process is repeated after about every 10 units

Answer 99

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has a high energy bond like ATP so it is energy producing. When you convert the UTP to UDP you are hydrolyzing a highly phosphate bond which leads the release of energy.

Answer 100

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anabolic enzyme so an anabolic hormone like insulin can stimulate it.
Insulin will dephosphorylate glycogen synthase which activates it and glycogen phosphorylase which inactivates it. This is because synthesis and degradation cannot go on at the same time.

Answer 101

A

no because it involves different enzymes and they are called futile cycle because if the cell is doing both at the same time it will die
Glucagon will phosphorylate glycogen phosphorylase causing activation and glycogen synthase causing inactivation
glycogen phosphorylase will change glycogen to G1P. There is a debranching enzyme involved which comes in and cleaves the alpha 1,6 bonds because glycogen phosphorylase cannot cleave it.
Muscles don’t have glucose 6 phosphatase so when glycogen is degrading in muscles it will go to G6P and then go into glycolysis or pentose phosphate pathway route. It is also a high energy demand tissue
In the liver the G6P will do some glycolysis but most of it will be converted to glucose so it can be released into blood because it has the glucose-6-phosphotase which changes G6P back into glucose

Answer 102

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due to deficiency of G6P phosphatase, so liver wont be able to release glucose into the blood causing G6P to accumulate in the liver which will lead to low glucose.
Fatty acids leading to ketone bodies and high fatty acid in the blood.
There is G6P build which can go glycolysis, so we will have high pyruvate and then high lactate formation.
The G6P can back to glycogen synthesis and so we will have glycogen accumulation leading to the hepatomegaly.

Answer 103

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gycogen phosphorylase deficiency

- will have glycogen accumulation and not G6P and therefore there wont be lactate formation.

Answer 104

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McArdle affects muscle so would have a presentation of muscle weakness/myalgia
pompe is a glucosidase deficiency which is seen as cardiomyopathy and skeletal muscle damage, also very serious in infantile.

Answer 105

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No because glycolysis has 3 irreversible reactions which are mediated by enzymes that are highly regulated and so you cannot go back to those but you need to bypass them and you have a couple of new enzymes coming in

Answer 106

A

pyruvate to oxaloacetate vy pyruvate carboxylase and biotin( B7) which requires ATP.
The formed oxaloacetate will form phosphoenolpyruvate which is a glycolysis intermediate using enzyme PEP carboxykinase
glucagon will activate PEP carboxykinase by increasing its expression and Acetyl CoA will also activate
Once we get to PEP we start to do opposite of glycolysis making 2-phosphoglycerate to 3-phosphoglycerate to 1-3 bisphosphoglycerate,then 2 glyceraldehyde 3- phosphate, and DAP, and both can be converted back to fructose 1, 6 bisphosphate
PFK-1 is an irreversible step so fructose 1,6 bisphosphate to fructose 6 phosphate through fructose 1,6 bisphosphate, then fructose-6-phosphate it will form glucose -6-phosphate by isomerization
G6P goes to glucose through the use of glucose -6-phosphotase

Answer 107

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glucagon will phosphorylate and activate enzyme

Answer 108

A

only present in the liver

Answer 109

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gluconeogenesis is making glucose from non-carbohydrate sources specifically from AA in skeletal muscle including, alanine, serine, creonine, tryptophan

Answer 110

A

Glycemic index: standard amount of available carbs and - Glycemic load: glycemic index times the actual amount of carbs in a serving
glycemic load

Answer 111

A

vegetables, oatmeal, water(LOL), celery

Answer 112

A

donuts, white bread, white pasta, processed food
If the starch looks white it is probably a higher glycemic load, if the starch looks pigmented it is probably a lower glycemic load because more colorful food is processed

Answer 113

A

Because a lot of sugar in a liquid makes the liquid thick and viscous which will start to cause circulation dysfunction, first in the small vessels
Typical body range is 70-100

Answer 114

A

insulin
High
yes, become hypoglycemic

Answer 115

A

processing fiber, fat, protein
Removing the fiber content, increase glycemic load because it is a non-starch polysaccharide that is not digestible by human enzymes

Answer 116

A

Big molecule that can obstruct smaller molecules
Fiber can uptake and trap other sugar molecules which improves insulin sensitivity, and lipid effects
brown flour lost its fiber so it is not trapping the sugar, so you can see a high glycemic spikes with processed grains
White grain has gotten rid of the bran and some of the germ which is unfortunate because it loses some of the vitamins which have to be added back (fortified)
Soluble: dissolves a bit in water and makes a gel like substance and changes viscosity (psyllium like meta-mucil in supplemental form, beta-glucan which is in cognac roots) vs Insoluble: Remains as particles dissolving
Oatmeal, barley, mushrooms
Insoluble fibers good for constipation

Answer 117

A

Decreases glycemic index, absorb fats so it has to metabolize more than one thing at a time so it cant concentrate on glucose; if you have fat in there it will occupy its time to digest fat
Combining carbs with fat or especially protein can slow down the absorption (for diabetic patients)

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Week 4 Flashcards

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