Fed State Metabolism Flashcards

1
Q

Why can’t we digest cellulose?

A
  • lots of linear beta linkages
  • structure allows for cellulose molecules to stack, not very hydrated
  • our enzymes cannot access the cellulose molecules very well when they are stacked
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2
Q

What does amylase in our saliva break starches into?

A
  • maltoses

- dextrins

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3
Q

Which bonds does amylase hydrolyze?

A

-1-4 glycosidic bonds

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4
Q

What transporter transports glucose into intestinal epithelial cells?

A

-SGLT1

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5
Q

Where are GLUT 4 transporters present?

A
  • Adipose tissue

- Muscle Tissue

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6
Q

Where are SGLT 1 transporters present?

A
  • Duodenum
  • Jejunum
  • Renal Tubules
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7
Q

Where are GLUT 5 receptors present?

A

the jejunum

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8
Q

What happens when insulin binds its receptor on adipose and muscle cells?

A

-GLUT4 is upregulated and inserted into the membrane so more glucose can be uptaken

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9
Q

What will happen to extra glucose in the liver?

A
  • protein synthesis
  • glycogen synthesis
  • VLDL synthesis
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10
Q

Where does most fat synthesis occur?

A
  • liver

- then transported to adipose tissue

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11
Q

What will happen to extra glucose in the muscle?

A
  • protein synthesis

- a little bit of glycogen synthesis

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12
Q

What are the three regulated steps in glycolysis?

A
  1. Glucose –> glucose 6-phosphate
  2. Fructose 6-phosphate –> fructose 1,6-bisphosphate
  3. Phosphoenol Pyruvate –> Pyruvate
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13
Q

What are the only tissues that undergo anaerobic metabolism? Why?

A
  • blood: no mitochondria

- Muscle: sometimes needs ATP very quickly, no time for oxidative phosphorylation

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14
Q

What is the first step of glycogen synthesis? Enzyme?

A
  • conversion of glucose 6-phosphate into glucose 1-phosphate

- phosphoglucomutase

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15
Q

What type of bonds are formed by the elongation of glycogen molecules?

A

-alpha 1-4 bonds

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16
Q

What type of bonds are formed by branching of glycogen molecules?

A

-alpha 1-6 bonds

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17
Q

What activates/inhibits glycogen synthase?

A
  • Activate: glucose 6 phosphate (high energy state)

- Inhibits: AMP, Ca, PKA (cAMP)

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18
Q

What is von Gierke disease?

A
  • a defect in glucose 6-phosphatase or the glucose transport system that prevents effective gluconeogenesis
  • results in glycogen accumulation and massive liver enlargement
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19
Q

What is Andersen Disease?

A
  • defect in the branching enzyme of glycogen synthesis resulting in abnormally long chains with fewer branches
  • generally fatal by age 2
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20
Q

What is McArdle/Hers Disease?

A
  • defects in muscle and liver phosphorylase activity, respectively
  • retards the ability of glycogen to be utilized as an energy source
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21
Q

What protease cleaves proteins in the stomach?

A

-pepsin

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22
Q

What activates pepsin (from pepsinogen)?

A

-low pH

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23
Q

Where does pepsin cleave proteins?

A

at aromatic residues

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24
Q

Why is having a low pH in the stomach good for digestion?

A
  • it denatures the proteins we eat

- makes them more accessible to pepsin

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25
Q

Why are proteases released as inactive zymogens instead of active enzymes?

A

-to prevent self-digestion of the secretory tissue and proteases

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26
Q

What are the two ways in which amino acids are absorbed into intestinal epithelial cells?

A
  • sodium-amino cotransporter

- proton-peptide cotransporter

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27
Q

What happens to peptides when they enter the intestinal epithelial cell?

A

-they are cleaved by peptidases into single amino acids then excreted through the basolateral membrane

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28
Q

What are the essential amino acids according to Steen?

A
  • Histidine
  • Methionine
  • Threonine
  • Valine
  • isoleucine
  • Phenylalanine
  • Leusine
  • Lysine
  • Tryptophan
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29
Q

What enzyme converts glutamate to glutamine in most tissues?

A

-glutamine synthetase

30
Q

What enzyme converts glutamine to glutamate in the liver?

A

glutaminase

31
Q

Which organ creates most of the urea we excrete?

A

-liver

32
Q

What do most tissues use as a nitrogen carrier to the liver?

A

-glutamine

33
Q

What does muscle tissue use as a nitrogen carrier to the liver?

A

-alanine

34
Q

What is the net reaction of the urea cycle?

A

2 R-NH2 + HCO3 –> H2N-CO-NH2 (Urea)

35
Q

What amino acid delivers nitrogen to the urea cycle?

A

-aspartate

36
Q

Where do the nitrogens in urea come from?

A
  • one from ammonium from oxidative deamination (or from kidneys)
  • one from aspartate
37
Q

What vitamin is required for amino transferases?

A

-vitamin B6

38
Q

What doe glutamate dehydrogenase use as a reducing agent when synthasizing alpha-ketoglutarate from glutamate, and vice versa?

A
  • NAD+

- NADP+

39
Q

Why isn’t arginine an essential amino acid?

A

-it is synthesized as an intermediate in the urea cycle

40
Q

Where does the urea cycle take place?

A

-split between both the mitochondria and cytosol of liver cells

41
Q

What results from arginosuccinate lyase defficincy?

A

-the inability to synthesize arginine

42
Q

What is the treatment for arginosuccinate lyase defficiency?

A
  • low protein diet

- must be high in arginine though

43
Q

What breaks down triglycerides into diglycerides, monoglycerides, and fatty acids?

A

-lipases

44
Q

How are fatty acids absorbed into the intestine and beyond?

A
  • fatty acids are absorbed via diffusion into intestinal epithelial cells
  • there they are reconverted back into triglycerides
  • These triglycerides are then packaged into micelles called chylomicrons, and secreted into the lymph
45
Q

What are chylomicrons?

A
  • lipoproteins that are very triglyceride rich

- they contain specific apolipoprtoteins that mediate the uptake of chylomicrons by adipose and liver

46
Q

What happens to chylomicrons once they reach the blood stream?

A
  • travel to adipose tissue and muscle where they unload TAGs for storage of energy
  • Travel to the liver where they are broken down and repackaged as VLDLs, which are then sent to the adipose tissue or muscle
47
Q

Where does the lymphatic system dump into the blood stream?

A

Left Subclavian vein

48
Q

What’s the difference between chylomicrons and VLDLs?

A
  • they have same function of delivering fat to the rest of the body, they just have a different origin
  • also, VLDL’s are smaller than chylomicrons
49
Q

What does lipoprotein lipase do?

A
  • breaks down TAGs from chylomicrons and VLDL’s so that they can be absorbed into tissues
  • the entire chylomicron or VLDL is not eaten by the cell, there is a progressive decrease in TAGs
50
Q

What is the main substrate of Fatty Acid synthesis?

A

-malonyl CoA

51
Q

What enzyme catalyzes the entire process of fatty acid synthesis?

A

-fatty acid synthase

52
Q

How is Acetyl CoA transported out of the mitochondria?

A

The citrate/pyruvate shuttle

  • citrate is exported out of the mitochondria and converted to acetyl CoA and oxaloacetate
  • Oxaloacetate is then converted to pyruvate using ATP and transported back into the mitochondria
53
Q

What enzyme converts Acetyl CoA into Malonyl CoA?

A

-Acetyl CoA carboxylase

54
Q

How is acetyl CoA carboxylase present normally in the cell? How is it activated?

A
  • it is in an inactive dimer

- converted to active polymer form in the presence of citrate and other high energy signals like insulin

55
Q

What cofactor serves as a flexible arm to carry the synthetic intermediates of fatty acid synthesis between various active sites of fatty acid synthase?

A

-phosphopantatheine

56
Q

When is the process of fatty acid synthesis complete?

A
  • when it gets to palmitate

- a 16 carbon fatty acid

57
Q

What is the purpose of the pentose phosphate pathway?

A
  • For FA synthesis: generates NADPH
  • Source of 5-C sugars for ribonucleotides
  • provides for the breakdown or interconversion of 5-C sugars to glycolytic intermediates, and vice versa
58
Q

How many NADPH’s are produced per glucose 6-phosphate that enters the pentose phosphate pathway?

A

-2 NADPH

59
Q

Where are the only locations along a fatty acid that post-synthetic desaturation can occur? What are the implications of this restriction?

A
  • C4, 5, 6, and 9 counting from the carboxylate carbon
  • this means that some fatty acids that we require for other pathways cannot be synthesized, and must be acquired from our diet
60
Q

Describe how glucose stimulates insulin release.

A
  • Increased glucose concentration stimulates insulin release by B-cells of the pancreas.
  • Glucose enters the B-cells via GLUT 2 receptors, which leads to an increase in intracellular ATP. The increase in ATP inhibits the Sulfonylurea/Potassium channel, which decreases potassium flux, thus depolarizing the cell. Depolarization leads to influx of calcium ions (via V-Ca channels) which triggers vesicular release of insulin.
61
Q

What are the two main signaling metabolites who’s levels are affected by insulin?

A
  • Fructose 2,6-bisphosphate

- Malonyl CoA

62
Q

Which tissue(s) utilize Gln from protein degradation for energy?

A. Brain

B. Brain and blood

C. Kidney and intestine

D. Blood

E. Muscle

A

C. Kidney and Intestine

63
Q

Intestine can utilize which of the following nutrients:

A. Glucose

B. FAs

C. Glucose and FAs

D. Glucose, FAs, and Gln

E. Glucose, FAs, Gln, and ketone bodies

A

E. Glucose, FAs, Gln, and ketone bodies

64
Q

Resting muscle prefers which energy store during fasting?

A. Glucose

B. FAs

C. Glucose and FAs

D. ketone bodies and glucose

E. Triglycerides

A

B. Fatty acids

65
Q

In the fed state, adipose tissue uses which nutrient for energy?

A. Glucose

B. FAs

C. Ketone bodies

D. Ala and Gln

E. Both Glucose and FAs

A

A. Glucose

66
Q

In which of the following states is liver gluconeogenesis inactive?

A. Fed

B. Fasted

C. Starved

D. Stressed

E. Exercised

A

A. Fed

67
Q

Insulin drops when:

A. you eat a big meal

B. you enter a fasting state

C. you exercise

D. A and C

E. B And C

A

E. When you enter a fasting state and when you exercise.

68
Q

Lipolysis is increased in response to all but which of the following hormones:

A. Glucagon

B. Insulin

C. Norepinephrine

D. Cortisol

E. Growth Hormone

A

B. Insulin

69
Q

When digesting a substantial meal, fat is transported as:

A. Free fatty acids on serum albumin (NEFA)

B. VLDL

C. Free triglycerides

D. Chylomicrons

E. B And D

A

E. VLDL and Chylomicrons

70
Q

In the post-absorptive states 3-5 hours after feeding, the main source of blood glucose is:

A. Muscle

B. Liver glycogen

C. Liver Gluconeogenesis

D. Kidney Gluconeogenesis

E. Intestinal breakdown of food

A

B. Liver Glycogen

71
Q

All but which of the following are gluconeogenic precursors?

A. Glutamine (Gln)

B. Alanine (Ala)

C. Glycerol (GOL)

D. Lactate (Lac)

E. Fatty acids (FA)

A

E. Fatty Acids (FA)

72
Q

Which of the following are circulating energy sources during starvation:

A. Glucose

B. Fatty Acids

C. Acetoacetate

D. 3-hydroxybutyrate

E. All of the above

A

E. All