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2) Biochemistry II > Regulation of Body Mass, Metabolic Syndrome, and Type II Diabetes > Flashcards

Regulation of Body Mass, Metabolic Syndrome, and Type II Diabetes Flashcards

1
Q

What are the effects of increased glucose post-prandial?

A

Increased glycolysis and glycogenesis

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2
Q

What happens 2 hours post-prandial?

A
  • Glucose decreases

- Liver glycogen releases glucose (glucagon)

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3
Q

What happens 4 hours post-prandial?

A
  • More glucagon is secreted
  • More TG hydrolysis
  • FA becomes the major fuel
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4
Q

What happens to non-essential amino acids in prolonged fasting?

A

They are deaminated

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5
Q

Which proteins are preferentially depleted in the liver and heart?

A

Lys-Phe-Glu-Arg-Gln

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6
Q

In prolonged fasting, what happens to oxaloacetate?

A
  • Diverted to gluconeogenesis

- Prevents Acetyl-CoA entry into the TCA cycle –> accumulation of Acetyl-CoA

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7
Q

What is oxidized as fuel during prolonged fasting?

A

Fatty acids, produces Acetyl-CoA

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8
Q

What does an accumulation of Acetyl-CoA during prolonged fasting lead to?

A

Favors ketone body synthesis

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9
Q

What is the main difference between a normal weight person and an obese person’s stores?

A

More adipose tissue for obese people (better hibernation, fasting)

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10
Q

How long can someone survive fasting if hydrated?

A

30 to 40 days

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11
Q

When do severe symptoms appear after fasting? When does death occur? Due to what?

A
  • Symptoms: 35 to 40 days
  • Death: 40 to 61 days
  • Organ failure or myocardial infarction
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12
Q

What do people die from during starvation?

A
  • Not from starvation/lack of nutrients

- Infectious diseases due to a weakened immune system

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13
Q

Differentiate Type 1 and Type 2 diabetes.

A
  • Type 1: insufficient production of insulin (problem in insulin concentration)
  • Type 2: insulin resistance (problem in insulin signaling)
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14
Q

What is the cause of Type 1 diabetes?

A
  • Usually due to an autoimmune destruction of B-cells

- Usually develops early in life (childhood diabetes)

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15
Q

What is the cause of Type 2 diabetes?

A

B-cells work so hard, that they eventually give up and do not respond appropriately to insulin

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16
Q

What is elevated in diabetes? What is the consequence?

A
  • Blood glucose
  • Increased osmolality
  • Excessive urination and thirst
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17
Q

What is the consequence on proteins due to glucose abnormalities?

A

Proteins get glycosylated, which leads to abnormal functions

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18
Q

What happens in Type I diabetes? What are the consequences?

A
  • Fat breakdown is accelerated, which leads to an increase in ketone bodies
  • Increase in blood (H+) leads to ketoacidosis
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19
Q

What does ketoacidosis activate in Type I diabetes? What does that lead to?

A
  • Bicarbonate buffering system is activated, which leads to altered breathing patterns
  • Breakdown of acetoacetate produces acetone, which is expelled via the breath
20
Q

What does untreated Type I diabetes lead to?

A
  • Dramatic weight loss

- Breakdown of proteins and lipids as an energy source

21
Q

What hormones does adipose tissue release?

A
  • Peptide hormones called adipokines

- Carry information about fuel stores to the brain

22
Q

What are orexigenic neurons?

A

Increase appetite and eating behaviour

23
Q

What are anorexigenic neurons?

A

Decrease appetite by inducing satiety

24
Q

What are the consequences of leptin?

A

Activates a-MSH, which activates anorexigenic neurons (less eating)

25
Q

What are the consequences of insulin?

A

Inactivates NPY, which inactivates orexigenic neurons (less eating)

26
Q

What are the consequences of ghrelin?

A

Activates NPY, which activates orexigenic neurons (more eating)

27
Q

What are the consequences of satiety signals, such as PYY?

A

Inactivates NPY, which inactivates orexigenic neurons (less eating)

28
Q

What happened to homozygous ob/ob mice?

A
  • Ate continually

- Obese, elevated cortisol, shivered, infertile, insulin resistance, died early

29
Q

What happened to homozygous ob/ob mice when leptin was injected?

A

The mice lost weight and temperature returned to normal

30
Q

Why does leptin administration to obese people not restore normal body mass?

A
  • Since they have higher levels of leptin

- Theory of leptin resistance

31
Q

What are db/db mice? What does the db gene encode for?

A
  • Obese and diabetic

- db gene encodes the leptin receptor (Lepr) in the brain, and is mostly expressed in the hypothalamus

32
Q

Where is ghrelin secreted? Where are the ghrelin receptors?

A
  • Secreted from the stomach

- Receptors: brain, heart, adipose tissue

33
Q

How does ghrelin work? What is the consequence of injecting ghrelin?

A
  • Works via GPCR to increase the sensation of hunger

- Injection of ghrelin immediately increases appetite

34
Q

What is PYY?

A
  • Appetite-suppressing hormone

- Peptide with 36 AA with two Tyrosine (Y) residues at the end

35
Q

Where is PYY secreted from? What does it activate/inhibit? What is the result

A
  • Secreted from the small intestine and colon
  • Inhibits the release of orexigenic NPY neurons
  • Results in reduced hunger
36
Q

What are most bacterial products?

A

Short-chain FA: acetate, propionate, butyrate

37
Q

What is the consequence of propionate?

A
  • Acts through GPCR 43 and 41
  • Stimulates adipocyte differentiate
  • Inhibits lipolysis
  • Fat is not hydrolyzed, and accumulates in adipose tissue
38
Q

Some microorganisms create __________ that affect adipose tissue

A

fermentation products

39
Q

What do enlarged adipocytes produce?

A

Macrophage chemotaxis protein (MCP-1)

40
Q

What is the effect of MCP-1?

A

Attracts macrophages, which infiltrate adipose tissue

41
Q

What is the effect of macrophage infiltration?

A
  • Exports fatty acids to muscle
  • Interferes with GLUT4 (insulin-sensitive)
  • Produces insulin resistance (Type II diabetes)
42
Q

How does insulin resistance lead to the accumulation of fat?

A
  • If glucose is not utilized, it is stored as glycogen

- But, since there is a limit for glycogen storage, excess glucose is converted to fatty acids

43
Q

Which would be most important to produce sugars required in high concentrations for mitosis?

A) Pentose phosphate, oxidative
B) Gluconeogenesis
C) Lactate fermentation
D) Pentose phosphate, non-oxidative 
E) None would contribute the specific sugars required in advance of mitosis
A

A) Pentose phosphate, oxidative phase

44
Q

What product of the preparatory phase of glycolysis is required in the payoff phase, but at twice the concentration?

A) DHAP
B) Pyruvate
C) NAD+
D) ADP

A

D) ADP

45
Q

Which of the following strategies is NOT actually applied in the coordinated regulation of glucose metabolism?

A) A change in the expression of metabolic enzymes
B) An allosteric change in the activity of metabolic enzymes
C) A change in the cellular location of existing metabolic enzymes
D) Phosphorylation or dephosphorylation of an enzyme in a metabolic pathway
E) All of the above strategies in cells function to regulate glucose metabolism

A

E) All of the above strategies in cells function to regulate glucose metabolism

2) Biochemistry II (23 decks)

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