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Biochemistry 2 > Body Mass Diabetes > Flashcards

Body Mass Diabetes Flashcards

1
Q

Does hexokinase 4 have a high or low affinity for glucose? What about hexokinase 1?

A

Hexokinase 4: low affinity (Liver doesn’t use glucose until it is very high in [])

Hexokinase 1: high affinity

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2
Q

What does post-prandial mean?

A

post food intake

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3
Q

What happens to glucose levels immediately after a meal? What is secreted as a result? What two glycolytic pathways become activated?

A

Glucose levels increase

Insulin is secreted: glycolysis and glycogenesis increase

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4
Q

What happens to glucose levels 2 hours post-prandial? What is secreted as a result?

A

Glucose levels begin to drop.

Glucagon is secreted

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5
Q

What is secreted 4 hours post-prandial?

A

more glucagon

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6
Q

What becomes a major fuel 4 hours post prandial? What is being hydrolized?

A

FA - more TGA hydrolysis

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7
Q

During prolonged fasting, what does the body start to break down? For what purpose?

A

The liver breaks down non-essential (glucogenic!) AAs to provide fuel to the brain

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8
Q

What 2 reactions do the non-essential AAs degraded by the liver undergo? What does this break the AAs into?

A

Transimation and deamination reactions

Carbon skeleton + NH3(+)

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9
Q

What happens to the extra amino groups of the non-essential AAs after undergoing transamination/deamination reactions?

A

Converted to urea, which is exported via the bloodstream to the kidneys and excreted in the urine

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10
Q

What are the carbon skeletons of the non-essential glucogenic amino acids converted to? What does this lead to?

A

Pyruvate or intermediates of the TCA cycle. This leads to gluconeogenesis in the liver

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11
Q

What does gluconeogenesis yield?

A

Glucose for export to the BRAIN!!!

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12
Q

Where do FAs come from that are imported into the liver?

A

Adipose tissue

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13
Q

What happens to FAs that enter the liver from adipose tissue?

A

They are oxidized as fuel, producing acetyl-CoA

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14
Q

Why is the acetyl-CoA that was produced from FAs unable to enter the TCA cycle? What happens to acetyl-CoA?

A

because oxaloacetate is constantly being depleted by the use of the TCA cycle intermediates for gluconeogenesis. Acetyl-CoA accumulates!

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15
Q

What does the accumulation of acetyl-CoA in the liver favor the formation of?

A

Acetoacetyl-CoA + ketone bodies

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16
Q

What happens to the ketone bodies formed via the accumulation of acetyl-CoA in the liver? What happens to the excess ketone bodies?

A

They are exported to the brain via the bloodstream. Brain uses them as fuel. The excess end up in the urine

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17
Q

What is necessary for starvation?

A

The accumulation of fat

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18
Q

Proteins containing what sequence are preferably depleted in the liver and heart?

A

Lys-Phe-Glu-Arg-Gln

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19
Q

In terms of fuel reserves in the body, what is the main difference between obese and normal weight people?

A

Adipose tissue.

Extra fat = extra fuel…but also means increased inflammation, electrolyte imbalance, etc.

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20
Q

How many days can one survive on a hunger strike?

A

30-40 days IF HYDRATED

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21
Q

When on a hunger strike, when do severe symptoms begin to appear? Examples?

A

35-40 days (hallucinations, seizures, susceptible to infection, etc.)

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22
Q

People that are starving die of what?

A

Infection, not lack of nutrients by itself

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23
Q

What is type 1 diabetes? What is the cause? When does it develop?

A

Insufficient production of insulin.

Cause: Autoimmune destruction of beta-cells

Early in life - childhood

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24
Q

What is type 2 diabetes? When does it develop? How do cells interact with insulin?

A

Insulin resistance.
Also associated with reduced insulin because beta-cells eventually give up.

Develops in late adulthood

Cells don’t respond appropriately to insulin

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25
Q

In which type of diabetes is blood glucose elevated?

A

Both types

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26
Q

What do people that have diabetes do a lot?

A

Pee a lot and drink lots of water - always thirsty (increased osmolality)

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27
Q

Osmolality of blood increases with what?

A

Dehydration

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28
Q

What happens to proteins in diabetes?

A

They get glycosylated: become abnormally functional

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29
Q

In type 1 and advanced type 2 diabetes, what accelerates? What does this lead to?

A

Fat breakdown accelerates –> ketone bodies

30
Q

In type 1 diabetes, what does raised blood [proton] lead to?

A

ketoacidosis

31
Q

In type 1 diabetes, what does the activation of the bicarbonate buffering system lead to?

A

altered breathing pattern

32
Q

In type 1 diabetes, what does the breakdown of ketone body acetoacetate produce? How is it expelled? What does this cause behaviorally?

A

Acetone which is expelled via breaths

Causes slow and deep breaths

33
Q

What does untreated diabetes lead to?

A

dramatic weight loss

34
Q

Adipose tissue is also what?

A

An endocrine organ

35
Q

What do adipose tissues release?

A

Peptide hormones called adipokines.

36
Q

What is the function of adipokines that are released from adipose tissue?

A

Carry information about fuel stores to the brain - signal to the brain to control appetite and food intake

37
Q

What are two examples of adipokines?

A

Leptin

Adiponectin

38
Q

What hormone do anorexogenic neurosecretory cells carry? What message does this hormone carry to neurons in the hypothalamus?

A

alpha-MSH

“Eat less, metabolize more”

39
Q

What hormone do orexogenic neurosecretory cells carry? What message does this hormone carry to neurons in the hypothalamus?

A

NYP

“Eat more, metabolize less”

40
Q

What hormone(s) activate the release of alpha-MSH from anorexogenic neurosecretory cells?

A

Leptin (secreted from adipose)

41
Q

What hormone(s) activate the release of NPY from orexogenic neurosecretory cells?

A

Ghrelin (secreted from stomach)

42
Q

What hormone(s) inhibit the release of NPY from orexogenic neurosecretory cells?

A

Leptin (secreted from adipose)

PYY(36-6) & GLP-1 (secreted from gut)

Insulin (secreted from pancreas)

43
Q

Once the neurosecretory cells in the hypothalamus receive hormonal input, where do they relay the signals to?

A

To cells of muscle, adipose tissue, and liver/.

44
Q

What does the leptin hormone do?

A

It reduces appetite

45
Q

Where was the leptin gene first identified? What was the behavior of ob/ob mice?

A

Obese mice.

Ate continually, obese, elevated cortisol (stress hormone), shivered (uncontrollable body weight), infertile, insulin resistance, died early.

46
Q

What happened to the obese mice when leptin was injected into their body?

A

The mice lost weight & body temp returned to normal.

47
Q

How does the injection of leptin affect obese people?

A

They do not lose weight, do not restore normal body mass

48
Q

What does the db gene encode?

A

It encodes the leptin receptor (Lepr) in the brain (mainly in hypothalamus?)

49
Q

How can the db/db mice be characterized?

A

obese and diabetic

50
Q

What is Ghrelin?

A

A short-term orexigenic peptide that is secreted from the stomach.

51
Q

Where can ghrelin receptors be found?

A

Brain, heart, adipose tissue

52
Q

What receptor/signaling pathway does Ghrelin bind to? Purpose?

A

GPCP

Purpose: to increase the sensation of hunger

53
Q

What happens immediately after the injection of ghrelin in the body?

A

Increased appetite

54
Q

How can the PYY hormone be characterized?

A

Appetite suppressing. “Eat less, metabolize more”

55
Q

How many AAs does the PYY peptide contain? It has __ _____ residues at the end.

A

36 AA

2 tyrosine

56
Q

Where is PYY secreted from?

A

Small intestine, colon

57
Q

What does PYY inhibit? What does this result in?

A

The release of orexigenic NYP neurons.

Result: reduced hunger

58
Q

What affects gut microflora?

A

Diet.

Obese and lean people have different gut microflora.

59
Q

What do some microorganisms create that affects adipose tissue?

A

Fermentation products

60
Q

What are the majority of bacterial products? Give 3 examples

A

Short-chain FA.

  1. acetate
  2. propionate
  3. butyrate
61
Q

What receptor does propionate act through?

A

GPCR 43 & 41

62
Q

What does propionate stimulate? What does it inhibit?

A

Stimulates adipocyte differentiation

Inhibits lipolysis

63
Q

In an individual with a healthy body mass, what does TAG uptake from diet = ?

A

= TAG catabolized

64
Q

In overweight individuals, what does excess caloric intake result in?

A

Enlarged adipocytes, overloaded with TAGs and unable to store more

65
Q

What do enlarged adipocytes secrete? What does this attract?

A

MCP-1 which attracts macrophages

66
Q

What do the macrophages that were attracted to adipose tissue due to the secretion of MCP-1 do?

A

They take over the adipose tissue and produce TNF-alpha (tumor necrosis factor).

67
Q

What does TNF-alpha favor?

A

It favors the export of fatty acids from adipocytes to muscle.

68
Q

What happens as FAs are exported from adipocytes to muscle?

A

Ectopic (small) lipid deposits form in muscles.

69
Q

What do ectopic lipid droplets in the muscle interfere with?

A

Interferes with GLUT4 movement to the myocyte surface…this causes insuline resistance.

70
Q

What is one held belief about insulin resistance due to TAG overload?

A

Insulin resistance leads to obesity. But I believe that….obesity leads to insulin resistance.

Biochemistry 2 (8 decks)

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