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Gastrointestinal System > Neurochemical Control of Food Intake > Flashcards

Neurochemical Control of Food Intake Flashcards

1
Q

How is BMI calculated?

A

Weight in kg/(Height in m)^2

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2
Q

What does a BMI of 25 mean?

A

Normal

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3
Q

What does a BMI of 25 to 30 mean?

A

Overweight

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4
Q

What does a BMI of over 30 mean?

A

Obese

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5
Q

How does obesity occur?

A

When the calorie intake is greater than the calories burned

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6
Q

What are the three ways the body can deal with the excess dietary calories?

A

Convert excess fuel to fat and store it in adipose tissue

Burn excess fuel by extra exercise

Waste fuel by diverting it to heat production

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7
Q

Where does thermogenesis occur?

A

Uncoupled mitochondria

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8
Q

What does excess adiposity lead to?

A

Common chronic diseases like diabetes, fatty liver and heart failure

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9
Q

What is the primary physiological role of white adipose tissue?

A
  1. Function as a daily buffer of circulating lipids

Store dietary lipids in the fed states

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10
Q

What do white adipose tissues do in the fasted state?

A

Release free fatty acids in the fasted states

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11
Q

What do white adipose tissues do in the fed state?

A

Store dietary lids in the fed states

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12
Q

Based on studies and graphs what are the results of DCR and VLCD diets?

A

A percentage of starting body weight is lost during the first 12 months but then is gradually regained.

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13
Q

What is the lipostat theory?

A

Fat-borne factors act on the brain to regulate energy homeostasis and control levels of adiposity through different mechanisms

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14
Q

What mechanisms control the levels of adiposity?

A

Inhibiting eating behavior
Increasing energy consumption

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15
Q

When are the mechanisms of controlling adiposity levels initiated?

A

Whenever the body exceeds a specific value known as the setpoint

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16
Q

When are the mechanisms inhibited?

A

When the body weights drops below set point, patients starts eating and again and decreases energy consumption.

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17
Q

What happens to the body during diet that affects the set point?

A

When starting a diet, the fat reserve decreases, which causes the brain to think you are running out of energy and basically starving, no matter how overweight you may be. Thus the brain forces you to eat.

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18
Q

What is leptin?

A

A peptide hormone encoded by the ob gene.

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19
Q

Where is leptin mainly secreted?

A

Mainly secreted by the adipocytes

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20
Q

What is the function of leptin?

A

It carries the message about the level of fat reserves in the body

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21
Q

What is monogenic obesity?

A

Obesity resulting from a mutation or deficiency in a single gene (ob gene)

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22
Q

In mice; what happens when there are two defective copies of the ob gene?

A

Their serum cortisol levels are elevated

They grow abnormally

They exhibit unrestrained appetite

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23
Q

What is the result of having two defective copies of the ob gene (as seen in mice)?

A

They become severely obese

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24
Q

What is monogenic obesity like in humans?

A

They exhibit an unrestrained appetite

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25
Q

What is the treatment of monogenic obesity in humans?

A

Leptin injections

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26
Q

How do leptin injections work?

A

Increased energy expenditure and reduced eating, marked weight loss

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27
Q

What is the difference in genes between obese people and monogenically obese individuals?

A

Obese people do not have a defective ob gene, and they also have high levels of leptin.

Individuals suffering from monogenic obesity have defective ob gene and thus cannot produce leptin

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28
Q

What is leptin resistance?

A

Desensitization to leptin, when too much is given.

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29
Q

What is the mechanism of leptin?

A

It regulates adipose-tissue mass by promoting lipolysis and thermogenesis through a negative feedback, through the sympathetic nervous system.

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30
Q

What is the process of lipolysis?

A

Leptin is released from the adipose tissues, which are neural signals via sympathetic neurons.

The adipose cells circulating have receptors for nor-adrenaline which activates the release of adenocyclase when bound. There is phosphorylation of ATGL, HSL, and MGL.

Fat stored in adipocytes gets converted into fatty acids and glycerol and moves to the liver to be metabolized.

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31
Q

How is thermogenesis initiated?

A

By promoting uncoupling proteins activity

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32
Q

Where does leptin act in the brain?

A

Hypothalamic arcuate nucleus

33
Q

Which are the appetite-stimulating neurons?

A

The orexigenic

34
Q

How do orexigenic neurons work?

A

Stimulate eating by producing and releasing neuropeptide Y (NPY) which causes the next neuron in the circuit to send the signal to the brain to eat more.

35
Q

Which are the appetite-suppressing neurons?

A

The anorexigenic

36
Q

How do anorexigenic neurons work?

A

Anorexigenic neurons in the arcuate nucleus produce α-MSH. The release of α-MSH causes the next neuron to send the signal to the brain to eat less

37
Q

What is α-MSH formed by?

A

Its precursor polypeptide precursor pro-opiomelanocortin (POMC)

38
Q

What are orexigenic and anorexigenic neurons activated by?

A

Leptin, when leptin bind to their receptors, it gets phosphorylated and releases STAT3

39
Q

What is STAT3?

A

It is a protein that regulates the signal sent to brain through the neurons to either increase or decrease appetite

40
Q

What is insulin?

A

A hormone secreted from the β-cells in the pancreas

41
Q

Where are insulin receptors expressed? How does that link to leptin?

A

In both NPY and POMC neurons, it also regulates caloric homeostasis as it acts on the same neurons and in the same way as leptin

42
Q

What happens if the POMC neurons are activated?

A

Appetite is reduced

43
Q

What is the function of leptin and insulin?

A

The regulation of long-term level of fat stored in the body.

44
Q

Is obesity a genetic condition?

A

Rarely, obesity occurs in families according to CLEAR inheritance patterns caused by changes in a single gene

45
Q

What is the most commonly implicated gene in familial obesity?

A

MC4R which encodes the melanocortin 4 receptor

46
Q

What is the effect of mutations in the MC4R gene?

A

Diminishment of its function

47
Q

How common are mutation in the MC4R gene in the obese population?

A

A small fraction, <5%

48
Q

What is the main clinical sign of kids who suffer from the MC4R mutation?

A

Affected children feel extremely hungry and become obese because of hyperphagia

49
Q

What are L cells?

A

Endocrine cells and not absorbing cells

50
Q

What is the function of L cells?

A

To identify what kind of nutrient/substance has arrived in the intestine

51
Q

Where are GLP1 and GLP1/PYY mainly found?

A

Duodenum/Jejunum
Rectum

52
Q

Where is Gherkin primarily found?

A

In the stomach

53
Q

Where is GIP mainly found?

A

Duodenum

54
Q

What is Gherlin?

A

The hunger signal

A peptide hormone that is synthesized and released from endocrine cells of the stomach.

55
Q

Does appetite change immediately if there is an imbalance in leptin?

A

No, however there are other hormones that have an immediate effect on appetite

56
Q

What is the function of Gherlin?

A

Excites orexigenic neurons in the arcuate nucleus

Inhibits anorexigenic POMC nuerons

57
Q

When is Gherlin released?

A

Before a meal, in order to stimulate hunger and tell the body to eat

58
Q

What is the relation between Gherlin and insulin?

A

Negative correlation

59
Q

How does the size/volume of the stomach relate to appetite?

A

Usually enlarged gastric capacity is related to overeating

60
Q

What is the relation between glucose and L cells?

A

L cells detect the glucose through glucose transporters.

Glucose binds with sodium and the positive charge of the sodium causes changes in the membrane potential.

61
Q

What is the result of membrane changes caused by the sodium?

A

Increase in calcium secretion which releases the gut hormones

62
Q

What are the gut hormones?

A

GLP 1
GIP
CCK
SCT

63
Q

What is the effect of glutamine on GLP1?

A

Triggers and potentiates GLP1 secretion by raising cytosolic Ca2+ and cAMP

64
Q

How do different amino acids have different effects on the concentration of insulin released?

A

Different amino acids cause different levels of glucose secretion and thus insulin

65
Q

How does insulin give a heads up about storage of glucose?

A

Insulin activates the β-cells in the pancreas and gives a heads-up to store glucose

66
Q

What is the incretin effect?

A

The phenomenon where oral glucose elicits higher insulin secretory responses than does intravenous glucose

67
Q

Where are GLP1 and PYY synthesized and secreted?

A

L cells in the large intestine

68
Q

What are the functions of GLP1?

A

Stimulating insulin secretion and directly activating POMC neurons (anorexigenic)

69
Q

How does GLP1 reduce food intake?

A

Through signaling mechanisms requiring functional GLP1 receptors in the arcuate nucleus

70
Q

What is Semaglutide?

A

A glucagon-like peptide 1 analogue (GLP1 analogue)

71
Q

What is Tirzepatide?

A

A novel GIP and GLP1 receptor agonist, combination of both, works even better than mono therapy

72
Q

What are the two common types of bariatric surgeries?

A

Roux-en-Y gastric bypass
Vertical sleeve gastrectomy

73
Q

Which kind of patients does bariatric surgery specifically benefit?

A

Type 2 diabetes patients

74
Q

How does bariatric surgery help type 2 diabetes patients?

A

Reduced plasma glucose levels after bariatric surgery (due to loss of body weight and adiposity) improve insulin sensitivity

75
Q

Bariatric patients have elevated post…?

A

Post-prandial insulin secretion

76
Q

What happens during the RYGB procedure?

A

The esophagus is attached to the pylorus, completely bypassing the stomach.

Decreased absorption

77
Q

What happens during the vertical sleeve gastrectomy?

A

Removal of about 80% of the stomach.

Adrenaline levels will be much less because the patient gets fuller faster and thus eats less.

78
Q

How does bypass surgery help GLP1 secretion?

A

Increased nutrient flow to the distal gut

Increased postprandial GLP1 triggers higher insulin levels

Gastrointestinal System (28 decks)

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