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Metabolism > Role of the GIT in Obesity > Flashcards

Role of the GIT in Obesity Flashcards

1
Q

Weight is regulated in the

A

Hypothalamus

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2
Q

Which nucleus in the hypothalamus regulates body weight?

A

Arcuate nucleus

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3
Q

What are the two classes of nerves in the arcuate nucleus?

A

NPY (NPY and AgRP)

POMC (CART and aMSH)

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4
Q

NPY nerves release _______ when they fire which ________ appetite

A

NPY and agouti-related protein (AgRP); increase appetite

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5
Q

POMC nerves release ________ when they fire which _________ appetite

A

CART (cocaine and amphetamine related transcript) and aMSH; decrease appetite

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6
Q

Which hormones from the stomach regulate food intake at the arcuate nucleus?

A

Ghrelin

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7
Q

Which hormones from the small bowel regulate food intake at the arcuate nucleus?

A

CCK, PYY, GLP-1, Oxyntomodulin, Uroguanilin

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8
Q

Which hormones from the pancreas regulate food intake at the arcuate nucleus?

A

insulin, amylin, PP

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9
Q

Ghrelin ________ appetite by activating _______

A

increases; NPY and its mRNA

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10
Q

Leptin ________ appetite

A

decreases;

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11
Q

Ghrelin and leptin work

A

antagonistically

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12
Q

Ghrelin rises _________ and drops __________

A

before a meal; after a meal - diurnal variation

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13
Q

ILP-5 ________ appetite via ________

A

increases; relaxin5 receptor (GPCR)

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14
Q

ILP-5 is expressed

A

colon; less so in ileum, none in jejunum

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15
Q

Which hormone is the most powerful driver of hunger?

A

NPY > Ghrelin > ILP-5

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16
Q

CCK is made in the

A

upper bowel/I cells of small intestine

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17
Q

CCK is made as a

A

preprohormone

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18
Q

Which CCK peptide has the highest potency?

A

CCK8

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19
Q

CCK is secreted from

A

I cells in small intestine

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20
Q

The half-life of CCK is

A

short (~mins)

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21
Q

CCK stimulates

A

emptying of the gallbladder and release of digestive enzymes

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22
Q

CCK acts through which receptors?

A

CCK1 and CCK2

23
Q

CCK _________ food intake and is involved in _________

A

inhibits; digestion

24
Q

CCK mediates its effects mainly via

A

CCK1R on the vagus nerve

25
Q

Why doesn’t CCK work as a tx in obesity?

A

Reduces food intake but increases number of meals

26
Q

PYY is made in the

A

L cells of the GIT (ileum)

27
Q

PYY ________ food intake and _______ body weight

A

reduces; decreases (chronic)

28
Q

PYY is cleaved by

A

DPP4; the enzyme that degrades GLP-1, oxyntomodulin

29
Q

What is the action of PYY?

A

reduces food intake (and body weight if used chronically); increases feelings of satiety (but also nausea)

30
Q

Oxyntomodulin is a product of which gene?

A

Glucagon

31
Q

Oxyntomodulin is released from

A

L cells of the lower small intestine in response to food

32
Q

Oxyntomodulin ________ food intake and _________ energy expenditure

A

reduces; increases

33
Q

Oxyntomodulin may mediate its effects via which receptor?

A

GLP-1 R

34
Q

Oxyntomodulin is inactivated by

A

DPP4

35
Q

T/F Oxyntomodulin is more potent than GLP-1

A

True

36
Q

What is the benefit of combining PYY and oxyntomodulin?

A

they work synergistically to further reduce food intake

37
Q

GIP

A

gastric inhibitory peptide/glucose-dependent insulinotropic polypeptide

38
Q

What are the incretin hormones that stimulate insulin secretion?

A

GIP and GLP-1

39
Q

GIP is released from

A

duodenal and jejunal K cells after ingestion of nutrients

40
Q

What is the action of GIP?

A

stimulates insulin release, activates lipoprotein lipase (clears fat from plasma for storage)

41
Q

What are the actions of GLP-1?

A

increases period of postprandial satiety, slows gastric emptying

42
Q

GLP-1 decreases intake of

A

food quantity, calories, and fluid

43
Q

Liraglutide

A

human GLP-1 w/attached FA molecule (enters brain more readily)

44
Q

What is the concern with using liraglutide?

A

it increases HR; BP drops with weight loss but the HR does not change

45
Q

Uroguanylin is produced in

A

the distal gut

46
Q

What are the actions of uroguanylin?

A

decreases food intake via the brain; decreases intestinal fluid absorption via the gut

47
Q

What happens to leptin following weight loss?

A

leptin decreases dramatically with weight loss (70% below fasting) and starts to rise only in proportion to weight gain

48
Q

What happens to ghrelin following weight loss?

A

ghrelin increases (it still follows diurnal variation with meals) tf more hungry

49
Q

What happens to PYY following weight loss?

A

PYY decreases; making you more hungry

50
Q

What happens to CCK following weight loss?

A

CCK decreases; making you more hungry

51
Q

Why do hunger hormones increase and satiety hormones decrease following weight loss?

A

Defensive mechanism to maintain body weight

52
Q

T/F Hunger hormones and satiety hormones go back to baseline 1yr after weight loss

A

False; Ghrelin is still increased, PYY and CCK are still decreased - this is why it is so hard to maintain weight loss

53
Q

T/F Gut hormones play an important role in the defense of body weight

A

True; levels of hunger hormones (ghrelin) are increased and satiety hormones (CCK, PYY) are decreased even 1yr post weight loss

54
Q

How do gut bacteria influence body weight?

A

processing of dietary indegestable polysaccharides to short-chain fatty acids (butyrate, acetoacetate) which protect against bowel cancer - this increases calories and fat absorption in the liver; increased activity of LPL and tf fat storage

Metabolism (16 decks)

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