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ENI > Metabolic Hormones > Flashcards

Metabolic Hormones Flashcards

1
Q

Where is gastrin produced?

A

G cells in distal stomach

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2
Q

Where is secretin produced?

A

duodendum

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3
Q

Where is cholecystokinin produced?

A

Duodenum

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4
Q

Where is gastric inhibitory peptide produced?

A

Duodenum

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5
Q

Where is glucagon-like peptide (GLP-1) produced?

A

Ileum L cells

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6
Q

Where is motilin produced?

A

duodenum and jejunum

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7
Q

Where is ghrelin produced?

A

Stomach

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8
Q

What is the release stimuli for gastrin?

A

Presence of peptides and AA in the stomach
Stomach distention
Vagal stimulation
Hypercalcaemia

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9
Q

What are the effects of gastrin?

A

Stimulates release of gastric acid from parietal cells

Stimulates pepsinogen release from chief cells

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10
Q

What is the release stimuli for secretin?

A

H+ in the small intestine

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11
Q

What are the effects of secretin?

A

This signals to the exocrine pancreas that food is on its way and it should start secreting bicarb and digestive enzymes now

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12
Q

What is the release stimuli for Cholecystokinin CCK?

A

Fatty acids, monoglycerides and AA in the small intestine

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13
Q

What are the effects of Cholecystokinin?

A

This is the gall bladder squeezing hormone, when products of digestion reach the duodenum then CCk signals for the exocrine pancreatic secretion. CCK is more enzymes and secretin is more bicarb.

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14
Q

What is the release stimuli for Gastric Inhibitory Polypeptide?

A

Fat, glucose and amino acids in small intestine

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15
Q

What are the effects of Gastric Inhibitory Polypeptide?

A

Inhibits gastric secretion and motility (tries to deal with the large amount of food coming)
Causes release of insulin in response to elevated blood glucose concentration
Stimulation of lipoprotein lipase activity in adipocytes

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16
Q

What does GLP-1 do?

A

GLP-1 is stimulated when it senses too much nutrient in this part of the gut so it tells us to slow down food movement and tells us to stop eating (as well as telling the pancreas to secrete insulin)

Suppresses glucagon driven gluconeogenesis
Slowed gastric emptying
Promotes satiety (hypothalamus)

17
Q

What is the release stimuli for motilin?

A

Secretion is associated with fasting

(?) high pH in the duodenum

18
Q

What are the effects of Motilin?

A

Maintains motility in the stomach and intestine

Stimulates the production of pepsin

19
Q

What does leptin do?

A

Leptin causes satiety (anorexigenic)

20
Q

What does ghrelin do?

A

Ghrelin stimulates appetite (orexigenic)

21
Q

What does the satiety centre respond to?

A

Responds to high glucose levels

Inhibits eating

22
Q

What does the appetite centre respond to?

A

Responds to low glucose levels

Stimulates eating

23
Q

Where do the appetite and satiety centres lie?

A

Satiety lies either side of the ventral third ventricle

Appeteite centre lies laterally to this

24
Q

What is the lipostat hypothesis of obesity?

A

Adipose tissue produces a hormonal signal- leptin
Leptin level proportionate to the amount of fat
Signal acts upon membrane bound receptors in the hypothalamus to decrease food intake and increase energy output.
Genetic lack of leptin leads to obesity so Leptin can be described as an anorexigenic hormone

25
Q

What is the CCK (appetite) /peptide YY hypothesis?

A

CCK is synthesised in the small intestine and acts upon G protein coupled receptors.
CCK also found in cells in the brain - expansion of the stomach after a meal causes release of CCK from these brain cells. This release of CKK slows gastric emptying ad decreases food intake.

26
Q

What is the Ghrelin hypothesis?

A

Produced predominantly by the lining of stomach (also from intestine and hypothalamic nuclei).
Increases before meals, decreases after.
Stimulates appetite at hypothalamus
Ghrelin can be described as an orexigenic hormone
Ghrelin receptors are also found in other areas of the brain, including the hippocampus and regions known to be involved in reward systems

ENI (33 decks)

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