section 4 Flashcards

1
Q

explain Lipostatic hypothesis and Glucostatic hypothesis.

A

Lipostatic hypothesis Suggest that adipose tissues produce something to regulate appetite
Seen by hiberniting animals
Body requirement of fat accumulation that regulate amount needed

Glucostatic hypothesis: Insulin was already discovered. They is a balance glucose level and everything is produce to keep that glucose level

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2
Q

(TF) visual and olfactory sensation doesn’t impact food intake.

A

False
food intake is regulated by endocrine, metabolic factors, visual, olfactory, taste sensation, memory, emotions and life conditions

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3
Q

Explain briefly metabolic role these hormones:
Secretin
GIP
GLP-1
Ghrelin

A

Secretin: (from exocrine pancreas) help absorption in intestin
GIP: regulate incretin activity, help insulin and glucagon to regulate glucose level
GLP-1: also impact insulin and glucagon -> glucose level
Ghrelin: + stimulate NPY neurons -> eat more -> only orexic hormone

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4
Q

What is the satiety center ?

A

VMH (Specific nuclei). by experiment of lesioning result to hyperphagia (animal overeat w/o VMH). Give signal eat enough

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5
Q

What is the hunger center ?

A

lateral hypothalamus nucleus if lesion lead to anorexia (animal don’t know when to eat)

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6
Q

What control the satiety and hunger center ?

A

SCN. regulated by light which regulate circadian rythym for whole body. lesion of SCN -> hyperphagia and obesity

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7
Q

Which hormones regulate HPT (hypothalamus-pituitary thyroid) and HPA (hypothalamus-pituitary-adrenal) in central regulation of feeding ?

A

PVN and ARC

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8
Q

Which 2 organs are crucial in central regulation of feeding ?

A

Hypothalamus and Brain stem (neurotransmetters)

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9
Q

Explain briefly how alpha-MSH and NPY neurons regulate food intake.

A

They receive hormonal input from peripheral organs in Arcuate neurons and translate into signal to hypothalamus. alpa-MSH=anorexic; NPY=orexic
More fat -> more leptin -> + regulate a-MSH & inhibit NPY neurons -> anorexic hormone -> lipostatic hypothesis
Insulin (pancreas) -> inhibit NPY -> anorexic hormone
PYY and GLP -> inhibit NPY -> anorexic hormone
Grelin -> + stimulate NPY neurons -> eat more -> only orexic hormone

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10
Q

Explain endocannabinoid system.

A

both endocannabinoid (AEA & 2-AG) are produce in tissues by enzymes -> GPCR receptors (CB1 and CB2) that inhibit cyclic AMP synthesis -. anabolic effect (store energy)

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11
Q

What is the precursor of both endocannabinoids?

A

arachidonic acid

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12
Q

what happend when inhibiting endocannabinoid system?

A

weight lost/ increase catabolism system
more satiety and less lipogenesis

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13
Q

explain the blood supply to the pancreas.

A

aorta -> hepatic artery -> divide into smaller arteries different part pancreas

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14
Q

explain the blood supply from the pancreas.

A

Splenic and mesenteric veins -> portal vein -> collect all blood from GIT -> liver to metabolize it

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15
Q

Name each Islets of Langerhans and which hormone they secrete.

A

alpha-cells: Glucagon
beta-cells: Insulin
gamma-cells: Somatostatin
E-cells: Ghrelin
F-cells: Pancreatic polypeptide

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16
Q

Which Islets of Langerhans received blood supply first?

A

Beta-cells detect glucose levels -> secrete insulin if needed

17
Q

Explain briefly beta-cells synthesis.

A

a lot of proliferation before 5yr old then decrease. lifespan of 25yrs. Stem cell in periphery of islets transform into beta cells when needed
B-differentiation -> stop being beta function before dying

18
Q

(TF) glucagon always stimulate insulin synthesis.

A

False. Glucagon stimulate insulin but also indirectly inhibit insulin (through somatostatin)

19
Q

(TF) C-peptide better representation of beta cells than insulin.

A

True

20
Q

(TF) C-peptide is metabolized by liver.

A

False. Insulin metabolized by liver and C-peptide metabolized by kidney

21
Q

What is the Glucagon synthesis progression

A

Preproglucagon -> proglucagon -> glucagon

22
Q
A