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Endocrinology Y2 > Obesity and the Endocrine Control of Food Intake > Flashcards

Obesity and the Endocrine Control of Food Intake Flashcards

1
Q

Where in the Brain is food intake regulated - SPECIFIC

A

Hypothalamus ARCUATE NUCLEUS

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2
Q

What ables the ARCUATE NUCLEUS to regulate food intake

A

circumventricular region)- allows access to peripheral hormones

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3
Q

2 neuronal populations in the arcuate nucleus?

A

Stimulatory (NPY/Agrp neuron)

Inhibitory (POMC neuron)

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4
Q

Inhibitory neuronal population in the arcuate nucleus?

A

POMC neurons

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5
Q

Stimulatory neuronal population in the arcuate nucleus?

A

NPY/Agrp neuron)

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6
Q

What hormonal inputs regulate food intake (3)

A

ghrelin, PYY, and normal leptin

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7
Q

What neuronal input regulates food intake

A

Vagus

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8
Q

Hormones of the arcuate nucleus? (2)

A

Agrp and POMC

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9
Q

What stimulates hunger

A

You trigger hunger by the release of Agrp from the arcuate nucleus which is an endogenous antagonist of MC4R, this blocks the inhibitory signal of α-­‐MSH and stimulates food intake

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10
Q

What receptor controls hunger in the PVN

A

MC4R

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11
Q

MC4R receptor is important in

A

hunger

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12
Q

Why aren’t you hungry all the time

A

Under normal conditions, the POMC will be broken down to α‐MSH which is an endogenous agonist of the MC4R, which suppresses food intake

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13
Q

MC4R stimulation impact on food intake?

A

Decreased

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14
Q

MC4R inhibition impact on food intake?

A

Increased

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15
Q

MC4R inhibitor?

A

NPY/Agpr neurons

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16
Q

MC4R agonist?

A

Alpha-MSH

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17
Q

Alpha MSH is cleaved from

A

POMC

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18
Q
  • No XXXXX mutations associated with appetite have been discovered
A

NPY/Agrp

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19
Q
  • X deficiency and Y cause morbid obesity (X in the arcuate nucleus and y is PVN)
A

X POMC

Y MC4-R mutations

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20
Q
  • OB GENE CODES FOR X
A

LEPTIN

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21
Q

What was observed in ob/ob mice (7)

A
  • Obese
  • Diabetic
  • Infertile
  • Stunted linear growth
  • Decreased body temperature
  • Decreased energy expenditure
  • Decreased immune function
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22
Q

What was missing in ob/ob mice

A

Leptin

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23
Q

Where is leptin released from

A

white adipose tissue

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24
Q

Leptin levels when low body fat?

A

Low

25
Q

Leptin levels when high body fat?

A

High

26
Q

Physiological effect of leptin?

A

Inhibits feeding

27
Q

Neuronal MoA of leptin?

A
  • Activates POMC and inhibits NPY/Agrp neurons
28
Q
  • Leptin circulates in plasma concentrations proportional to XX
A

fat mass

29
Q

Why is leptin ineffective as a weight loss pill?

A

Obese people tend to have leptin resistance

30
Q

On who is leptin effective as a weight loss pill?

A

LEPTIN IS EFFECTIVE IN TREATING LEPTIN DEFICIENT CHILDREN AND ADULTS

31
Q

How is leptin an anti-starvation hormone rather than an anti-obesity one

A
  • Presence of leptin tells the brain that one has sufficient fat reserves, but it doesn’t stop you from wanting to eat
32
Q
  • Central administration of insulin of food intake?
A
  • Central administration reduces food intake
33
Q

Does insulin have receptors on the hypothalamus?

A

Yes

34
Q

Central or peripheral administration of leptin will decrease X and increase Y

A

food intake

thermogenesis

35
Q

Effect of leptin on puberty?

A

Lack of leptin means the hypothalamus doesn’t release GnRH

36
Q

Ghrelin is activated from its inactive form by …

A

GHRELIN O-ACYLTRANSFERASE

37
Q

Effect of ghrelin on arcuate nucleus neuronal populations?

A
  • Stimulates NPY/Agrp neurons
  • Inhibits POMC neurons
  • Increases appetite
38
Q

Ghrelin is secreted by…

A

The stomach

39
Q

The stomach secretes what food intake controlling hormone

A

Ghrelin

40
Q

What cells and where secrete PYY

A

enteroendocrine/L- cells in the distal small intestine and colon

41
Q

What cells and where secrete GLP-1

A

enteroendocrine/L- cells in the distal small intestine and colon

42
Q

enteroendocrine/L- cells in the distal small intestine and colon secrete what food intake controlling hormones (2)

A

PYY and GLP-1

43
Q

Effect of PYY on arcuate nucleus neuronal populations?

A
  • Inhibits NPY neurons

- Stimulates POMC neurons

44
Q

Effect of ghrelin on food intake

A

Increases

45
Q

Effect of PYY on food intake

A

Decreases appetite

46
Q

Effect of GLP-1 on food intake?

A

reduces food intake (suppresses appetite)

47
Q

GLP 1 stands for

A

Glucagon like peptide

48
Q

When is GLP-1 released

A

Post prandially

49
Q

When is PYY released

A

Post prandially

50
Q

When is ghrelin released

A

High in morning, goes down after food and cycles

51
Q

Effect of GLP-1? (2)

A
  • Well characterised incretin role in stimulating glucose-stimulated insulin release and also reduces food intake (suppresses appetite)
52
Q

What are GLP1 based drugs used to treat?

A

Diabetes mellitus

53
Q

GLP1 in inactivated by … 1/2 life?

A

by DPP‐4 (dipeptidyl peptidase 4)

about a minute in circulation

54
Q

What is Saxenda

A

Long‐acting GLP-1 receptor agonist

55
Q

Example of a Long‐acting GLP-1 receptor agonist ?

A

Saxenda

56
Q

Why is PYY not a good drug target?

A

Has a narrow therapeutic index.
If you inject someone with PYY, you will get a big, transient increase in drug concentration and then a relatively rapid drop
At high levels, it will cause nausea
There is a relatively small sweet spot in terms of drug concentration that gives the effects that you want

57
Q

What is the thrifty gene hypothesis

A

Specific genes selected for to increase metabolic efficiency and fat storage- BUT in an environment with plentiful food and low exercise these genes predispose to obesity/diabetes

58
Q

What is the adaptive drift (drifty gene) hypothesis?

A
  • Normal distribution of body weight; the fat are eaten, the thin starve This was probably true for humans originally
  • 10-20k yrs ago, humans learned to defend themselves
  • Thus obesity wasn’t selected against
  • Putting on body fat was then a neutral change (genetic drift)
  • In current context, the inheritors of these genes become obese

Endocrinology Y2 (18 decks)

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