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P1: GI > Control of Food Intake > Flashcards

Control of Food Intake Flashcards

1
Q

What starts to expand when you eat?

A

→ The fundic area expands to accomodate food

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2
Q

What two hormones are used in accommodation?

A

→ VIP and NO

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3
Q

What is PYY and what does it do?

A

→ Is a satiety factor and increases gut motility

Peptide YY

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4
Q

What do you feel when emptying occurs?

A

→ A sense of hunger (ghrelin)

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5
Q

Where do contractions occur and what are they mediated by?

A

→ Occur in the antrum

→ Mediated by AcH

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6
Q

What relaxation occurs when food is swallowed?

A

→ Receptive relaxation

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7
Q

What is receptive relaxation done by?

A

→ Vagal innervation

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8
Q

What kind of relaxation occurs in the stomach to allow accommodation?

A

→ adaptive relaxation

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9
Q

What is CCK stimulated by?

A

→ Lipids

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10
Q

What is affected if you cut vagus nerves?

A

→ Accommodation

→ Gastric compliance

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11
Q

What is the difference between appetite and hunger?

A

→ Appetite is a psychological desire

→ Hunger is a physiological craving

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12
Q

What is hyperphagia/polyphagia?

A

→ Abnormal desire for food

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13
Q

What does the hypothalamus control?

A

→ Hunger + thirst

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14
Q

Functions of the prefrontal cortex

A

→ Food seeking
→ Integration of sensory information from inside and outside the body
→ Receives emotional + cognitive information from the limbic system
→ Makes choices by translating the homeostatic and environmental information into adaptive behavioral responses,

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15
Q

What is the limbic system?

A

→ Complex system of nerves and networks in the brain

associated with instinct and mood

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16
Q

What sites is feeding behavior modulated by?

A

→ Lateral hypothalamus

→ Ventromedial hypothalamus

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17
Q

What is the role of the lateral hypothalamus?

A

→Hunger + thirst center

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18
Q

What is the role of the ventromedial nucleus ?

A

→ Satiety center

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19
Q

What happens if there is a lesion to the VMN?

A

→ Increased appetite with weight gain

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20
Q

What does the dorsomedial nucleus do?

A

→ Modulates energy intake (hunger center)

release NPY into DMN= increased feeding

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21
Q

What acts on the dorsomedial nucleus to increase feeding?

A

→ NPY into the DMN increases feeding

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22
Q

What does the paraventricular nucleus do and how?

A

→ Modulates feeding behavior
→Paraventricular nucleus and perifornical hypothalamus

→NPY, opioids, and GABA =↑ feeding
→leptin =↓ food intake

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23
Q

What does the arcuate nucleus produce?

A

→ Orexigenic signals

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24
Q

What are the types of relaxation of the reservoir?

A

→receptive (mechanical stimulation of pharynx – mechanoreceptors, sight)
→adaptive (vagal innervation (NO/VIP), tension of stomach)
→feedback (nutrients, CCK).

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25
Q

How do the inhibitory vagal fibres relax the stomach?

A

→inhibitory vagal fibres release ACH

→ACH activate inhibitory enteric pathways that release NO, VIP and ATP in order to relax the muscle

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26
Q

What is vagotomy?

A

impairs accommodation and emptying: a cause for early satiety in some patients

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27
Q

Define satiety

A

state of being full after eating food (joyous moments – no longer need to continue eating)

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28
Q

Define aphagia

A

the inability or refusal to swallow

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29
Q

What is the role of satiety signals?

A

→to prolong the interval until hunger or the onset of the next meal

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30
Q

Summarise the factors that control food intake

A

→hypothalamic control

→BMI

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31
Q

What are some diurnal variations in food metabolism?

A

→Carbohydrates metabolised during the day
→Fats metabolised at night
→Hypothalamus responds to the switch between carbohydrate and fat metabolism

32
Q

How does the hypothalamus control food intake?

A

→The base of the hypothalamus has several nuclei that regulate energy homeostasis- bout 12 of them
→ Control the appetite; size of helping, and our ingestive behaviour
The nuclei communicate with each other

33
Q

What happens with stimulation of ventromedial nuclei and removal?

A

→aphagia (swallowing difficulty)

→ removal= hyperphagia

34
Q

What happens with stimulation of lateral hypothalamus?

A

→increased feeding

35
Q

What happens with lesion of the lateral hypothalamus?

A

aphagia

36
Q

What is opioid’s effect?

A

(growth hormone releasing hormone)

→increased appetite

37
Q

What is the effect of naltrexone?

A

(opioid antagonist) reduces the positive ‘hedonic valence’ of food

38
Q

What is the hedonistic system?

A

pleasant sensation

39
Q

What is the arcuate nucleus?

A

Neurons produce orexigenic signals (NPY, the opioids, dynorphin, β-endorphin, POMC, galanin, amino acids, glutamate, and GABA) =increased feeding

40
Q

What is GABA effects on feeding behaviour?

A

→Injection of GABA into the VMH reliably increases food intake
→Injection of GABA into the origin of the nigrostriatal dopamine (DA) neurons in the substantia nigra (SN) suppressed food intake

41
Q

What is the suprachiasmatic nucleus?

A

→Human body clock is located in the suprachiasmatic nuclei
→Perception of the light-dark cycle (circadian rhythms)? Appetite or the sensation of hunger =mood/drive to eat

→Also stomach nerves

42
Q

What is the medial amygdaloid nucleus?

A

→It is a sub-region of the amygdaloid complex

→Participates in the regulation of food intake

43
Q

What are the ligands involved in regulation of appetite and food uptake?

A

→5-HT (via 5-HT2C and 5-HT1A)-

44
Q

Regulation of appetite in the hypothalamus by 5-HT2C agonist

A

→balance between an appetite stimulating pathway that releases agouti-related peptide (AgRP) and neuropeptide Y (NPY)
→an appetite suppressing pathway that releases alpha-melanocyte stimulating hormone (alpha-MSH).
→The appetite suppressing neurons make the precursor pro-opiomelanocortin (POMC)
→broken down into alpha-MSH
→binds to melanocortin 4 receptors (MC4R) to suppress appetite

45
Q

How is food intake controlled centrally?

A

→5-HT (5-HT2C and 5-HT1A), dopamine, GABA =reduced appetite

→anorexigenic factors

46
Q

What does zimelidine do?

A

→inhibits the reuptake of 5-HT from synaptic cleft, allowing 5-HT to
persist in the synaptic cleft

47
Q

What is the role of the prefrontal cortex?

A

influences food-seeking behaviour
→Integrates sensory information from inside and outside the body;
→Receives emotional and cognitive information from the limbic system
→Helps one make choices by translating all of the homeostatic and environmental information into adaptive behavioural response

48
Q

What is the role of the limbic system?

A

→areas concerned with instinct, learning, reproductive behaviour; emotions/mood, pleasure (fear, anger, etc.)

49
Q

Under what control is the cortico-limbic mechanisms?

A

executive control

50
Q

What do higher functions do?

A

modulate responses to both CNS and peripheral cues (e.g. gut; environment)

51
Q

Factors that affect if food is sought or not and the type we ingest….

A

Food preferences
Emotions; psychological; physiological
Environment
Life style

52
Q

What is the role of the circadian rhythm?

A

→limits food intake to certain times (in some people)

53
Q

What does the brain do in high and low glucose levels?

A

↓[glucose]blood →induces hunger

↑[glucose]blood → induces satiety

54
Q

Why do diabetic patients feel hungry despite ↑[glucose]blood?

A

The blood glucose is not being taken up

55
Q

What do cold and hot environments do?

A

→stimulate feeding while hot environments inhibit appetite

56
Q

What is calcitonin?

A

hormone that reduces appetite

57
Q

What are insulin’s effects in the brain?

A

→Different parts of the brain that insulin reduces levels of orexigenic factors that inhibits feeding
→Inhibits NPY/AgRP(co-expressed with NPY and acts to increase appetite) = reduce food intake, reduce body fat

Insulin and leptin act agonistically in reducing food intake via action on receptors within the brain​

58
Q

What hormones are secreted by the endocrine pancreas?

A

→insulin, glucagon, and amylin

59
Q

What does insulin do to the liver and the forebrain

A

→to reduce energy intake as well as to suppress hepatic glucose production.

60
Q

What does glucagon do?

A

→acts mainly at the liver

→increases glucose production while generating a signal to reduce energy intake that is relayed to the hindbrain

61
Q

What does amylin do?

A

→acts directly at the hindbrain to reduce energy intake
inhibits glucagon secretion, delays gastric emptying, and acts as a satiety agent.
o-released with Insulin

62
Q

What is the area postrema?

A

a medullary structure in the brain that controls vomiting.

63
Q

What type of cells release CCK?

A

I-cells from the intestine and nerve ending

64
Q

What is CCK?

A

→Fat ingestion causes CCK release and the slowing of gastric emptying – state of sense of fullness
→inhibit further food intake
→Injection of CCK in the brain → reduction of appetite

65
Q

What is somatostatin?

A

growth hormone inhibiting hormone

→satiety factor

66
Q

What is leptin?

A 
Fat cells (adipocytes) secrete leptin- gene expressed mainly in adipocytes
→Controls fat stores by operating a feedback mechanism between adipose tissue and brain
→increased adipose tissue size and increased leptin secretion
67
Q

What can administration of leptin lead to?

A

decrease food intake, induce weight loss and increase energy expenditure

68
Q

What does leptin increase the expression of?

A

anorexigenic factors (pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), corticotrophin-releasing hormone (CRH), neurotensin

69
Q

What other things can leptin do?

A

→Stimulates metabolic rate

→Inhibits neuropeptide Y, which stimulates feeding

70
Q

Can one be resistant to the effects of leptin?

A

Yes; →binge eating, despite adequate or growing adipose tissue (obese)

71
Q

What are the properties of Ghrelin?

A

→An appetite-inducing hormone (an orexin) – stimulates hunger
→Fast-acting and stimulates food intake
→Suppresses the ability of leptin to stimulate anorexigenic factors

72
Q

Which organs release ghrelin?

A

Released by stomach, pancreas, adrenals

73
Q

When does ghrelin levels increase?

A

↑ preprandially and ↓ after a meal

→Increases central orexins, e.g. NPY, and AgRP (generate hunger signal

74
Q

What inhibits ghrelin?

A

by leptin

→Leptin and ghrelin act reciprocally on food intake

75
Q

What is obestatin?

A

→Produced by epithelial cells of stomach

→Encoded by ghrelin gene, but it opposes the effects of ghrelin on food intake

76
Q

How does obestatin mediate its effects?

A

via different receptors to ghrelin

P1: GI (15 decks)

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