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SGUL - Physiology 1 > Control of Food Intake > Flashcards

Control of Food Intake Flashcards

1
Q

Why should food intake be studied?

A
  • Physiological process common to all animals
  • Combat endocrine disorders
  • Understand its clinical significance
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2
Q

Describe ghrelin.

A
  • Secreted by the stomach fundus
  • Increases the sense of hunger and stimulates gastric emptying
  • Stimulates neuropeptide Y and AgRP neurons
  • Suppresses the ability of leptin to stimulate anorexigenic factors
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3
Q

Describe PYY

A
  • Signals satiety and inhibits gut motility
  • Exert inhibition of AgRP neurons in animals
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4
Q

Describe obestatin

A
  • Peptide derived from the same prehormone as ghrelin
  • Opposes the effects of ghrelin
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5
Q

Describe amylin

A

Reduces food intake through the medulla of the brainstem and by delaying gastric emptying

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6
Q

Describe enterogasterones

A
  • Secreted by the mucosa of the duodenum in the lower GI tract
  • Response to dietary lipids that inhibit the aboral motion of chyme
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7
Q

Give examples of enterogasterones

A

Secretin
CCK (cholecystokinin)
GIP(gastric inhibitory peptide)

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8
Q

Describe what is involved in the relaxation of the fundus

A

Mediated by reflexes

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9
Q

What are the three ways in which fundus relaxation can be mediated?

A
  • Receptive (mechanical stimulation of the pharynx)
  • Adaptive (vagal innervation (NO/VIP) to influence tension of the stomach)
  • Feedback (nutrients, CCK).
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10
Q

What is receptive, adaptive and feedback-mediated reflexes mediated by?

A

Non-adrenergic, non-cholinergic (NANC) mechanisms

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11
Q

What may happen when the stomach is ready to receive food?

A

Noradrenaline is released from the sympathetic nerve fibres which help the stomach to relax

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12
Q

Describe the actions of PACAP (pituitary adenylate cyclase-activating peptide).

A

Stimulate adenylate cyclase activity in the anterior pituitary

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13
Q

Where is PACAP found?

A
  • Brain
  • Gut (the myenteric and submucosal ganglia)
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14
Q

What does PACAP stimulate?

A
  • Mediates the neuronal regulation of gastric acid secretion (thus mediating intestinal motility).
  • Stimulates the relaxation of colonic smooth muscle
  • Stimulates pancreatic secretions (insulin and glucagon secretion in humans).
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15
Q

How can gastric surgery impair accommodation and emptying? PART 1

A
  • Prior gastric surgery may result in gastroparesis (delayed gastric emptying).
  • Around 5% of patients who undergo a vagotomy develop symptoms of early satiety (as well as nausea, and bloating from gastric stasis), in the absence of a mechanical obstruction.
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16
Q

How can gastric surgery impair accommodation and emptying? PART 2

A
  • Disturbance of fundic and antral contractility have been reported
  • Non-motor factors may be involved, as symptoms do not always correlate with delays in gastric emptying.
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17
Q

Define hunger.

A

Discomfort caused by the lack of food and the desire to eat - characterised by a strong craving for food/ sensation of emptiness in the stomach

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18
Q

Define appetite.

A

Desire to satisfy the body’s needs for food - a hunger-stimulated response

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19
Q

Define satiety.

A

Being full after eating food

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20
Q

Define aphagia.

A

Inability or refusal to swallow

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21
Q

Define hyperphagia.

A

Abnormal desire for food

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22
Q

Give a summary of the factors that influence food intake.

A
  • external factors - eg. food availability, daily routine
  • emotional state - stress, depression
  • physiological regulation
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23
Q

What main input from the brain controls food intake?

A
  • Hypothalamus
  • Base of the hypothalamus has several nuclei that regulate energy homeostasis.
  • Controls the appetite and ingestive behaviour
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24
Q

Besides the hypothalamus, what other inputs control our feeding behaviour?

A

Orexigenic and anorexigenic neurotransmitters within the hypothalamus.

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25
Q

What is the effect of orexigenic neurotransmitters?

A

Increase appetite

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26
Q

What is the effect of anorexigenic neurotransmitters?

A

Decrease appetite

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27
Q

Feeding behaviour/food intake is modulated by many hypothalamic sites.

List some of them. PART 1

A
  • Lateral Hypothalamus (LH) - acts as a hunger centre
  • Ventromedial Nucleus (VMN) = satiety centre
    [the VMN and LH have the ability to restrain feeding if required; a lesion would increase appetite, with weight gain that tends to persist]
  • Dorsomedial Nucleus (DMN) = modulates energy intake [releasing NPY into the DMN increases feeding]
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28
Q

Feeding behaviour/food intake is modulated by many hypothalamic sites.

List some of them. PART 2

A
  • Paraventricular Nucleus (PVN) = modulates feeding behaviour
    [controls feeding behaviour; if NPY, opioids, GABA, etc. given, leads to increased feeding, while if leptin was given, it leads to decreased feeding]
  • Arcuate Nucleus (ARC) = neurons produce orexigenic signals (NPY, opioids, dynorphin, β-endorphins, POMC, galanin, amino acids, GABA and glutamate)
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29
Q

What is the role of the suprachiasmatic nucleus (SCN)?

A

Controls circadian rhythms

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30
Q

What is appetite regulated by?

A

Balance between 2 pathways:
- Appetite-stimulating pathway that releases agouti-related peptide (AgRP) and neuropeptide Y (NPY)
- Appetite suppressing pathway that releases α-melanocyte stimulating hormone (α-MSH).

31
Q

List the steps involved in appetite suppression.

A
  • Appetite-suppressing neurons make the precursor pro-opiomelanocortin (POMC), which is broken down into α-MSH
  • This binds to melanocortin 4 receptors (MC4R) to suppress the appetite.
32
Q

List the steps involved in appetite stimulation

A

Occurs when no occupancy of MC4R receptors by α-MSH

33
Q

What are the effects of serotonin 5-HT2C agonist?

A
  • Binds to 5-HT2C receptors on POMC neurons in the appetite-suppressing pathway
  • Activates POMC neurons
  • Releases α-MSH, which binds to MC4R
34
Q

Describe diurnal variation in food intake.

A
  • Carbohydrates are metabolised during the day
  • Fats are metabolised at night
  • Hypothalamus responds to the switch between carbohydrate and fat metabolism
35
Q

Describe the role of the prefrontal cortex and the limbic system in the executive control of food intake. PART 1

A
  • Receives sensory information from inside and outside the body
  • Receives emotional and cognitive information from the limbic system
  • Connected to cortical areas involved in motor planning and execution.
36
Q

Describe the role of the prefrontal cortex and the limbic system in the executive control of food intake. PART 2

A
  • Homeostatic and environmental information is translated into adaptive behavioural responses
37
Q

What is the limbic system?

A
  • Complex system of nerves and networks in the brain.
  • Involves area around the cortex concerned with instinct and mood.
  • Control over fear, pleasure, anger
  • Drives hunger, care of offspring
38
Q

How has it been proved that feeding is dependent on both stimulating AND inhibiting forces in the hypothalamus?

A
  • Removal of the lateral hypothalamus causes hypophagia
  • Removal of the ventromedial hypothalamus causes hyperphagia
  • Feeding is regulated by a balance of stimulating and inhibiting forces in the hypothalamus.
39
Q

Are diabetics hyperphagic or hypophagic?

A

Hyperphagic

40
Q

Why are people with IDDM not usually obese?

IDDM - insulin-dependent diabetes mellitus

A

-Insulin is required for adipocytes to store fat
- Excess calories consumed are wasted via excretion in the urine.

41
Q

What is the physiological role of glucagon?

A
  • Stimulate glucose production via hepatic glycogenolysis or gluconeogenesis
  • Maintain euglycaemia during stages of rapid glucose utilisation or fasts
42
Q

What is the hypothesised role of glucagon in food intake?

A
  • Secreted as food is ingested
  • Provides a satiety signal leading to termination of the meal
43
Q

Where and how is insulin secreted?

A
  • Secreted into the blood from the pancreas in proportion to the amount of fat stored in white adipose tissue.
44
Q

Outline how insulin works in energy homeostasis. PART 1

A
  • Small amount of insulin is transported into the brain where it acts on insulin receptors on neurons with either net catabolic or anabolic activity (e.g the arcuate nucleus of the hypothalamus).
45
Q

Outline how insulin works in energy homeostasis. PART 2

A
  • Neurons in turn influence energy homeostasis (food intake and energy expenditure)
  • Influence the amount of fat stored in the body by exerting a net catabolic action.
46
Q

What hormone(s) inhibit lipolysis?

A

Insulin

47
Q

What hormone(s) induce lipolysis?

A

Ghrelin, NA, adrenaline, GH, testosterone and cortisol

48
Q

How does insulin participate in the regulation of energy homeostasis?

A
  • Secreted from the endocrine pancreas.
  • Acts on both the liver and forebrain to reduce energy intake as well as to suppress hepatic glucose production.
49
Q

How does glucagon participate in energy homeostasis?

A
  • Acts at the liver
  • Increases glucose production
  • Generates a signal to reduce energy intake that is relayed to the hindbrain.
50
Q

How does amylin participate in energy homeostasis?

A
  • Acts at the hindbrain to reduce energy intake.
  • Acts upon the NTS and AP (area postrema), and induces their stimulation.
51
Q

What are the effects of somatostatin on control of food intake?

A
  • Evidence that somatostatin decreases appetite.
  • Similar mechanism of action to CCK and appears to work via the vagus nerve, like CCK.
52
Q

What is leptin’s role in the control of food intake?

A
  • Hormone secreted by white adipocytes and gastric cells.
  • Generally as adipose tissue size increases so does leptin secretion
53
Q

What is the role of gastric leptin?

A
  • Delay of gastric emptying
  • Absorption of nutrients by the intestinal wall
  • Secretion of gastric, intestinal, and pancreatic hormones.
54
Q

What is the role of leptin secreted by adipocytes?

A

Acts on hypothalamus for long-term regulation of food intake.

55
Q

How does low blood glucose affect ghrelin? PART 1

A
  • Ghrelin is produced by cells called P/D1 cells in the upper section of the stomach.
  • Increased glucose levels inhibit its expression in the P/D1 cells.
  • A drop in blood glucose levels below the threshold activates the expression of ghrelin.
56
Q

How does low blood glucose affect ghrelin? PART 2

A
  • Reaches the arcuate nucleus of the hypothalamus (ARC) via the bloodstream
  • Activates the expression of agouti-related peptide (AgRP) and NPY (and cannabinoids).
  • Both AgRP and NPY generate hunger signals by stimulating the orexigenic neuron
57
Q

What is the role of obestatin in the control of food intake? PART 1

A
  • Produced in the epithelial cells of the stomach.
  • Encoded by the ghrelin gene, but opposes the effects of ghrelin .
  • Suppresses food intake (suppresses appetite, so decreases body weight gain).
58
Q

What is the role of obestatin in the control of food intake? PART 2

A
  • Antagonises ghrelin-induced food intake (and growth hormone secretion).
  • Imbalance of ghrelin and obestatin may have a role in obesity, as a decreased ghrelin/ obestatin ratio has been found to characterise obesity in women.
59
Q

Describe the volume of the stomach when we have not eaten (fasting)

A

Volume is small

60
Q

What happens to the stomach when we begin to eat food?

A
  • Fundic area of the stomach enlarges to accommodate food.
  • Mediated by NO and VIP
61
Q

What motion allows the stomach to empty?

A

Contraction of the antrum area using ACh

62
Q

In order to relax what do fats and lipids release in order for the stomach to relax to it can receive food?

A

CCK

63
Q

What is vagotomy and what does it cause?

A
  • Operation in which one or more branches of the vagus nerve are cut, typically to reduce the rate of gastric secretion
  • Reduces accommodation and gastric compliance
64
Q

Where is the thirst centre located?

A

Lateral hypothalamus

65
Q

What is the amyloid nucleus and what is its role?

A
  • Sub-region of the amygdaloid complex;
  • Participates in the regulation of food intake
66
Q

What does zimelidine do?

A

Inhibits the reuptake of 5 -HT from the synaptic cleft, allowing 5-HT to persist in the Synaptic cleft

67
Q

What do glucostat receptors detect?

A
  • ↓[glucose]blood →induces hunger
  • ↑[glucose]blood → induces satiety
68
Q

Why do other factors can stimulate feeding and inhibit appetite?

A
  • Cold environments stimulate feeding while hot environments inhibit appetite
  • Distension of a full stomach inhibits appetite; contraction of an empty one stimulates appetite
69
Q

What is the effect of stimulating leptin?

A
  • Decrease food intake, induce weight loss and increase energy expenditure
70
Q

What is the ligand of the medial amygdaloid nucleus?

A

5-HT

71
Q

What condition happens if you stimulate the hypothalamus?

A

Aphagia

72
Q

What condition happens if there are lesions to the hypothalamus?

A
  • Hyperphagia
73
Q

How does leptin control fat stores?

A
  • Operates a feedback mechanism between adipose tissue and the brain
  • Increases the expression of anorexigenic factors
  • Stimulates metabolic rate
  • Inhibits neuropeptide Y which stimulates feeding

SGUL - Physiology 1 (68 decks)

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