Control of food intake Flashcards

1
Q

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

A

In an empty stomach, the volume is small.

50ml

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2
Q

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

A

The fundic area of the stomach enlarges to accommodate food. NO and Vasoactive intestinal polypeptide allow this to happen.

1.5L

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3
Q

What motion allows the stomach to empty?

A

We get contraction of the antrum area of the stomach

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4
Q

What hormone stimulates appetite?

A

Ghrelin

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5
Q

What causes the stomach to relax when we swallow food?

A

Co-ordinated by:

  1. Receptive
  2. Adaptive
  3. Feedback relaxation

Inhibitory vagal fibres release acetycholine that activate the enteric pathways that release NO, PACAP, VIP and ATP to relax the muscle

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6
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

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7
Q

What is vagotomy and what does it cause?

A

A surgical operation in which one or more branches of the vagus nerve are cut, typically to reduce the rate of gastric secretion (e.g. in treating peptic ulcers).

Reduces accommodation and gastric compliance

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8
Q

Define Hunger

A

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

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9
Q

Define appetite

A

Psychological desire/drive to satisfy the body’s needs of food; a hunger-stimulated response

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10
Q

Define satiety

A

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

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11
Q

Define aphagia

A

The inability or refusal to swallow

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12
Q

Define Hyperphagia/polyphagia

A

An abnormal desire for food (extreme unsatisfied drive to eat)

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13
Q

What is food intake controlled by?

A

It is controlled by the Hypothalamic control

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14
Q

Give 2 reasons for differences in BMI?

A

Genes (70%)

How much we eat and its composition

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15
Q

Foods are metabolised at different times in the day:

Carbs

Fats

When are they metabolised?

A
  • Carbohydrates metabolised during the day
  • Fats metabolised at night
  • Hypothalamus responds to the switch between carbohydrate and fat metabolism
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16
Q

What else can appetite be influenced by?

A

Family gatherings, food palatability, emotional, habitual, and circadian factors

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17
Q

How does the hypothalamus control food intake?

A

• The base of the hypothalamus has several nuclei that regulate energy homeostasis
→ Control the appetite; size of helping, and our ingestive behaviour

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18
Q

What is the satiety centre in the body?

A

Hypothalamus (ventromedial nuclei - wall of paraventricular)

19
Q

What happens when we get stimulation of ventromedial nuclei?

A

Aphagia

20
Q

What happens when we get lesions of ventromedial nuclei?

A

Hyperphagia (an increased appetite or excessive hunger)

21
Q

Where is the thirst centre located?

A

Lateral hypothalamus

22
Q

Do opioids increase appetite

A

Yes

23
Q

What does the dorsomedial nucleus control (DMN)?

A

Modulates energy intake (hunger centre)

24
Q

What does the release of NPY cause and where does it act?

A

DMN and increases feeding

25
Q

What does the Paraventricular nucleus (PVN) do?

A

Modulates feeding behaviour

26
Q

NPY, opioids, and GABA all do?

A

Increase feeding, GABA has mixed effects

27
Q

What does leptin do? (1)

A

Decreases food intake

28
Q

What is the Suprachiasmatic nucleus and what does it control?

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

29
Q

What is the amyloid nucleus and what is its role?

A

• A role for medial amygdaloid nucleus in feeding
• behaviour has been proposed
It is a sub-region of the amygdaloid complex;
Participates in the regulation of food intake

30
Q

What do Ligands: 5-HT (via 5-HT2C and 5-HT1A) do? (2)

a and fi

A

Decreases appetite

31
Q

What does the release of 5-HT, dopamine and GABA cause?

A

Decreases appetite

32
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

33
Q

What other inputs control feeding behaviour?

A
  • Orexigenic and anorexigenic neurotransmitters have been found in the hypothalamus
  • Orexigenic neurotransmitters: ↑appetite
  • Anorexigenic neurotransmitters: ↓ appetite
34
Q

Higher functions can modulate the CNS and peripheral cues what does this cause as a result?

A

inhibition or stimulation of food intake

35
Q

What overall factors affects how much we eat?

A
  • Food preferences
  • Emotions
  • Environment
  • Life style
  • Circadian rhythm – limits food intake to certain times (in some people)
  • Individual-based requirements (e.g., neural, metabolic, and hormonal) may alter feeding behaviour
36
Q

What receptors does blood glucose stimulate?

A

Stimulates gluco-receptors in hypothalamus

37
Q

What do glucostat receptors detect

A

o ↓[glucose]blood →induces hunger

o ↑[glucose]blood → induces satiety

38
Q

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

A
  • Cold environments stimulate feeding while hot environments inhibit appetite
  • Afferent input
  • Distension of a full stomach inhibits appetite; contraction of an empty one stimulates appetite
39
Q

Describe what happens when the pancreas releases?

A
  1. Insulin is released.
  2. Transported to the brain capillaries
  3. Causes a catabolic reaction so we get reduced food intake and reduce body fat/ or an anabolic reaction occurs and we get increased food intake and increase body fat
  4. Produces white fat
40
Q

Describe the regulation of energy homeostasis

A

On image

41
Q

Where is leptin produced?

How does it work?

What are the results of leptin secretion?

A
  • Fat cells (adipocytes) secrete leptin (16kDa protein) - gene expressed mainly in adipocytes
  • Controls fat stores by operating a feedback mechanism between adipose tissue and brain
  • ↑ adipose tissue size → ↑ leptin secretion: High correlation of leptin levels with body fat in humans and animals
  • Administration of leptin can decrease food intake, induce weight loss and increase energy expenditure
42
Q

Where is ghrelin released?

When are ghrelin levels high and low?

What does release of gherlin increase?

When can ghrelin be inhibited by?

A

• Released by stomach, pancreas, adrenals in response to nutritional status
 Circulating levels of ghrelin ↑ preprandially and ↓ after a meal
• Increases central orexins, e.g. NPY, and AgRP (generate hunger signals)
• Secretion of ghrelin can be inhibited by leptin
• Suppresses the ability of leptin to stimulate anorexigenic factors
• Could loss of ghrelin activity determine the success of gastric bypass?
• Leptin and ghrelin act reciprocally on food intake
• Stimulation of their receptors in hypothalamus → changes in food intake

43
Q

Where is Obestatin released and what does it cause?

A

• Produced by epithelial cells of stomach
• Encoded by ghrelin gene, but it opposes the effects of ghrelin on food intake
Suppresses food intake (suppresses appetite; ↓ body weight gain)
Antagonises ghrelin-induced food intake (and growth hormone secretion)
• Obestatin mediates its effects via different receptors to ghrelin
• Imbalance of ghrelin and obestatin may have a role in obesity?
[Decreased ghrelin/obestatin ratio characterise obesity in women?]