Control of food intake Flashcards

1
Q

What is the stomach volume when fasting and during food accommodation?

A

Fasting: 50ml

During food accommodation: 1.5L

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2
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 due to the increase in ghrelin hormone.

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3
Q

Define appetite.

A

The physiological desire/drive to satisfy the body’s need for food; hunger a stimulated response.

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4
Q

Define satiety.

A

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

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5
Q

Define aphagia.

A

The inability or refusal to swallow.

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6
Q

Define Hyperphagia/polyphagia.

A

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

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7
Q

What happens during accommodation of food?

A

Inhibitory NANC neurotransmitters VIP and NO enlarge and expand the fundus area of the stomach.

PYY (Peptide YY) also released, providing a satiety feeling and also decreases gut motility.

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8
Q

What are the 3 types of relaxation of the gastric reservoir?

A
  • Receptive
  • Adaptive
  • Feedback
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9
Q

What is receptive relaxation?

A

Vagovagal reflex that is stimulated by chewing and swallowing, causing relaxation of smooth muscle of stomach.
Mechanoreceptors are involved.

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10
Q

What is adaptive relaxation?

A

Stomach stretches when food enters, causing an increase in intragastric pressure, causing relaxation of gastric reservoir through NANC inhibition.
Mechano and/or chemoreceptors involved

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11
Q

What is feedback relaxation?

A

Presence of nutrients, particularly lipids in the small intestine, and CCK trigger relaxation of the gastric reservoir.

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12
Q

What are receptive, adaptive and feedback relaxation mediated by?

A

NANC inhibition as well as reflex chains involving release of Noradrenaline (NA) from sympathetic fibres.

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13
Q

What is the role of NANC inhibitors in relaxation of gastric reservoir?

A

In order for relaxation of gastric reservoir, inhibitory vagal pathways innervate inhibitory enteric pathways that release NO, VIP, PACAP and/or ATP.

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14
Q

What mediates contraction of the stomach?

A

Excitatory vagal pathways which innervate excitatory enteric pathways that release acetylecholine (Ach).

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15
Q

What is the control centre for appetite, food intake, hunger and thirst?

A

Hypothalmus

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16
Q

How does the hypothalamus control appetite, food intake, hunger and thirst?

A

The base of the hypothalamus contains several nuclei that regulate energy homeostasis (energy inflow and energy expenditure).

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17
Q

What is are the roles of Orexigenic and Anorexigenic Neurotransmitters in Hypothalamus?

A

Orexigenic Neurotransmitters increase appetite

Anorexigenic Neurotransmitters decrease appetite

18
Q

What is the role of the Pre-frontal cortex in controlling food intake?

A

Pre frontal cortex involved in FOOD-SEEKING:

  • integrate sensory information from inside and outside the body
  • receives emotional and cognitive information from limbic system
  • translates this homeostatic and environmental information into adaptive behavioural responses (e.g. eating).
19
Q

What is the role of the limbic system in controlling food intake?

A

System of nerves and networks in areas of the brain concerned with instinct and mood, and may control emotions e.g. pleasure, fear, anger, HUNGER etc.

20
Q

What is the role of lateral hypothalamus?

A

Hunger/thirst centre

21
Q

What is the role of the ventromedial nucleus (VMN)

A

Satiety centre

22
Q

What is the role of the Dorsomedial Nucleus (DMN).

A

Hunger centre (release of NPY into DMN increases feeding).

23
Q

What is the role of the Paraventricular Nucleus (PVN).

A

Modulates feeding behaviour.

Release of NPY, opioids, GABA into PVN increasing feeding.

Release of leptin into PVN decreases feeding.

24
Q

What is the role of the arcuate nucleus?

A

Modulates feeding behaviour

Release of orexigenic signals into arcuate nucleus (NPY, opioids, dynorphin, β-endorphin, POMC, galanin, amino acids, GABA and glutamate) increase feeding.

25
Q

What is the role of Suprachiasmatic Nucleus (SCN)?

A

Controls circadian rhythms, which could affect mood/drive to eat

Located on either side of hypothalamus, directly above optic chiasm.

26
Q

What is the role of Medial-Amygdaloid Nucleus?

A

Regulates appetite and food intake as 5HT binds to receptors (5-HT2C and 5HT1A) decreasing appetite.

27
Q

Describe The Appetite Suppressing Pathway.

A
  • 5HT2C agonist e.g. mcPP binds to 5HT2C receptors on POMC neurones (appetite suppressing neurones)
  • POMC neurones activated and POMC precursor (pro-opiomelanocortin) is broken down into ⍺-MSH
  • ⍺-MSH released by POMC neurones and bind to MC4R receptors, causing suppression of appetite.
28
Q

What are the Anorexigenic factors that suppress appetite?

A

5HT (by binding to 5HT2C and 5HT1A)
Dopamine
GABA
Insulin

29
Q

Describe the Appetite Stimulating Pathway.

A

Agouti Related peptide (AgRP) and Neuropeptide Y (NPY) released by AgRP/NPY neurone, which is the appetite stimulating neurone.

Appetite suppressing neurone POMC doesn’t release ⍺-MSH hormone, therefore MCR4 receptors not occupied, causing for stimulation of appetite.

30
Q

What are the Orexigenic factors stimulating appetite?

A

Opioids

31
Q

What does the stimulation of VMN cause(satiety centre)?

A

Aphagia

32
Q

What do the lesions of VMN cause?

A

Hyperphagia

33
Q

What do Lesions of Lateral Hypothalamus cause?

A

Aphagia

34
Q

What us the role of Zimelidine?

A

inhibits reuptake of 5HT from synaptic cleft, causing for suppression of appetite.

35
Q

When are carbohydrates and fats metabolised?

A

Carbohydrates - During the day

Fat - all night

36
Q

Give 4 different signals that affect apetite.

A

1) Concentration of glucose in the blood will stimulate glucoreceptors in the hypothalamus.
- Decreased glucose up-regulated hunger
- Increased glucose up-regulates feeling of satiety.

2) Cold environments stimulate feeding while hot environments inhibit feeding. This is useful as allows to put fat on when cold.

3) Afferent inputs to stomach:
- Distension of full stomach inhibits appetite
- Contraction of empty stomach stimulates appetite

4) Deposition of fat (which releases leptin) may also control appetite

37
Q

What is the role of gut hormones?

A

Released with a meal

Fat ingestion causes CCK release and slowing of gastric emptying

CCK (from I cells in the intestine or nerve endings) and somatostatin inhibit further food intake

Injection of CCK in the brain could reduce appetite

38
Q

What is the role of pancreatic hormones (isulin, glucagon and amylin)

A

Insulin acts on insulin receptors in arcuate nucleus of hypothalamus with either net catabolic or anabolic effect, influencing homeostasis.

  • Catabolic effect: insulin inhibits NPY and AgRP synthesis, causes for increased food intake and increased body fat
  • Anabolic effect: insulin stimulates POMC and CART neurones, causes for decreased food intake and decreased body fat

Glucagon acts at the liver where it increases glucose production while generating a signal to reduce energy intake that is relayed to the hindbrain.

Amylin acts directly at the hindbrain to reduce energy intake.

39
Q

What is the Area postrema (AP)?

A

A medullary structure in the brain that controls vomiting

40
Q

What is leptin?

A

A hormone produced by white adipose (fat) cells that acts as a satiety factor in regulating appetite.

Increases expression of anorexigenic factors POMC, CART, CRH and neurotensin.

Inhibits NPY which generally stimulates feeding. Also inhibits ghrelin

Stimulates metabolic rate

41
Q

What is ghrelin?

A

Appetite inducing hormone produced by P/D1 Cells and stimulates hunger.

Can be released by pancreas and adrenals.

Stimulates food intake:

  • increases expression of orexigenic factors NPY and AgRP
  • suppresses the ability of leptin to stimulate anorexigenic factors

Secretion of ghrelin can be inhibited by leptin.

42
Q

What is obestsatin?

A

Hormone produced by epithelial cells of the stomach which suppresses appetite and reduces body weight gain.