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Gastrointestinal > Feeding and Satiety > Flashcards

Feeding and Satiety Flashcards

1
Q

What are the BMI ranges for normal, overweight, obese and morbidly obese?

A

Normal - up to 25.
Overweight - 25-29.9.
Obese - 30-39.9.
Morbidly obese - >40.

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2
Q

What other conditions can obesity contribute to?

A

Stroke (hypertension), resp disease (sleep apnoea), heart disease (lipids, diabetes, hypertension), gallbladder disease, osteoarthritis, dementia, NAFLD, diabetes, cancer, hyperuricaemia and gout.

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3
Q

What are 3 functions of fat in our bodies?

A

Energy storage, prevention of starvation and energy buffer during prolonged illness.

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4
Q

What is the result of the brain re-programming after long-term obesity?

A

Your brain views the extra weight as normal and dieting as threat to body survival i.e. defends new weight.

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5
Q

What are the 3 ways that the CNS influences energy balance and body weight?

A
  1. Behaviour - feeding and physical activity.
  2. ANS activity - regulates energy expenditure.
  3. Neuroendocrine system - secretion of hormones.
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6
Q

What is the neural centre responsible for controlling energy intake and body weight?

A

The hypothalamus.

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7
Q

What are the 3 basic concepts that underlie the hypothalamuses control of body weight?

A
  1. Satiety signalling.
  2. Adiposity negative feedback signalling.
  3. Food reward.
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8
Q

Define satiation, stiety and adiposity.

A

Satiation: sensation of fullness generated during a meal.
Satiety: period of time between termination of one meal and the initiation of the next.
Adiposity: state of being obese.

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9
Q

What regulates meal initiation, termination and inter-meal frequency?

A

Short term processes.

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10
Q

What do satiation signals do during meals and why?

A

Increase to limit meal size.

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11
Q

List the proteins involved in satiety signals and what effect do they have?

A

Cholecytokinin (CKK), peptide YY (PYY3-36), glucagon-like peptide 1 (GLP-1), oxyntomodulin (OXM), obestatin. They make you feel full.

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12
Q

What is the hunger signalling protein called?

A

Ghrelin.

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13
Q

What type of peptide is ghrelin?

A

An octanoylated peptide.

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14
Q

Where is ghrelin produced and secreted?

A

Oxyntic cells in stomach.

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15
Q

What are the functions of ghrelin?

A

Stimulates food intake (hypothalamus), decreases fat utilisation (helps control fat metabolism, increased lipogenesis in liver and adipose tissue).

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16
Q

What hormones are produced in peripheral tissues to act on hypothalamic neurones to communicate the status of fat stores in the brain?

A

Leptin (made and released from fat cells) and insulin (made and released from pancreatic cells).

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17
Q

What happens to the levels of leptin and insulin in blood as more fat is stored?

A

They increase.

18
Q

What gene mutation caused obesity in mice (mimics starvation, causes unrestrained appetite and obesity)?

A

Ob/Ob spontaneous mutation (the gene that codes for leptin).

19
Q

What other gene mutation causes obesity in mice and what other effects did this have?

A

Having no functional leptin receptor (db/db mutation). Also became hyperglycaemic, hyperinsulinaemic and insulin resistant.

20
Q

What other gene mutations can cause obesity in humans?

A

POMC and MC4-R.

21
Q

Where are there high levels of leptin receptors (Ob-Rb)?

A

In the hypothalamus.

22
Q

What effect does intracereberoventricular (ICV) leptin and insulin have on rodents?

A

Inhibits food intake and decreases body weight.

23
Q

What are the functions of leptin?

A

Food intake/energy expenditure/fat deposition, peripheral glucose homeostasis/insulin sensitivity, maintenance of immune system, maintenance of reproductive system, angiogenesis, tumourigenesis, bone formation.

24
Q

How do the peripheral and hypothalamic actions of insulin differ?

A

They are opposite (peripheral insulin is anabolic).

25
Q

What pathways cause the food reward and what else are they implicated in?

A

Dopamine pathways. Substance abuse and drug addiction.

26
Q

Why can leptin not be used therapeutically in common obesity?

A

Most obese individuals have severe leptin resistance.

27
Q

Why does diet-induced obesity result in leptin resistance?

A
  1. Defective leptin transport into brain. 2. Altered signal transduction following leptin binding to its receptor.
28
Q

What previous anti-obesity drugs have been withdrawn due to side effects?

A

Noradrenergics, serotonergics, Fen-phen.

29
Q

What system did rimonabant target and what were the side effects of this drug?

A

The endocannabinoid system. Severe depression, promotes development of neurodegenerative disease.

30
Q

What used to be the only drug prescribed to treat obesity?

A

Orlistat.

31
Q

What is the mechanism of orlistat and what are the side effects?

A

Inhibits pancreatic lipase decreasing triglyceride absorption (reduces efficiency of fat absorption).
Side effects: cramping, severe diarrhoea.

32
Q

Other than the side effects, what are the downsides of orlistat?

A

You need to take vitamin supplements (fat-soluble vitamins), may not be particularly effective over long term.

33
Q

Name a drug that is going to be marketed in the UK soon.

A

Contrave.

34
Q

Name a new anti-obesity drug coming.

A

Liraglutide (Saxenda).

35
Q

What type of drug is liraglutide and how is it taken?

A

Glucagon-like peptide 1 receptor antagonist. Has to be injected.

36
Q

What side effects are still to be ruled out with liraglutide?

A

Thyroid and pancreatic cancer.

37
Q

What are the benefits of bariatric surgery?

A

Produces substantial weight loss that is also sustainable, induces high level of complete resolution of type 2 diabetes.

38
Q

How may bariatric surgery resolve type II diabetes?

A

Altered secretion of peptides from stomach and gut that affect beta cells and hypothalamus e.g. GLP-1, PYY3-36, ghrelin.

39
Q

How may brown adipose tissue help with obesity?

A

Increases energy expenditure by uncoupling of oxidative metabolism from ATP production.

40
Q

What is the protein in brown adipose tissue that causes the uncoupling?

A

Uncoupling protein 1 (UCP1).

41
Q

Can white adipose tissue be changed to brown adipose tissue?

A

Some can.

42
Q

What causes more activity of brown adipose tissue and why is this not widely used?

A

2,4-dinitrophenol (DNP), can kill people due to hyperthermia.

Gastrointestinal (26 decks)

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