Physiology: Feeding & Satiety Flashcards

1
Q

What physiological imbalance leads to obesity?

A

Small constant mismatch between energy intake and energy expenditure

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2
Q

What is energy homeostasis?

A

over time energy intake is matched to energy expenditure

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3
Q

Obesity BMI range

A

Up to 25 -> normal

25 - 29.9 -> overweight

30 - 39.9 -> obese

> 40 -> morbidly obese

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4
Q

Describe obesity as a disease

A

group of conditions with multiple causes

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5
Q

What are the major factors influencing obesity? (2)

A
  • Genetics (susceptibility genes linked to fat storage and also regulation of energy intake and expenditure)
  • Environment (wide variety of high calorie food, reduced physical activity e.g. cars, jobs)
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6
Q

What are some diseases does obesity contributes to? (11)

A
  • Stroke (hypertension)
  • Dementia (Alzheimer’s)
  • Respiratory disease (sleep apnoea)
  • Type 2 Diabetes
  • Hypertension
  • Cardiovascular disease (lipids, diabetes, hypertension)
  • Increased cancer risk (especially colon, breast, uterus, prostate)
  • NAFLD (Non-Alcoholic Fatty Liver Disease)
  • Gall bladder disease
  • Osteoarthritis
  • Hyperuricaemia -> gout
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7
Q

Functions of fat (3)

A
  • Energy storage
  • Prevention of starvation
  • Energy buffer during prolonged illness
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8
Q

How does the brain respond to long-term obesity?

A

Brain defends body weight because it views the new weight as normal and dieting as threat of starvation.

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9
Q

In what 3 ways does the CNS influence energy balance and body weight? What is the site of integration of these influences and what is the neural centre responsible?

A
  1. Behaviour - feeding and physical activity
  2. ANS - regulates energy expenditure
  3. Hormonal - secretions of hormones

Site of integration: brain

Neural centre responsible: hypothalamus

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10
Q

Lesioning of which part of the hypothalamus causes obesity?

A

Ventromedial

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11
Q

Lesioning of which part of the hypothalamus causes leanness?

A

Lateral (lateral leanness)

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12
Q

Define satiation.

Define satiety.

Define adiposity.

A

Satiation: sense of fullness generated during a meal. (signals increase during meal time to limit meal size)

Satiety: period of time between meals. (satimety)

Adiposity: the state of being obese.

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13
Q

What 3 concepts underlie the control of energy intake and body weight?

A
  1. Satiety signalling
  2. Adiposity negative feedback signalling
  3. Food reward
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14
Q

What are the 5 Satiation Signals and discuss their location of secretion, release, and action?

A
  1. Cholecystokinin
    - secreted from enteroendocrine cells in duodenum and jejenum.
    - released in proportion to lipids and proteins in a meal.
    - signals via sensory nerves to hindbrain and stimulates hindbrain directly (Nucleus of solitary tract NTS)
  2. Peptide YY (PYY3-36)
    - secreted from endocrine mucosal L-cells of GI tract
    - release increases post-prandially
    - inhibits gastric motility, slows emptying and reduces food intake (hypothalamus)
  3. Glucagon-like Peptide 1 (GLP-1)
    - product of pro-glucagon gene
    - released from L cells in response to food ingestion
    - inhibits gastric emptying and reduces food intake (hypothalamus, NTS)
  4. Oxyntomodulin (OXM)
    - from pro-glucagon gene, and small intestinal L cells and oxyntic cells
    - released after meal
    - acts to suppress appetite
  5. Obestatin
    - peptide produced from gene that encodes ghrelin
    - released from cells lining the stomach and small intestine
    - not sure but may reduce food intake and antagonise action of ghrelin
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15
Q

What is the hunger signal? What produces it? When is it produced? How are its levels raised?

A

Ghrelin

  • produced + secreted by oxyntic cells in stomach
  • levels increase before meals and decrease after.
  • levels raised by fasting and hypoglycaemia
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16
Q

What does peripheral ghrelin do?

A
  1. stimulates food intake
  2. decreases energy expenditure
  3. decreases fat utilisation

overall increases body weight

17
Q

What do ghrelin-containing hormones in brain do?

A
  1. helps control fat metabolism
  2. increases lipogenesis
  3. decreases lipid oxidation (liver and adipose) (lipid oxidation causes cell damage)
18
Q

What can be injected into hypothalamic centres to increase food intake? (3)

A

-Glutamate
-gaba
-opioids.
Effects are short lasting.

19
Q

What neurotransmitters suppress food intake?

A

Monoamines (drugs developed based on these systems but most withdrawn with bad side effects)

20
Q

What are the two adiposity signals (reporting fat status), where are they produced and what do they act on?

A

Leptin (produced in fat cells) and Insulin (produced in beta pancreatic cells)

Act on hypothalamic neurons.

Levels of these increase in blood with increase in fat.

21
Q

What happens with reduced leptin?

A

Reduced leptin mimics starvation -> unrestrained appetite

22
Q

Where are there high levels of leptin receptors?

A

Hypothalamus

23
Q

List biological roles of leptin

A
  • food intake/energy expenditure/fat deposition
  • peripheral glucose homeostasis/insulin sensitivity
  • immune system maintenance
  • reproductive system maintenance
  • angiogenesis
  • tumourgenesis
  • bone formation
24
Q

What therapy can be effective in ob defected people? In what group of people is it ineffective?

A

Injected leptin therapy

Ineffective in people with leptin resistance

25
Q

What can cause leptin resistance?

A

diet-induced obesity (defected leptin transport + problem with leptin receptors)

26
Q

List some anti-obesity drugs (4)

A
  • sibutramine (decreases food intake, withdrawn but can still be bought online)
  • Orlistat (reduces fat absorption in small intestine, bad gastric side effects, need vitamins at same time, approved in europe, over the counter)
  • Contrave/Mysimba (approved in europe)
  • Liraglutide (drug used for type 2 diabetes that is a GLP-1 agonist + shows weight loss effects at high dose, has to be injected)
27
Q

What surgery is performed for obesity?

A

Bariatric surgery - gastric by-pass (50-60% weight loss, Type 2 diabetes resolution, reduced calorie intake because of by-pass but also altered secretion of peptides from stomach that affects hypothalamus and beta cells, e.g. PPY3-36, GLP-1, ghrelin

28
Q

What are some metabolic stress consequences

A
  • obesity
  • dyslipidaemia
  • Type 2 Diabetes
  • Insulin Resistance
  • Metabolic Syndrome
  • CVS disease