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The GI Block > Physiology > Flashcards

Flashcards in Physiology Deck (17):
1

What are the possible consequences of obesity?

-Stroke (hypeprtension) -Respiratory disease (sleep apnoea) - Heart Disease (Lipids, diabetes, hypertension) -Gallbladder disease -Osteoarthritis -Dementia -NAFLD -Diabetes -Cancer (uterus, breast, prostate, colon) -Hyperuricemia, gout

2

Why do we need fat?

-Energy storage -Prevention of starvation -Energy buffer during prolonged illness

3

Once a person has gained weight it is difficult to lose it. What is the neurological reasoning for this?

Increased body fat alters brain function Long-term obesity induces brain re-programming i.e. your brain views the extra weight (fat) as normal & dieting as threat to body survival and defends the new weight

4

How does the CNS influence energy balance and body weight?

1) Behaviour- feeding and physical activity 2) ANS Activity- regulates energy expenditure 3) Neuroendocrine System- secretion of hormones Integration (in the hypothalamus) of these determines final output- feeding behaviour e.g. lesioning ventromedial hypothalamus causes obesity e.g. lesioning lateral hypothalamus causes leanness

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5

What three basic concepts underlie the control system of energy homeostasis?

1. Satiety signalling

2. Adiposity Negative Feedback Signalling

3. Food Reward

6

Define

a) satiation and

b) satiety.

 

a) Satiation is a sensation of fullness generated during a meal

b) Satiety is the period of time between termination of one meal and the initiation of the next

 

7

Define adiposity

 

Adiposity is the state of being obese

8

What are the 5 main satiation signals?

  1. Cholecystokinin
  2. Peptide YY
  3. Glucagon-like peptide
  4. Oxyntomodulin
  5. Obestatin 

9

Describe cholecystokinin

  • secreted from enteroendocrine cells in duodenum and jejunum
  • released in proportion to lipids and proteins in meal
  • signals via sensory nerves to hindbrain 
  • and stimulates hindbrain directly (nucleus of solitary tract)

10

Describe peptide YY 

  • secreted from endocrine mucosal L-cells of GI tract
  • levels increase rapidly post-meal (post-prandially)
  • inhibits gastric motility, slows emptyinh and reduces food intake 

11

Describe glucagon-like peptide 1

  • product of pro-glucagon gene
  • also released from L cells in response to food ingestion
  • inhibits gastric empyting and reduces food intake 

12

Describe oxyntomodulin

 

  • also from pro-glucagon gene and released from oxyntic cells of small intestine after meal
  • acts to suppress appetite
  • mechanism unclear

13

Describe obestatin

  • peptide produced from gene that encodes ghrelin 
  • released from cells lining stomach/small intestine
  • suggested to reduce food intake- may antagonise the actions of ghrelin- actions unclear at present 

14

What is ghrelin?

Octanolyated peptide

  • produced and secreted by oxyntic cells in stomach
  • ghrelin levels increase before meals and decrease after meals
  • levels are raised by fastin and hypoglycaemia 
  • peripheral ghreli stimulates food intake and decreases fat utlization

15

What two hormones report fat status to the brain?

  1. Leptin- made & released from fat cells
  2. Insulin- made & released from pancreatic cells

Levels in blood increase as more fat is stored.

Function= inform brain (hypothalamus) to alter energy balance- eat less and increase energy burn

This malfunctions in obese states 

16

What deficiencies might an obese human have?

  • Leptin deficiency
  • Leptin receptor deficiency
  • POMC deficiency
  • MC4-R deficiency

17