Physiology

Question 1

What are the possible consequences of obesity?

Answer 1

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

Question 2

Why do we need fat?

Answer 2

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

Question 3

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

Answer 3

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

Question 4

How does the CNS influence energy balance and body weight?

Answer 4

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

Question 5

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

Answer 5

1. Satiety signalling
2. Adiposity Negative Feedback Signalling
3. Food Reward

Question 6

Define

a) satiation and
b) satiety.

Answer 6

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

Question 7

Define adiposity

Answer 7

Adiposity is the state of being obese

Question 8

What are the 5 main satiation signals?

Answer 8

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

Question 9

Describe cholecystokinin

Answer 9

• 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)

Question 10

Describe peptide YY

Answer 10

• 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

Question 11

Describe glucagon-like peptide 1

Answer 11

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

Question 12

Describe oxyntomodulin

Answer 12

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

Question 13

Describe obestatin

Answer 13

• 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

Question 14

What is ghrelin?

Answer 14

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

Question 15

What two hormones report fat status to the brain?

Answer 15

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

Question 16

What deficiencies might an obese human have?

Answer 16

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