Feeding and Satiety Flashcards

1
Q

what is energy homeostasis

A

physiological process whereby energy intake is matched to energy expenditure over time via feedback loop - promoting body fuel stability (energy stored as fat)

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2
Q

what is obesity in terms of BMI

A

small constant mismatch between energy intake and energy expenditure;
>30 - obese
>40 - morbidly obese

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3
Q

factors influencing obesity

A

genetics - susceptibility genes, increasing the risk of developing disease
environmental

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4
Q

consequences of obesity

A
stroke (hypertension)
respiratory disease - sleep apnea
heart disease
gallbladder disease
osteoarthritis 
dementia - alzheimer's
NAFLD 
diabetes
cancer
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5
Q

obesity’s affect on the brain

A

alters brain function/brain re-programming - brain views extra weight as normal and dieting as a threat to body survival

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6
Q

how does the CNS influence energy body balance and body weight

A

behaviour - feeding and physical activity
ANS activity - regulates energy expenditure
neuroendocrine system - secretion of hormones

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7
Q

control centre of the brain for feeding behaviour

A

hypothalamus;
lesioning ventromedial hypothalamus - obesity
lesioning lateral hypothalamus - leanness

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8
Q

concepts underlying the hypothalamus

A

satiety signalling - feeling full
adiposity negative feedback signalling - state of being obese
food reward

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9
Q

what are satiation signals

A

short term processes regulating meal initiation, termination and inter-meal frequency (increase to limit meal size)

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10
Q

different types of satitation signals

A
cholecystokinin (CCK)
peptide YY
glucagon-like peptide
oxyntomodulin (OXM)
obestatin
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11
Q

describe cholecystokinin

A

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 (NTS)

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12
Q

describe peptide YY

A

secreted from endocrine mucosal L-cells of G-I tract
Levels increase rapidly post-prandially
Inhibits gastric motility, slows emptying and reduces food intake (Hypo)

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13
Q

describe glucagon-like peptide (GLP-1)

A

product of pro-glucagon gene.
released from L cells in response to food ingestion
Inhibits gastric emptying and reduces food intake (Hypo, NTS)

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14
Q

describe oxyntomodulin

A

from pro-glucagon gene and released from oxyntic cells and L-cells of small intestine after meal.
Acts to suppress appetite – mechanism and site unclear.

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15
Q

describe obestatin

A

peptide produced from gene that encodes ghrelin and released from cells lining stomach/small intestine.
Suggested to reduce food intake – may act to antagonise the actions of ghrelin – actions unclear at present.

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16
Q

what is ghrelin

A

a hunger signal
octanoylated peptide produced and secreted by oxyntic cells in stomach
there are ghrelin-containing neurones in the hypothalamus

17
Q

ghrelin function

A

levels increases before meals and decreases after meals

levels are raised by fasting and hypoglycaemia

18
Q

ghrelin in the hypothalamus

A

control fat metabolism
increase lipogenesis
decreases lipid oxidation (liver and adipose)

19
Q

peripheral ghrelin

A

stimulates food intake;

decreasing energy expenditure and fat utilisation –> increasing body weight

20
Q

central appetite controllers

A

glutamate, gaba and opiods

monoamines

21
Q

function of flutamate, gaba and opiods

A

increase food intake when injected into hypothalamic centres - effects modest/short lasting

22
Q

function of monamines

A

suppress food intake - many drugs developed to act on these system (many are withdrawn)

23
Q

hormones reporting fat stores to the brain

A

adiposity signals - levels will increase in blood as more fat is stored;
leptin (from fat cells)
insulin (pancreatic beta-cells)

24
Q

function of the hormones reporting fat stores to the brian

A

inform the hypothalamus to alter energy balance - eat less and increase energy burn
this malfunctions in obese state

25
Q

mutation in leptin gene

A

a reduced leptin will mimic starvation, causing an unrestrained appetite and obesity

26
Q

biological roles of leptin

A

food intake.energy expenditure/fat disposition
peripheral glucose homeostasis/insulin sensitivity
maintaince of immune system
maintenance of reproductive system
angiogenesis
tumourigenesis
bone formation

27
Q

describe the food reward effect on the brain

A

dopamine pathway activated in foods strongly linked to sugar and fat

28
Q

describe leptin therapy in obesity

A

limited by severe leptin resistance present in most obese individuals

29
Q

how does diet-induced obesity result in leptin resistance

A

defective leptin transport into brain

altered signal transduction following leptin binding to its receptor

30
Q

describe adaptive thermogenesis

A

Thermogenic adipocytes – increase energy expenditure uncoupling of oxidative metabolism from ATP production