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GI > 1- physiology of feeding + satiety > Flashcards

1- physiology of feeding + satiety Flashcards

1
Q

what is energy homeostasis?

A
  • a physiological process whereby energy intake is matched to energy expenditure over time
  • promotes body fuel stability - energy primarily stored as fat
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2
Q

how do you calculate BMI?

A

weight (kg)/square of height (m)

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3
Q

what are some consequences obesity?

A
  • stroke
  • respiratory disease
  • heart disease
  • osteoarthritis
  • dementia
  • covid-19
  • diabetes
  • cancer
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4
Q

why need fat?

A
  • energy storage
  • prevent starvation
  • energy buffer during prolonged illness (when ill use up lots of energy so need it from stored fat)
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5
Q

what is consequence of disease of adipose tissue?

A

difficult to lose wight as over time (long term obesity) induces brain re-programming so your brain views the extra weight (fat) as normal + dieting as a threat to body survival

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6
Q

how does CNS influence energy and body weight?

A

1)Behaviour- feeding and physical activity

2)ANS activity- regulates energy expenditure

3)Neuroendocrine system- secretion of hormones

= site of integration of these factors is the brain, specific neural centre responsible is hypothalamus

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7
Q

what are 3 basic concepts underlying control system of body weight + energy intake?

A
  1. satiety signalling
  2. adiposity negative feedback signalling
  3. food reward
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8
Q

what is satiety?

A

= period of time between termination of 1 meal and initiation of the next

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9
Q

what is satiation?

A

= sensation of fullness generate during a meal

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10
Q

what is purpose of peptide hormones released during a meal?

A

variety of peptide hormones released by specialised cells in gut + stomach, they are released during a meal to limit meal size (can go wrong in obesity)

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11
Q

what are 3 examples of peptide hormones that are released during a meal to limit size?

A
  • cholecystokinin (CCK)
  • peptide YY (PYY3-36)
  • glucagon-like peptide (GLP-1)
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12
Q

where is cholecystokinin (CKK) released from and what’s its function?

A
  • secreted fromenteroendocrinecells 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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13
Q

where is peptide YY released from and what’s it’s function?

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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14
Q

where is glucagon like peptide released from and whats it’s function?

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

*GLP-1 important as this is target of anti-obesity drugs

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15
Q

what do signals respond to that control energy balance and where are they sensed?

A
  • signals are produced in response to body nutritional status
  • these are sensed in hypothalamus
  • they act to modulate food intake + energy expenditure
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16
Q

what are 2 adiposity signals and what is their purpose?

A

leptin and insulin = act at hypothalamic neurons to say eat more or less →adiposity signals

17
Q

what must be communicated in order to control energy status to control amount of body fat?

A

brain

18
Q

what is leptin?

A

adiposity signal that is major one for controlling fat homeostasis in body

19
Q

what is insulin?

A

adiposity signal, major control factor for glucose homeostasis (but can also control fat homeostasis a bit)

20
Q

what is effect on adiposity signals as more fat is stored?

A

increased levels of adiposity signals as more fat stored

21
Q

what does reduced leptin mimic?

A

mimic starvation, causing unrestrained appetite

(more leptin = lean. less leptin = large)

22
Q

what is affect if deficient in normal functioning leptin receptor?

A

(plenty leptin but not functioning leptin) = obese and diabetic (hyperglycemic, hyperinsulinemic + insulin resistant)

*only explain less than 10% of obesity

23
Q

what are biological roles of leptin (has multiple)?

A
  • glucose homeostasis
  • maintenance of immune system (relationship to covid)
  • maintenance of reproductive system angiogenesis
  • tumorigenesis
  • bone formation

→so if leptin not working problem then big knock on effect

24
Q

what is ghrelin?

A

a hunger signal - another satiety peptide, has long term influences on energy expenditure + weight

  • it’s a octanoylated peptide, produced and secreted by oxyntic cells in stomach
25
Q

how does ghrelin levels differ around meals?

A

increase before meals and decrease after meals (makes sense as hunger signal)

26
Q

what can raise ghrelin levels?

A

Levels are raised by fasting and hypoglycaemia.

27
Q

what does peripheral ghrelin stimulate? what is mechanism?

A

stimulates food intake, decreases energy expenditure and decreases fat utilization – increases body weight
- acts to trigger central pathways to prepare body to process in-coming nutrients –for storage as fat so helps control fat metabolism, increase lipogenesis and decreases lipid oxidation

28
Q

what is effect of diet induced obesity on leptin?

A

leads to decreased leptin resistance

  • most obesity is associated with high leptin levels (corresponds with high fat level) = this means leptin use therapeutically is reduced as high resistance
29
Q

what are the 2 theories of why leptin resistance in diet induced obesity?

A
  1. Defective leptin transport into brain
  2. Altered signal transduction following leptin binding to its receptor
30
Q

what are prevention options for diet induced obesity?

A
  1. Lifestyle changes: dieting and exercise – do not appear to produce marked sustainable weight loss in the overall population
  2. Psychological therapies – cognitive behavioural therapy – not able to deliver on a mass scale
  3. Bariatric surgery – effective – but reserved for morbidly obese. substantial weight loss and often resolves type 2 diabetes very quickly + effectively (not totally sure why)
  4. Therapeutic agents to reduce body weigh
31
Q

what are therapeutic options for obesity?

A
  • there have been previous drugs like noradrenergic, serotonergics, sibutramine, rimonabant which were effective but had extreme side effects
  • GLP1 receptor agonists = more modern approach like luraglutide and semaglutide
32
Q

what are examples of GLP1 receptor agonists for obesity therapeutic agents?

A

luraglutide = has to be injected, was originally given for diabetes but then discovered also gave weight loss

semaglutide = later development (better version) - very effective, 15-20% weight loss and reduced cardiovascular + heart disease, huge impact (the maker can’t keep up with demand, very popular)

→companies are trying to make oral versions of these drugs

GI (56 decks)

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