Control of appetite, metabolic syndrome, developmental origins of health & disease Flashcards

1
Q

Which stimulatory hormones are involved in the control of appetite?

A

NPY & AgRP - promote hunger

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2
Q

Which inhibitory hormones are involved in the control of appetite?

A

POMC –> a-MSH & B-endorphine (through neurotransmitters) promoting satiety

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3
Q

How do hormones control appetite?

A

primary neurone –> secondary neurone –> modulated feeding behaviour

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4
Q

When is Ghrelin released? what is it?

A

peptide hormone released from stomach wall when EMPTY
released from stomach wall to hypothalamus
stimulate excitatory NYP & AgRP primary neurones
increasing appetite
filled stomach inhibits ghrelin release

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5
Q

Outline the control of appetite

A

satiety centre of hypothalamus: appetite control centre

hypothalamus’ arcuate nucleus

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6
Q

What is another hormone that is released from the gut to the hypothalamus apart from ghrelin which suppresses appetite?

A

PYY

released by cells in ilium & colon (small intestines), inhibits primary excitatory neurones, suppressing appetite

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7
Q

What happens when there is too much PYY and too little PYY

A

too much: patient becomes anorexic

too little: patient becomes obese

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8
Q

What’s a hormone released from the body to the hypothalamus?

A

Leptin - peptide hormone released to blood by fat cells (adipocytes)
stimulates POMC & suppresses NPY & AgRP - suppressing appetite

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9
Q

Aside from leptin, which other hormones are released from the body to the hypothalamus to suppress appetite?

A

insulin & amylin - both released from beta cells of pancreas

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10
Q

What is metabolic syndrome?

A

a cluster of risk factors associated to CVD

e.g. abdomin obesity, high BP, insulin resistance, raised fasting glucose, dyslipidaemia (high TAG, low HDL)

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11
Q

Which are the most significant risk factors of metabolic syndrome?

A
insulin resistance (high glucose conc = high insulin, beta cells can't keep up with production - so wear out) high glucose = type 2 diabetes
& central obesity (hypertension, high cholesterol, hyperglycaemia)

cause unknown

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12
Q

What are the treatments for metabolic syndrome?

A

primary: healthy lifestyle, calorie restriction, physical activity, healthy diet
secondary: drug intervention, STATINS reduce LDL - cholesterol
antihypertensive lower bp, antidiabetic - hyperglycaemia

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13
Q

Explain developmental origins of health & disease theory in relation to epigenetics

A

if a pregnant women had a low nutrient intake, the child could be programmed for similar life, so insulin & leptin resistance fo harsh environment
if offspring have a life of plenty (excess nutrient uptake) then metabolism will drive hem to obesity, diabetes, metabolic syndrome

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14
Q

How do their epigenetics change?

A

hormonal changes, metabolic changes, altered cellular differentiation
epigenetic regulation: histone modifications e.g. methylation of histones (non coding RNA) - long term effects on gene expression, increased risk of disease

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15
Q

what is the importance of the DoHaD theory?

A

better understanding of origins of some diseases

highlight importance of antenatal care - adequate & appropriate nutrition

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16
Q

what’s a socioeconomical issue of the DoHaD theory?

A

women greatest risk of poor nutrition, least likely to present for antenatal care

17
Q

examples of neg feedback

A
  1. release of cortisol from adrenal gland, suppressing release of TRH from hypothalamus & ACTH from pituitary gland
  2. hypoglycaemia stimulating release of insulin - decreasing blood glucose conc.
18
Q

example of positive feedback

A

blood clotting: signalling cascade to change blood from liquid –> solid

ovulation - LH surge

19
Q

What are hormones?

A

number of tissues that synthesise chemical signals

signals can be protein molecules, steroids, AA derivatives

20
Q

How do steroid & thyroid hormones travel in the blood? why?

A

they are lipophilic, so require specialist transport proteins e.g. albumin

21
Q

Describe how hydrophobic hormones travel and function?

A

transported in blood by specialist protein, can cross target cell plasma membrane, interact with intracellular receptors & bind with specific region of DNA to change rate of transcription of specific gene –> change rate of synthesis of specific protein –> protein determine response of target tissue

22
Q

difference between epigenetics & genetic mutation

A

genetic mutation: changes to nucleotide (DNA) sequence

epigenetics: methylation of DNA & changes in histone structure, affecting DNA transcription (copied to mRNA)

23
Q

appetite control in humans - why is it important?

A

to balance energy intake with energy expenditure