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Nutrients & Metabolic Disease > LT2 Hypothalamus > Flashcards

LT2 Hypothalamus Flashcards

1
Q

Why is it not just genectic mutation/drift that is causing the rapid increase in obesity rates?

A

Because the timeframe is too quick for it to be caused by genes alone

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2
Q

What is the % of heritability of fat mass?

A

40% to 70%

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3
Q

Give an example of one monogenetic mutation that causes obesity

A

Leptin and leptin receptor mutation

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4
Q

Define polygenic aetiology

A

A characteristic that is influence by two or more genes

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5
Q

What are our survival genes likely to do?

A

Drive obesity

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6
Q

Why are our survival genes likely driving obesity?***

A
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7
Q

Why is it difficult to lose weight, once gained?

A

Increased body fat alters brain function

Brain views extra fat as normal so dieting is seen as threat to body survival

Body defends heavier weight

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8
Q

CNS influence energy balance and body weight by what 3 mechanisms?

A

Behaviour = feeding and physical activity

ANS activity = regulates energy expenditure

Neuroendocrine system = secretion of hormones

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9
Q

Why is obesity a disease of the brain?

A

CNS controls energy intake and body weight

Brain integrates signals

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10
Q

What is the main CNS centre responsible for energy intake control?

A

Hypothalamus

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11
Q

What is the satiety centre in hypothalamus?

A

Ventromedial hypothalamus

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12
Q

What is the hunger centre in hypothalamus?

A

Lateral hypothalamus

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13
Q

What happens when ventromedial hypothalamus is removed?

A

Causes obesity because satiety signals not received

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14
Q

What happens when lateral hypothalamus is removed?

A

Causes leanness because hunger signals are not received

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15
Q

Why is an individuals weight stable over lengthy periods of time?

A

Because energy balance is controllled by feedback loops

They act to maintain constancy of total body energy stores

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16
Q

Why do most people regain weight after stopping dieting?

A

Because of the feedback loops bringing the body back to usual weight

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17
Q
A
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18
Q

How is food intake and energy expenditure modulated? (flowchart)

A

Signals produced in response to body energy status

Sensed by the brain

Signals in brain act to modulate food intake and energy expenditure

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19
Q

Where is the hypoethalamus located?

A

At the base of the brain, in the diencephalon

Attached above the pituitary gland

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20
Q

Define sagittal section

A

Vertical slice through the body

Divides it into left and right sides

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21
Q

Name the 6 areas of the hypothalamus

A

Arcuate nucleus (ARC)

Ventromedial nucleus (VMN)

Dorsomedial nucleus (DMN)

LHA/PFA = lateral hypothalamus / perifornical area

Paraventricular nucleus (PVN)

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22
Q

What is the central role of ARC?***

A

Nutrient homeostasis = integrate signals

Required for optimal functioning of organism

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23
Q

Define First-Order Neurones

A

Sensory neurons that detect the stimulus = afferent, PNS

Sensory neurons that pass through a spinal nerve have their cell bodies in the dorsal root ganglion

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24
Q

Define Second-Order Neurones

A

Interneurons = that relay sensory information from the spinal cord/brainstem to the thalamus and cerebellum

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25
Q

Glutamate (agonist, area effected, effect, half-life)

A

NMDA
LHA
Stimulates feeding
Lasts less than 10mins = short lasting action

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26
Q

GABA (agonist, area effected, effect, half-life)

A

Muscimol (GABA_A receptor agonist)

VMN, DMN, or PVN
Stimulates feeding
Lasts about 30mins

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27
Q

Opioids (agonist, area effected, effect, half-life)

A

B-endorphin, dynophin, long-acting enkelphalin

ARC, VMN, DMN, or PVN
Stimulates feeding
Effects short-lived and modest

28
Q

Monoamines (agonist, area effected, effect, half-life)

A

Noradrenaline, dopamine, serotonin
SUPRESS food intake

29
Q

What system are many anti-obesity drugs developed to act on?

A

Monoamin system

30
Q

Why are most anti-obesity drugs withdrawn?

A

Side effects

31
Q

Name the neurotransmitters that stimulate feeding and the one that supresses it

A

Glutamate, GABA, Opioids = stimulate

Monoamins = supress

32
Q

What is the name for something that increases appetite or food intake and its opposite word

A

(AN) OREXIGENIC

33
Q

Name the orexigenic neuropeptides

A

NPY, MCH, Agouti
Galanin, Orexins, Ghrelin, Endocannabinoids

34
Q

Name the anorexigenic neuropeptides

A

α-MSH, CART, GLP-1, TRH, CRH, PYY

Leptin & Insulin (both hormones not neuropeptides)

35
Q

What 3 things does neuropeptide Y do?

A

When injected into hypothalamus = stimulates food intake, reduces energy expenditure and induces lipogenic enzymes in fat and liver cells

36
Q

Where are neuropeptide Y-containing neurones mainly found?

A

ARC and DMN

37
Q

What happens with repeated administraiton of NPY to hypothalamus?

A

Leads to obesity = because stimulates food intake, reduces energy expenditure and incduces lipogenic enzymes

38
Q

When is NPY gene expression increased?

A

After fasting or reduce feeding

39
Q

What are NB mice? And what happens when they lack NPY receptor subtypes?***

A

Y1 or Y5 are pre-disposed to mild obesity because of functional redundancy and developmental copmensation

40
Q

What does α-MSH stand for?

A

α-melanocyte stimulating hormone

41
Q

What is α-MSH?

A

Non-opioid peptide

42
Q

What does POMC gene encode?

A

α-melanocyte stimulating hormone

43
Q

What is the role of α-MSH?

A

Acts in the ARC of hypothalamus = INHIBITS food intake

44
Q

When is POMC gene expression reduced and increased?

A

Decreased after fasting

Increased after increase in energy balance

Because codes for α-MSH, which inhibits food intake

45
Q

What melanocortin receptor subtypes are expressed in the brain?

A

MC-3 & MC-4

46
Q

What happens if either MC-3 or MC-4 receptors are deleted?

A

Obesity in mice becuase no inhibition of food intake signal

47
Q

Location of NPY and POMC neurones

A
48
Q

What is the Agouti-releated protien?

A

Neuropeptide that increases appetite = produced in the hypothalamus

49
Q

What is the mechanism of action of Agouti-related protein?

A

Expression of AgRP localized to ARC

Acts as antagoinst to MC3 & MC4 receptors = causes increased food intake

50
Q

Is AgRP effect long or short lasting compared to NPY?

A

Long lasting

51
Q

What is AgRP co-expressed with?

A

NPY in ACR neurones

52
Q

What does CART stand for?

A

Cocaine and amphetamine regulated transcript

53
Q

What affect do cocaine and amphetamine have on CART mRNA?

A

Increase CART mRNA

Anorexigenic = inhibit food intake

54
Q

What is CART co-expressed with?

A

α-MSH in ARC POMC neurones

55
Q

What happens when there is low activity of CART in depression?

A

Hypothalamic hypoactivity = assciated with hyperphagia and weight gain

56
Q

What is hyperphagia?

A

Abnormally great desire for food; excessive eating

57
Q

Where are Second-Order Neurones found in hypothalamus?

A

PVN = paraventricular nucleus

LHA/PFA

58
Q

What do the two Second-Order Neurones do?

A

PVN = inhibits food intake

LHA/PFA = increases food intake

59
Q

What does PVN also regulate?

A

Pituitary hormone secretion

60
Q

Give two examples of hormones from hypothalamus (PVN)

A

TRH stimulate secretion of TSH & prolactin

Corticotropin-RH stimualtes adrenocorticotropin hormone (ACTH) secretion

61
Q

What does adrenocorticotropin hormone (ACTH) do?

A

Stimulates adrenal gland to produce cortisol

Cuases negative energy balance = reduced food intake, increased sympathetic outflow, increased energy expenditure

62
Q

Name two neurosecretory cells and what they release

A

Magnocellular neurones = release oxytocin and vasopressin

Parvocellulular = release CRH and TRH

63
Q

Where do magnocellular neurones release from?***

A

Magnocellular neurons primarily release oxytocin and vasopressin directly into the bloodstream via the posterior pituitary gland

64
Q

Where do parvocellular neurones release from?

A

Parvocellular neurons release hormones like CRH and TRH into the hypophyseal portal system, which then carries them to the anterior pituitary gland to stimulate further hormone production

65
Q

Name two majorpeptidergic neurones in LHA (important in energy homeostasis)

A

MCH neurone = releases melanin-concentrating hormone (MCH)

Orexin neurone = releases orexins-A/B

Both causes increased food intake

Nutrients & Metabolic Disease (13 decks)

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