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Endocrinology & Reproduction > Food intake > Flashcards

Food intake Flashcards

1
Q

why are we becoming obese

A

failure to maintain balance between energy intake and energy expenditure

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2
Q

development of an obesogenic environment

A
  • rapid environmental change
  • rapid behavioural change
  • slow evoluationary adaptation to obesogenic environment
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3
Q

treatments for obesity

A

surgical (gastric sleeve, bypass and band)

pharmacological (orlistat)

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4
Q

how is appetite regulated

A

peripheral signals

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5
Q

what internal signals act on the hypothalamus to regualte appetite

A
  • hormonal
  • metabolic
  • neural
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6
Q

what hormonal signals act on hypothalamus to regualte appetite

A

leptin, insulin & GI

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7
Q

what neural signals act on hypothalamus to regualte appetite

A

gastric distention

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8
Q

what metabolic signals act on hypothalamus to regualte appetite

A

glucose, lipid and AA metabolism

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9
Q

what do metabolic, hormonal and neural signals act on to regulate appetite

A

hypothalamus

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10
Q

how does the environemtn affect appetite?

A

palatabilty of food & adverse food behaviours act on the cortical which signal to hypothalamus

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11
Q

hungery & satiety are regualted by the

A

hypothalamus

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12
Q

where does the hypothalamus recieve information from on energy status

A

the adipose tissue, becuse it is the major energy depot.

signals travel to the brain via blood stream as endocrine signal

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13
Q

how does energy status reach the brain

A

signal travesl from adipose tissue to the brain, as an endocrine signal - via the blood

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14
Q

what does the ob gene encode

A

leptin

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15
Q

what gene encodes leptin

A

ob

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16
Q

ob/ob mouse

A

produces inactive leptin and so continuous feeding occurs leading to obesity, hyperphagia, hyperglycaemia etc

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17
Q

what does the db gene encode

A

leptin receptor

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18
Q

what gene encodes leptin receptor

A

db

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19
Q

db/db mouse

A

produces defective leptin receptor so the hypothalamus does not get signal to reduce feeding = obesity

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20
Q

liposatic/adipostatic theory

A

total body weight maintained by regualting fat contetn.

hypothalamus senses [circulating factor] which provides info on size of fat stores

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21
Q

what is circulating factor

A

leptin

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22
Q

do ob/ob mice have circulating factor?

A

no

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23
Q

do db/db mice have circlating factor?

A

yes, but they don’t have the receptor for it and so are unresponsive to it

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24
Q

set point hypothesis

A

blood borne factor controls b.weight at a defined set point by interaction with the hypothalamus. depletion f energy stores increases food intake to maintan energy homeostasis

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25
Q

is leptin a long or short term signal

A

long term

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26
Q

what type of hormone is leptin

A

polypeptide hormone

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27
Q

where is leptin mainly expressed

A

adipose tissue

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28
Q

circulating levels of leptin are proprtional to

A

total fat mass

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29
Q

when do levels of leptin decrease

A

after feeding

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30
Q

how do leptin levels change

A

in humans; they will increase after several days with over feeding but rapidly decrease with food restriction

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31
Q

could leptin treat obesity?

A

probably not. Leptin is more responsive to food restriction than it is over-eating. Thought to be a survival trait for starvation

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32
Q

how does leptin causes weight loss

A
  • decreases food intake

- increases energy expenditure via sympathetic innervation

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33
Q

what are leptin levels like in the obese

A

higher than usual (not expected) hence can’t be used to treat obesity q

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34
Q

when can leptin be effective weight loss treatment?

A

extremely rare cases where people are leptin deficientbecuase of a defective Ob gene

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35
Q

potential way for leptin to be effective

A

increase the body’s sensitivity to leptin

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36
Q

what is the leptin receptor

A

member of the cytokine family

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37
Q

where are leptin receptors expressed

A

mostly in the hypothalamus, also in liver muscle, adipose & other tissues

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38
Q

summary of how leptin resistance develops in obesity

A
  • expansion of adipose tissue
  • increased leptin secretion
  • increased serum [leptin]
    -continuous stimulation of leptin receptors
  • down regualtion of leptin receptor signalling
    = leptin resistance
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39
Q

what does falling serum leptin levels signal

A

tells the brain body is starving

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40
Q

what does leptin deficiency drive

A

hunger & surpasses energy expenditure

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41
Q

how does leptin reduce appetite

A

leptin binds to leptin receptor in the hypothalmus to cause a neuronal signal to the regionof brain that reduces appetite

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42
Q

how does leptin increase energy expenditreu

A

leptin stimulates the hypothalamus which directs signals via the sympathetic neuron to increase thermogenesis in adipose

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43
Q

what does increased leptin cause

A

reduced appetite

increased energy expenditure

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44
Q

what dissipates heat in thermogenesis

A

UCP-1 uncoupling protein

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45
Q

how does UCP-1 work

A

in thermogenesis, UCP1 dissipates heat by causing heat loss as energy in the proton gradient without energy being stored in reactive moleucles such as ATP

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46
Q

leptin binding to leptin receptor causes increased release of

A

anorexigenic peptides

POMC and CART

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47
Q

leptin binding to leptin receptor causes downregulated release of

A

orexigenic peptides

NPY and AGRP

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48
Q

orexigenic peptides

A

NPY and AGRP

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49
Q

anorexigenic peptides

A

POMC and CART

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50
Q

POMC and CART are what kind of petides

A

anorexigenic

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51
Q

NPY and AGRP are what kind of peptides

A

orexigenic

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52
Q

when are POMC and CART increased

A

when leptin binds to leptin receptor

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53
Q

when are NPY and AGRP reduced

A

when leptin binds to leptin receptor

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54
Q

what do POMC and CART do

A

decrease food intake
incease EE via increased sympathetic tone
increase fat oxidation

55
Q

what do NPY and AGRP do

A

increase food intake
decrease EE via reduced sympathetic tone
decrease fat oxidation

56
Q

hypothalamic peptides that regulate food intake

A

POMC and CART (anorexigenic)

NPY and AGRP (orexigenic)

57
Q

POMC is not actually a

A

peptide

58
Q

ARC

A

arcuate nucleus

59
Q

PVN

A

paraventricular nuclues

60
Q

LHA

A

Lateral hypothalamic area

61
Q

gene that produces anoreixic peptide

A

POMC

62
Q

1st order signal example

A

leptin binding to receptor initiaites production of POMC from the ARC nucleus

63
Q

where is POMC produced

A

ARC nucleus

64
Q

what does POMC produce

A

alpha-MSH

65
Q

where does alpha MSH come from

A

POMC

66
Q

what does alpha MSH do

A

Alpha-MSH binds to MC4 receptor on the PVN to decrease appetite

67
Q

how does POMC decrease appetite

A

POMC prouces alpha MSH which binds to MC4 receptor on the PVN to decrease apptite

68
Q

how does alpha MSH reduced appetite

A

binds to MC4 receptor on the PVN to decrease apptite

69
Q

what is coexpressed with POMC in ARC neurons

A

CART

70
Q

where are POMC and CART coexpressed

A

ARC

71
Q

what is AGRP

A

orexigenic peptide that is similar to the agouti protein responsible for yellow hair pigment in mice

72
Q

what is AGRP coexpressed with

A

NPY

73
Q

where is AGRP expressed

A

ARC nucuels of the hypothalamus

74
Q

Where is NPY expressed

A

ARC nucuels of the hypothalamus

75
Q

What is NPY

A

powerful orexigenic peptide

76
Q

what is NPY co expressed with

A

AGRP

77
Q

how does NPY work

A

binds to Y1 receptors on the POMC neuron to prevent anorexigenic action
binds to LHA neurones to stimulate orexigenic action

78
Q

which peptide prevents anorexigenic action and stimulates orexigenic action

A

NPY

79
Q

where does NPY bind

A

Y1 receptor on POMC neuron and LHA neurons

80
Q

what are AGRP and NPY inhibited by

A

high leptin

81
Q

when are POMC and alpha MSH present

A

high leptin

82
Q

satiey signal

A

POMC and alpha MSH

83
Q

hunger signal

A

NPY and AGRP

84
Q

what does leptin mediate

A

an adipostat feedback loop from fat cells to the brain to suppress appetite and cause peripheral lipolysis and FA oxidation

85
Q

what does a mutated POMC gene cause

A

hyperphagia
obesity
red hair

86
Q

what does POMC knockout in mice cause

A

obesity

impaired pigment

87
Q

what are involved in 2nd order signalling

A

MCH and orexin = orexigenic
CRH and TRH - anorexigenic
melanocortin receptos

88
Q

how many melancortin receptors are there

A

4

89
Q

what are the functions of melanocrotin receptors

A

MC1 skin and hair
MC2 adrenal
MC3 hypothalamus
MC4 hypothalmus

90
Q

which melanocortin receptor controls food intake

A

MC4

91
Q

agonist of MC4

A

alpha MSH

92
Q

antagonosit of MC4

A

AGRP

93
Q

What determines how active MC4R is

A

balance of alpha MSH (stimulates) and AGRP (inhibits)

94
Q

how does leptin influence MC4

A

leptin stimulates POMC which produces alpha MSH which stimulates MC4R

95
Q

what does effect does active MC4R have on food intake

A

reduces food intake

96
Q

MC4R mutations

A

associated with morbid obesity

97
Q

most common monogenic cause of inherited morbid obesty

A

MC4R mutations

98
Q

% of morbidly obese children with mutation of one MC4R allele

A

4%

99
Q

phenotype of MC4R obesity

A
  • hyperphagia starts ~8mnths
  • tendency towards tall stature
  • hyperinsulinemia
100
Q

effect of agouti on alpha MSH

A

agouti blocks the action of apha MSH at:
MC1R inhair follicles resulting in yellow pigmentation
MC3R and MC4R in the hypothalamus, resulting in obesisty

101
Q

MCR are blocked by what

A

agouti like proteins

102
Q

MCR are essentil for the control of

A

body weight

103
Q

anorexigenic peptides in 2nd order signalling

A

CRH and TRH

104
Q

orexigenic peptides in 2nd order signalling

A

MCH and orexin

105
Q

what are CRH and TRH

A

anorexigenic peptides in 2nd order signalling

106
Q

what are MCH and orexin

A

orexigenic peptides in 2nd order signalling

107
Q

where is CRH secreted

A

PVN

108
Q

CRH

A

corticotropin-releasing hormone

109
Q

TRH

A

thyrotropin-releasing hormone

110
Q

where is TRH secreted

A

PVN

111
Q

What does CRH do

A

acts on the anterior pituiaty to realse ACTH which stimulates cortisol release from adrenal cortex which reduces appeptire

112
Q

what does ACTH stimulate

A

cortisol release from the adrenal cortex

113
Q

where is cortisol released

A

adrenal cortex

114
Q

effect of cortisol on appeitte

A

reduces appetite

115
Q

what is cortisol

A

stress hormone

116
Q

ACTH

A

adrenocorticotropic hormone

117
Q

where is ACTH released

A

anterior pituitary

118
Q

when is TRH down-regualted

A

fasting

119
Q

how is TRH release stimulated

A

leptin increases production of alpha MSH which stimulates TRH release

120
Q

what does TRH do

A

TRH acts on the anterior pituitary to release TSH which stimulates release of TH from the thyroid gland which stimulates metabolic rate

121
Q

what does TRH act on

A

anterior pituitary

122
Q

where is TSH release from

A

anterior pituitary

123
Q

what does anterior pituitary release in 2nd order signalling

A

ACTH and TSH

124
Q

What does TSH stimulate

A

release of TH from thyroid gland

125
Q

where is TH released

A

thyroid gland

126
Q

MCH

A

melanin concentrating hormone

127
Q

where is MCH over expressed

A

ob/ob mouse hypothalamus

128
Q

when is MCH increased

A

fasting in both obese and normal

129
Q

Where are orexins produced

A

exclusively inthe lateral hypothalamic area LHA

130
Q

What does the LHA exclusively produce

A

orexins A and B

131
Q

what can cause narcolepsy

A

Orexin deficiency

132
Q

orexin deficieny can cause

A

narcolepsy

133
Q

why does orexin deficieny cause narcolepsy

A

possible survival link between energy homeostaisi and wakefullness

Endocrinology & Reproduction (15 decks)

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