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Physiology 3 Endocrine > Appetite Regulation > Flashcards

Appetite Regulation Flashcards

1
Q

what are examples of energy intake?

A

eating

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2
Q

what are examples of energy expenditure?

A

physical activity
metabolism
thermogenesis (internal heat production)

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3
Q

what happens when intake > expenditure?

A

TG storage

weight gain

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4
Q

what happens when intake < expenditure?

A

TG breakdown

weight loss

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5
Q

weight refers to the amount of _____ and NOT ____

A

amount of fat tissue - adiposity

NOT the total body weight

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6
Q

why is weight gain strongly “defended” biologically?

A

our bodies have evolved to conserve energy/weight but once we gain weight, we stay fat

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7
Q

what are 2 examples of energy imbalance leading to serious diseases?

A

obesity

type 2 diabetes mellitus (T2DM)

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8
Q

energy balance is regulated by multiple pathways, both _____ and _____

A

afferent and efferent

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9
Q

what are some examples of things that convey information about meal status (fed/hungry states)?

A

nutrient sensing (glucose, lipids)
CNS/PNS
hormones

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10
Q

what is the job of the hypothalamus?

A

point of convergence for appetite pathways and major locus for their integration

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11
Q

major peripheral systems in appetite regulation include ______. give some examples

A

organs/systems involved in absorption and storage of nutrients

olfactory, gustatory, GI, pancreas, liver, muscle, adipose tissue, bone

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12
Q

peripheral signals relay to ___ and ____ to influence behavioral and physiological responses

A

higher cortical centers and limbic system

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13
Q

T/F: hypothalamus and brainstem are ONLY stimulated by peripheral hormones and neural signals from endocrine tissues

A

FALSE - both stimulated and inhibited

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14
Q

what does the stomach have/do to send out a “fullness” signal?

A

stomach contains stretch receptors (gastric distension)

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15
Q

what are the 2 things responsible for satiation?

A
  1. release of satiety peptides from GI tract

2. gastric distension

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16
Q

what are 2 satiety gut peptides?
where are they secreted from?
what do they do?

A

cholecystokinin (CCK)
glucagon-like peptide 1 (GLP1)

secreted from stomach and intestines

act as hormones/neuropeptides that generate signals via vagal pathways

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17
Q

signals mediated by satiety peptides are typically ____ and _____

A

short acting

define meal size and frequency

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18
Q

how do most satiety peptides decrease appetite?

A

by delaying the rate of gastric emptying

slowing the return of hunger

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19
Q

what is bariatric surgery?

A

gastric bypass surgery - restricts/reroutes the GI tract

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20
Q

in addition to its appetite suppression effects, GLP1 is also an ____

A

incretin - peptide hormone that stimulates insulin secretion (improving glucose tolerance during a meal)

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21
Q

what are gliptins?

A

a new family of drugs used to treat T2DM by increasing GLP1 activity

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22
Q

ghrelin is NOT a ____ but it is unique as the only gut peptide to ______.

A

satiety peptide

increases appetite

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23
Q

how is ghrelin an appetite stimulator? (nervous system)

what does it increase/decrease in the body?

A

binds to appetite stimulatory neurons in hypothalamus

increases food intake and body weight
decreases fat breakdown (decrease energy expenditure)

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24
Q

what are the levels of ghrelin before and after a meal?

A

high ghrelin before a meal (hunger state)

low ghrelin immediately after a meal (fed state)

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25
Q

what are the results of vaccines against ghrelin?

A

reduced food intake (in rodents)

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26
Q

what kind of peptide is ghrelin?

A

gut

NOT SATIETY

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27
Q

what kind of peptide hormone is insulin?

A

pancreatic peptide hormone

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28
Q

what are the 3 things insulin does to control appetite?

A
  1. insulin responds to minute-minute basis based on nutrient levels –> changes nutrient metabolism and thus, energy expenditure
  2. insulin crosses BBB and binds to appetite suppressing receptors on hypothalamus
  3. insulin is also an adiposity hormone –> basal hormone levels parallel amount of adipose tissue in body
    ex. high fat levels (obesity) = high basal levels of insulin
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29
Q

T/F: reducing meal size and frequency is another way for insulin to reduce glucose in the bloodstream

A

TRUE

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30
Q

what is obesity commonly associated with?

what is that then closely associated with?

A

obesity –> hyperinsulinemia –> insulin resistance, obesity, T2DM

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31
Q

T/F: adipose tissue is a complex and highly metabolic endocrine “organ”

A

TRUE

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32
Q

what are the two forms of adipose tissue and their function?

A

BAT (brown) - lots of mitochondria, thermogenesis
WAT (white) - energy storehouse, breakdown of stored fat releases fatty acids and glycerol, endocrine center, secretes hormones and cytokines

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33
Q

T/F: adipose tissue is involved in the metabolism of steroid hormones

A

TRUE

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34
Q

Leptin, from the greek word meaning ___, is secreted by _____.

A

thin

adipose tissue

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35
Q

leptin binds to receptors on hypothalamus and causes what?

A

appetite inhibition

36
Q

T/F: leptin can serve as an anti-obesity drug

A

FALSE - obesity is closely associated with leptin resistance in obese patients

37
Q

T/F: leptin cannot be used as an anti-obesity drug because obese patients have leptin resistance

A

TRUE

38
Q

what are the two gene mutations for leptin?

what were the experimental findings?

A

leptin deficiency - obese mice became normal weight and had reduced appetite when injected with exogenous leptin, works with humans with leptin deficiency

leptin receptor deficiency - no change in obesity with treatment with exogenous leptin due to leptin resistance in obese patients/mice, most common in human obesity

39
Q

like insulin, leptin is also a ______, and its concentrations correlate with body fat levels. most obesity is associated with high levels of ___ and ____. during fasting, leptin levels are ____, much more quickly than would be expected from weight loss.

A

adiposity signal
insulin and leptin
reduced

40
Q

what happens when leptin levels are too low? (reduced fat stores because leptin is adiposity signal)

A

hypothalamic amenorrhea - loss of menstrual period due to too much exercise or malnutrition, can occur if leptin is too low –> maybe to prevent pregnancy during illness or famine

41
Q

what are the short and long term effects of appetite regulation?

A

short term - satiety peptides (CCK, GLP1)

long term - leptin, insulin, ghrelin

42
Q

____ and _____ act synergistically to inhibit appetite whereas ghrelin opposes the action of _____

A

insulin and leptin

leptin

43
Q

physical exercise promotes a _____ energy balance which means…..

A

negative energy balance - expenditure > intake, weight loss

44
Q

what does acute exercise do to levels of satiety peptides and ghrelin?

A

increase satiety peptide post-prandial levels

ghrelin levels stay the same or decrease

45
Q

what happens to leptin levels with long term exercise?

A

leptin levels decrease

think about it like this: leptin decreases because it is an adiposity signal, so fat stores decreased due to exercise

46
Q

exercise improves ___ sensitivity and ___ uptake into skeletal muscle, which helps to overcome ____ resistance. exercise is therefore prescribed in the treatments of ____ and _____, for appetite control, weight reduction, and decreased _____ resistance.

A

insulin sensitivity
glucose uptake
insulin resistance

obesity and T2DM
insulin resistance

47
Q

what are the roles of the two main neuronal circuits of the hypothalamus?

A

drives food intake and determining whether fat is stored or used for fuel

48
Q

what are the two neuronal circuits of the hypothalamus?

where in the hypothalamus do these circuits signal?

A
  1. orexigenic - appetite stimulating
  2. anorexigenic - appetite inhibiting

in the ARC region of the hypothalamus

49
Q

ghrelin, leptin, insulin act via _____ whereas satiety peptides act via ____

A

ARC

vagal pathway

50
Q

appetite regulatory hormones bind to their receptors which releases ____, which then target _______ neurons associated with weight loss/gain pathways

A

neuropeptides

secondary

51
Q

what is composed of the brain’s reward center?

A

higher cortical center and limbic system

52
Q

T/F: both hypothalamic neuronal circuits are active at the same time but vary in levels to fine tune appetite and energy usage

A

TRUE

53
Q

T/F: only the anorxigenic hypothalamic neuronal circuit is active all the time to inhibit appetite (prevents over-eating)

A

FALSE - both neuronal circuits (orexigenic, anorxigenic) are active at the same time

54
Q

Insulin and PYY are (orexigenic/anorexigenic)

A

anorexigenic

both are appetite INHIBITING

55
Q

in the hungry state, ghrelin levels are (elevated/reduced) and activate receptors on (anorexigenic/orexigenic) ARC neurons, signaling the need for (increased/decreased) food intake and energy conservation. the ghrelin receptors then activate 2 more neuropeptides _____ and _____. these neuropeptides bind to secondary neurons expressing ____ receptor. Activation of this receptors increases food ____ and reduces energy _____.

A 
elevated
orexigenic 
increased
neuropeptide Y (NPY) and agouti-related peptide (AgRP)
NCY receptor
food intake
energy expenditure
56
Q

leptin (activates/inhibits) orexigenic ARC neurons so they do not release neuropeptides ____ and ____.

A

inhibits (leptin is appetite-inhibiting)

NPY and AgRP

57
Q

in the fed state, appetite inhibitory neurons like leptin and insulin (activate/inhibit) (orexigenic/anorexigenic) circuits in the hypothalamus. the same hormones that inhibit ARC orexigenic neurons also (stimulate/inhibit) anorexigenic neurons. These neurons release 2 neuropeptides ____ and ____.

A

inhibit
orexigenic
stimulate
cocaine and amphetamine-related transcript (CART) and pro-opiomelanocortin (POMC)

58
Q

POMC is proteolytically process in the _____ and produces hormone ______, which binds to melanocortin receptors on secondary neurons. This activates downstream pathways that (activate/inhibit) food intake and promotes energy _____. This pathway can be overriden by ____, a component of the orexigenic system. it inhibits _____ receptors on secondary neurons.

A 
hypothalamus
alpha-melanocyte-stimulating hormone
inhibit
expenditure
AgRP
melanocortin receptors
59
Q

Melanocortin receptor defects or chronic inhibition of these receptors by AgRP are both causes of _____

A

obestiy

60
Q

prolonged imbalance of energy intake/expenditure causes net weight ____ and ____

A

weight gain or loss

61
Q

what are the 3 environmental factors influencing appetite?

A
  1. visual cues
  2. energy density
  3. sensory perception
62
Q

T/F: environmental factors only affect sub-conscious cognitive functioning related to food intake

A

FALSE - both conscious and sub-conscious

63
Q 
how does visual cues affect food intake:
what makes people eat more?
does education help?
what helps determine when people stop eating? 
how do children tend to overeat?
A

visual cues like portion size, packaging

education does not mediate a visual cue effect –> nutrition experts overeat too when given a larger bowl

visual cue of how much food has been eaten

if they are taught to ignore signs of fullness

64
Q

what is energy density?

A

amount of energy per gram of food (calorie)

65
Q

regarding energy density, adults claim what after meals of differing energy density?

how can low-energy dense first course help to decrease energy intake while making the person feel full?
hint: ex. (eating vegetable soup before a meal)

A

adults claim equal fullness after meals of varying energy density

lowers energy intake at a meal while providing comparable levels of fullness as a high-energy meal
(eating vegetable soup before a meal)

66
Q

how can sensory perception affect food intake:
what makes people eat more?
how does palatability or amount of food eaten affect satiation after a meal?

A

food that has good taste, smell, appearance, texture

it is not sure

67
Q

what were the results of the Pima Indians experiment? what did it prove?

A

2 genetically identical native groups in different locations, US and Mexico

US pima group had higher access to fatty foods and had more of a sedentary lifestyle –> 50% T2DM and 90% obesity

Mexican pima group were more active and ate healthier –> lower obesity/T2DM statistics

68
Q

What is the thrifty gene hypothesis?

A

idea that the ability to accumulate and retain fat stores is adaptational in times of famine

basically –> weight is both environmental and genetic

69
Q

T/F: certain ethnic groups are at increased risk for insulin resistance and T2DM

A

TRUE - minority groups like black, latinos, asians, native americans

70
Q

What are some risk factors for T2DM?

A 
family history
obesity
lack of activity
impaired glucose tolerance 
giving birth to baby > 9 pounds 
> 45 years old
metabolic syndrome
71
Q

What is metabolic syndrome?

A

cluster of conditions (like diabesity, hypertension, cholesterol abnormalities) that increase risk of coronary artery disease

72
Q

T/F: metabolic syndrome shows a low correlation with obesity

A

FALSE - high correlation

increase risk of coronary heart disease with increased obesity levels

73
Q

what are hormonal vs neural examples of appetite inhibition?

A

hormonal - satiety peptides

neural - gastric distension (full –> no more eating)

74
Q

what are hormonal vs neural examples of appetite stimulation?

A

hormonal - ghrelin

neural - gastric emptying

75
Q

what are some pancreatic endocrine peptides?

A

insulin
glucagon
pancreatic polypeptide
amylin

76
Q

define resistance to a hormone

A

lack of response to hormone (usually hormone levels are high)

77
Q

What is the most abundant neuropeptide in the brain?

A

NPY

78
Q

T/F: NPY decreases with prolonged stress

A

FALSE - increases

79
Q

What is one of the most potent and long-lasting appetite stimulators?

A

AgRP

80
Q

What does ARC stand for?

A

arcuate region of the brain

81
Q

What does AgRP inhibit?

A

Melanocortin receptors (MCR)

82
Q

T/F: CART is only distributed in the hypothalamus in the brain

A

FALSE - distributed everywhere in the brain but concentrated in the hypothalamus

83
Q

What neurons secrete POMC?

A

ARC neurons

84
Q

what gene deficiency causes obesity?

is it dominant or recessive?

A

MC4R deficiency = obesity

dominant

85
Q

What are some things associated with metabolic syndrome? (FYI: to be considered MS, needs 3 or more of these things)

A 
high insulin, glucose intolerance, fasting glucose
high TG or low HDL
obesity
cholesterol abnormalities
BP > 140/90 without treatment
86
Q

NPY and AgRP are appetite….

A

stimulating

87
Q

CART and POMC are appetite…

A

inhibiting

Physiology 3 Endocrine (9 decks)

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