Appetite Regulation Flashcards by Jochebed Kim

what are examples of energy intake?

eating

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what are examples of energy expenditure?

physical activity
metabolism
thermogenesis (internal heat production)

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what happens when intake > expenditure?

TG storage

weight gain

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what happens when intake < expenditure?

TG breakdown

weight loss

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weight refers to the amount of _____ and NOT ____

amount of fat tissue - adiposity

NOT the total body weight

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why is weight gain strongly “defended” biologically?

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

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

obesity

type 2 diabetes mellitus (T2DM)

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

afferent and efferent

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

nutrient sensing (glucose, lipids)
CNS/PNS
hormones

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what is the job of the hypothalamus?

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

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

organs/systems involved in absorption and storage of nutrients

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

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

higher cortical centers and limbic system

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

FALSE - both stimulated and inhibited

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

stomach contains stretch receptors (gastric distension)

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what are the 2 things responsible for satiation?

release of satiety peptides from GI tract

2. gastric distension

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

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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signals mediated by satiety peptides are typically ____ and _____

short acting

define meal size and frequency

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how do most satiety peptides decrease appetite?

by delaying the rate of gastric emptying

slowing the return of hunger

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what is bariatric surgery?

gastric bypass surgery - restricts/reroutes the GI tract

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

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

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what are gliptins?

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

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

satiety peptide

increases appetite

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how is ghrelin an appetite stimulator? (nervous system)

what does it increase/decrease in the body?

binds to appetite stimulatory neurons in hypothalamus

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

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

high ghrelin before a meal (hunger state)

low ghrelin immediately after a meal (fed state)

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what are the results of vaccines against ghrelin?

reduced food intake (in rodents)

what kind of peptide is ghrelin?

gut NOT SATIETY

what kind of peptide hormone is insulin?

pancreatic peptide hormone

what are the 3 things insulin does to control appetite?

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

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

TRUE

what is obesity commonly associated with? | what is that then closely associated with?

obesity --> hyperinsulinemia --> insulin resistance, obesity, T2DM

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

TRUE

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

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

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

TRUE

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

thin adipose tissue

leptin binds to receptors on hypothalamus and causes what?

appetite inhibition

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

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

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

TRUE

what are the two gene mutations for leptin? | what were the experimental findings?

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

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.

adiposity signal insulin and leptin reduced

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

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

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

short term - satiety peptides (CCK, GLP1) | long term - leptin, insulin, ghrelin

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

insulin and leptin leptin

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

negative energy balance - expenditure > intake, weight loss

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

increase satiety peptide post-prandial levels | ghrelin levels stay the same or decrease

what happens to leptin levels with long term exercise?

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

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.

insulin sensitivity glucose uptake insulin resistance obesity and T2DM insulin resistance

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

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

what are the two neuronal circuits of the hypothalamus? | where in the hypothalamus do these circuits signal?

1. orexigenic - appetite stimulating 2. anorexigenic - appetite inhibiting in the ARC region of the hypothalamus

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

ARC | vagal pathway

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

neuropeptides | secondary

what is composed of the brain's reward center?

higher cortical center and limbic system

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

TRUE

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

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

Insulin and PYY are (orexigenic/anorexigenic)

anorexigenic both are appetite INHIBITING

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 _____.

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

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

inhibits (leptin is appetite-inhibiting) | NPY and AgRP

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 ____.

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

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.

``` hypothalamus alpha-melanocyte-stimulating hormone inhibit expenditure AgRP melanocortin receptors ```

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

obestiy

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

weight gain or loss

what are the 3 environmental factors influencing appetite?

1. visual cues 2. energy density 3. sensory perception

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

FALSE - both conscious and sub-conscious

``` 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? ```

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

what is energy density?

amount of energy per gram of food (calorie)

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)

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)

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?

food that has good taste, smell, appearance, texture it is not sure

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

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

What is the thrifty gene hypothesis?

idea that the ability to accumulate and retain fat stores is adaptational in times of famine basically --> weight is both environmental and genetic

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

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

What are some risk factors for T2DM?

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

What is metabolic syndrome?

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

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

FALSE - high correlation increase risk of coronary heart disease with increased obesity levels

what are hormonal vs neural examples of appetite inhibition?

hormonal - satiety peptides neural - gastric distension (full --> no more eating)

what are hormonal vs neural examples of appetite stimulation?

hormonal - ghrelin neural - gastric emptying

what are some pancreatic endocrine peptides?

insulin glucagon pancreatic polypeptide amylin

define resistance to a hormone

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

What is the most abundant neuropeptide in the brain?

NPY

T/F: NPY decreases with prolonged stress

FALSE - increases

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

AgRP

What does ARC stand for?

arcuate region of the brain

What does AgRP inhibit?

Melanocortin receptors (MCR)

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

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

What neurons secrete POMC?

ARC neurons

what gene deficiency causes obesity? | is it dominant or recessive?

MC4R deficiency = obesity | dominant

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

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

NPY and AgRP are appetite....

stimulating

CART and POMC are appetite...

inhibiting

Appetite Regulation Flashcards

(87 cards)