19 | Appetite Flashcards
(20 cards)
satiety
feeling of fullness
- peptides
- gastric distention
satiety peptides
appetite-inhibitory peptides (released from GI)
-CCK (cholecystokinin)
-GLP-1 (glucagon like peptide, also incretin - improves glucose tolerance during a meal)
decrease appetite by delaying rate of gastric emptying, slowing return of hunger
major short-term endocrine regulators of appetite
satiety signals (3)
- vagal pathways
- short acting
- define meal size and frequency
ghrelin (4)
only gut peptide that increases appetite
- binds to appetite stimulator neurons in hypothalamus
- increases food intake and body weight
- decreases fat breakdown (dec. energy use)
- level inc before meal (hunger), fall after a meal (fed)
insulin (3)
-responds to levels of nutrients, affects their metabolism/energy use
-crosses BBB, binds to hypothalamus neurons that suppress appetite
(dec meal size and freq is a way for insulin to dec BG)
-adiposity hormones, levels parallel amount of adipose
adipose tissue
metabolic endocrine “organ”
- brown fat: rich in mitochondria, thermogenesis
- white fat: energy storage, breakdown releases FFA’s and glycerol. endocrine center. receptors for response to metabolic and endocrine signals. secretes hormones and cytokines. metabolism of steroid hormones.
leptin
- secreted by adipose tissue
- binds to hypothalamus neurons, inhibits appetite
- many obese people are leptin (+ insulin) resistant, rather than deficient
- adiposity signal, levels correlate with adipose
- rapid drop during fasting, can influence other hormonal axes (loss of menstrual periods with strenuous exercise or malnutrition)
longer term appetite regulators
leptin + insulin: inhibit appeptite
ghrelin: opposes action of leptin
- peripheral effectors
exercise + energy homeostasis
-promotes negative energy balance (energy use > food intake, weight loss)
-improvees insulin sensitivity and glucose uptake in skeletal muscle, overcome insulin resistance
acute exercise:
-promotes post prandial levels of satiety peptides
-ghrelin levels may decrease
-leptin levels fall long term
orexigenic circuit
appetite stimulating
- food intake, energy conservation signals
- activated by ghrelin
- inhibited by leptin
anorexigenic circuit
appetite inhibiting
-activated by leptin
hypothalamus
ARC region: anorexigenic and orexigenic nuerons
-receptors for ghrelin + leptin
-activation releases neuropeptides
-activate second order neurons associated with weight loss or gain pathways
-net signals to higher cortical centers and limbic system
(circuits active at same time, varying levels to fine tune appetite and energy use. prolonged imbalance - net weight gain or loss)
hungry state
- inc ghrelin activates orexigenic receptors
- secrete neuropeptide Y (NPY) and agouti-related peptide (AgRP)
- activate second order neurons with NPY-R
- initiates feeding behaviors, metabolic processes
fed state
- leptin activates anorexigenic receptors (and inhibit orexigenic)
- neurons release CART (cocaine + amphetamine related transcript) and POMC (pro-opiomelanocortin) peptides
- POMC cleaved to a-MSH, binds to melanocortin-rec on second order neurons
- inhibit feeding behavior, promote energy use
- path can be overriden by AgRp
melanocortin receptor + obesity
-receptor defects
-chronic inhibition by AgRp
can cause obesity, interruption of anorexigenic signals
visual cues
- tend to eat more with larger package, utensils, food portions
- cue of how much eaten can signal to stop eating
energy density
- amount of energy/g of food (kcal/g)
- modulates overall energy intake
- low energy dense meal with comparable levels of fullness can decrease intake
sensory perception
food taste, smell, appearance
-can influence palatability, and amount eaten
Pima Indian study + thrifty gene hypothesis
Pima Indians - genetically predisposed to obesity + T2DM
- two genetically identical populations, one in S. Arizona, other in remote Mexico
- US group had more sedentary lifestyle, easier access to high cal, processed foods
- Mexican group had higher activity levels, consume lower-fat, traditional foods
- in Mexican group, obesity was uncommon and prevalence of T2DM was comparable to US population (8% overall)
- but in US group almost half had T2DM, and 95% of them were obese
support thrifty gene hypothesis:
ability to accumulate and retain stores of fat is adaptational in time of famine
-shows primary influence of environmental factors on genetic predisposition to obesity and T2DM
metabolic syndrome
conditions that increase risk of coronary artery disease
-obesity
-hypertension
-T2DM
-cholesterol abnormalities
[high insulin levels, with inc fasting glucose or glucose intolerance and central obesity, abnormal cholesterol, or high BP]