exam 3: Eating Behaviors

Lateral Hypothalamus role in regulating eating behavior (remember lateral and ventromedial regions of hypothal have different effects on eating behavior)

-hunger center -*MCH* is found here, which stimulates appetite and reduces metabolic rate -secretes *orexin*, stimulating appetite/reducing metabolic rate -stimulated by *ghrelin* secretion (*after arcuate nucleus is stimulated first)

arcuate nucleus role in regulating eating behavior

-involved in stimulating hunger -*NPY* located here, stimulates feeding and insulin, decreases breakdown of triglycerides and body temp -contains *CART* (coke/amphet) and a-*MSH* (melanocyte), which inhibit lateral hypothal, thus inhibiting appetite

Behavioral causes of obesity

-modern people have increased access to cheap, high fat, low nutrient foods -socioeconomic status can be mediating variable (less money -> more likely to be obese) -changes in energy expenditure (sedentary jobs, less exercise)

Genetic factors of obesity

-obesity is 40-70% hereditary -OB mouse ex: genetic mutation makes them deficient in *leptin*, which causes hypothalamic regions to never get satiety signals, and the mouse overeats

ventromedial hypothalamus role in regulating eating behavior (remember lateral and ventromedial regions of hypothal have different effects on eating behavior)

-satiety center -lesions here produce overeating, leading to *obesity*

paraventricular nucleus (of hypothal) role in regulating eating behavior

-secretes AGRP, an antagonist to MC4 receptors, thus increasing eating -excites lateral hypothal (involved in stimulating hunger)

Endocannabinoids

can facilitate the release of MCH and Orexin to encourage eating behavior

system variable

characteristic that is regulated in homeostasis

glucoprivation

deprivation of glucose in the blood, leads to signals that encourage eating by stimulating glucose-sensitive neurons in the medulla, which then stimulate NPY/AGRP release

lipoprivation

deprivation of lipids/fats in the bloodstream, signals that encourage eating

obesity as a food addiction

difficult to treat with frequent relapse, and there are more mechanisms to intake food than lose weight because energy intake is prioritized

adipose tissue

fat tissue, functions as a communication mechanism in long-term body weight regulation by secreting different amounts of leptin to activate hypothalamic systems to regulate and reduce eating behavior

risk factors for anorexia

genetics, social pressures and focus on thinness, anxiety, OCD and perfectionism, and disruptions in interoceptive awareness

Pancreatic satiety signals

insulin secretion, activating receptors in the hypothalamus to encourage the absorptive phase of metabolism

AGRP

located in arcuate nucleus, stimulates MCH and Orexin to stimulate eating behavior and decrease metabolism. Inhibited by leptin.

Melanin Concentrating Hormone (MCH)

located in lateral hypothalamus, leads to excitatory effects on eating and reduction of metabolism

Orexin

located in lateral hypothalamus, leads to excitatory effects on eating behavior and reduction of metabolism. Also involved in stimulating other arousal centers.

neuronal changes in anorexia

lower dopamine in striatum, increases in dopamine during weight restriction. Also show serotonin dysregulation, which results in dysphoria and elevated mood during eating restriction

Satiety disturbances in anorexia

lower leptin levels as a result of less adipose tissue, delayed gastric emptying

physiological regulatory mechanism

maintains the constancy of some internal characteristic of the organism in the face of external variability

detector

monitors value of the variable in homeostasis

set point

optimal value of a system variable in homeostasis

Neuropeptide Y (NPY)

peptide localized in the arcuate nucelus, released on the lateral hypothalamus to excite MCH and Orexin to stimulate eating behavior and decrease metabolism

Ghrelin

peptide that is secreted when the stomach empties and stimulates the arcuate nucleus, leading to excitatory effects on eating behavior. Decreases in this signal lead to satiety signals.

CART and a-MSH

peptides activated by leptin, located in the arcuate nucleus, inhibit MCH and Orexin to suppress eating and increase metabolic rate

homeostasis

process by which the body's substances and characteristics are maintained at their optimal level using physiological regulatory mechanisms

Cholecystokinin (CCK)

released by duodenem, sends satiety signals to the brain via the vagus nerve

Peptide YY (PYY)

released in proportion to amount of calories consumed, release from intestines sends inhibitory signal to NPY and AGRP, thus decreasing eating behavior and increasing metabolic rate. produced in gastrointestinal system

hunger disturbances in anorexia

report lower hunger but have increased ghrelin and NPY, so some disconnect between physiological signals and interpretation. Also show abnormal brain activation *during food presentation, less activity in amygdala, insula, and orbitofrontal cortex*

correctional mechanism

restores the system variable to set point in homeostasis

Liver satiety signals

sends signals to the brain after receiving nutrients from the intestines

environmental cues for initiating eating behavior

smells, sights of food can trigger desires to eat. Time signals and cultural practice can also dictate eating times