hunger chapter
Cholecystokinin (CCK) limits meal size in 2 ways
1. constricts the sphincter muscle between the stomach and the duodenum, causing the stomach to hold its contents and fill more quickly than usual 2. stimulates the vagus nerve to send signals to the hypothalamus, causing cells there to release a neurotransmitter that is a shorter version of the CCK molecule itself-- the body uses the same chemical in the periphery and in the brain for closely related functions
glucagon
A protein hormone secreted by pancreatic endocrine cells that raises blood glucose levels; an antagonistic hormone to insulin.
master area of controlling appetite
arcuate nucleus
why does rat overeat with damage to VMH?
because it's storing too much fat damage increases insulin production, and therefore, much of each meal is stored as fat
as time passes after a meal what happens?
blood glucose level drops-->insulinlevels drop --> glucose enters cells more slowly ---> hunger increases
what happens if insulin level remains constantly low?
blood glucose levels may be 3x normal levels but because little enters the cells, the cells are starving so the person will eat more --> excrete more glucose and lose weight ex: ppl with type 1 diabetes
lateral hypothalamus
controls insulin secretion, alters taste responsiveness, and facilitates feeding in other ways
Where does excess glucose go?
converted glycogen and stores it some enters the fat cells, converted to fat and stored
splanchnic nerve
convey info about the nutrient contents of the stomach
vagus nerve
conveys info about the stretching of the stomach walls to the brain
smoking ______ appetite
decreases
effect of lesion on lateral preoptic area
deficit in osmotic thirst due partly to damage to cells and partly to interruption of passing axons
effect of lesion on preoptic area
deficit in physiological mechanisms of temperature regulation
what is the main signal to end a meal?
distension of the stomach
rats with damage to PVN do what?
eat large meals
rats with damage to VMH do what?
eat normal sized meals but eat more frequently
insulin
enables glucose to enter cells, except brain cells which don't need insulin to enter
satiety-sensitive cells send an _____ message to the PVN, releasing _______
excitatory, melanocortins
ghrelin binds to the same receptors as
growth-hormone releasing hormone (GHRH)
animals that are preparing for hibernation have constantly _____ insulin levels
high
in what ways does the lateral hypothalamus facilitate feeding?
improves taste, enhances corrtical responses to food, and increases secretions of insulin and digestive juices
could you be satiated from taste alone?
in sham-feeding experiments (everything an animal swallows leaks out of a tube connected to the esophagus or stomach-- taste contributes to satiety, but it is not sufficient
effect of lesion on ventromedial hypothalamus
increased meal frequency, weight gain, high insulin level
paraventricular nucleus
increased meal size, especially increased carbohydrate intake during the first meal of the active period
What does the VMH do?
inhibits feeding
the hunger cells in the arcuate nucleus _____ the PVN and PVN _____ the lateral hypothalamus the inhibitory transmitters are
inhibits, inhibits, GABA, neuropeptide Y (NPY), agouti-related peptide (AgRP)
2 pancreatic hormones that regulate the flow of glucose into cells
insulin and glucagon
what area releases orexin and what does it do?
lateral hypothalamus, and increases animals' persistance for food
melanocortin receptors in the PVN are important for ______, damage to these receptors leads to _____
limiting food intake, overeating
what is the body's long term mechanism to compensate for day-to-day mistakes
monitoring fat supplies
could you become satiated without tasting your food?
most found the untasted meals unsatisfying, however, and reported a desire to taste or chew something
can we CCK to help people lose weight?
no, it produces short term effects only
syndromal obesity
obesity that results from a medical condition
duodenum releases a hormone called
oleoylethanolamide (OEA)
duodenum
part of the small intestine adjoining the stomach; first digestive site that absorbs nutrients
overweight people ___ leptin but....
produce, but have become less sensitive to it
normal mice ____ leptin obese gene mice ____ leptin
produce, fail to produce
problems with nonnutritive sweetners being added to foods and drinks
rats learned that taste is a poor predictor of energy and so they overate other foods and stopped compensating afterward. they also became less active
what evidence from rats suggests that bulimia resembles an addiction?
rats that alternate between food deprivation and a very sweet diet gradually eat more and more , and they reach to deprivation of the sweet diet with head shaking and teeth chattering, like the symptoms of morphine withdrawal
an animal with damage to lateral hypothalamus does what?
refuses food and water
As obesity develops, the effect of leptin _______ so that it ______ eating
reverses, increases
What does leptin do?
signals brain about fat reserves, providing long term indicator if you have been over/undereating
the stomach conveys satiety messages to brain via...
splanchnic and vagus nerve
What does glucagon do?
stimulates the liver to convert some of its stored glycogen back to glucose
What does OEA do?
stimulates the vagus nerve, sending a message to the hypothalamus that delays the next meal
______ _____ is enough to produce satiety
stomach distension
what happens when insulin levels stay constantly high
the body continues moving blood glucose into the cells, including liver cells and fat cells, long after a meal. before too long, blood glucose drops because glucose is leaving the blood without any new glucose entering --> increased hunger
what does ghrelin do?
triggers stomach contractions, acts on the hypothalamus
increasing ___ does helpo the brain produce ____ which induces sleepiness
tryptophan, melatonin
effect of lesion in lateral hypothalamus
undereating, weight loss, low insulin level (because of damage to cell bodies); underarousal, underresponsiveness (because of damage to passing axons)