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Ingestive Behaviors
| Term | Definition |
|---|---|
| Thirst | The body attempts to maintain an isotonic state by regulating fluid and ion intake. |
| Osmoregulatory | Osmoregulatory thirst is actually regulated by the organs of the lamina terminalis (LT) The LT lines the 3rd ventricle, which is in the middle of the hypothalamus. |
| Osmoregulatory prt 2 | -The LT is not separated from the blood by the BBB, allowing osmoreceptors on cells in the LT to directly respond to solute levels in the blood. -Ions more concentrated outside the cell, water leaves. This results in cell shrinkage. |
| prt 3 | Following H2O consumption, ions are lss concentrated outside the cell, and water enters. This results in cell swelling. |
| volumetric | -Volumetric thirst is due to large loss of fluid from the extracellular space. |
| prt 2 | -Hypovolemia activates baroreceptors in the heart and kidneys, which triggers the release of vasopressin from the posterior pituitary gland, which descends from the hypothalamus. |
| Anatomy of thirst detection and perception | -Thirst signals from the hypothalamus are routed through the thalamus to the insular cortex. -thirsty subjects have high levels of activity in the insular and anterior cingulate cortices. |
| prt 2 | -Renin is also released from the kidneys, which helps create angiotensin. -These cause motivation to consume both liquid and salt. |
| Osmoregulatory vs Volumetric Thirst | One system focuses on the levels of intracellular fluid and triggers osmometric thirst. The other monitors extracellular levels - more specifically, plasma or blood volume - |
| prt 2 | and triggers volumetric thirst. Volumetric thirst is associated wth a neeed for both salt and water. |
| Osmoreceptors vs. baroreceptors | Osmoreceptors reside in hypothalamus and respond to changes of extracellular fluid (ECF) osmolality. Baroreceptors are mechanoreceptors that sense blood pressure in the vessel wall. |
| What fuels the body> | The brain uses glucose for energy, while the rest of the body uses glucose and/or fatty acids. Energy stores exist in glycogen stores in the liver (short-term), and triglyceride stores in adipose tissue (long-term |
| Compare and contrast the absorptive and fasting phases of metabolism. | -When there is food in the digestive system, blood glucose rises (absorptive phase). -Brain and body use glucose. -Insulin is released. -Extra glucose is stored as glycogen. -Fat is stored as triglycerides. |
| Compare and contrast the absorptive and fasting phases of metabolism. prt 2 | When digestive system is empty, sympathetic nervous system causes release of glucagon. -Glycogen is converted to glucose for the brain. -Triglycerides are converted to fatty acids for the body, and more glucose for the brain. |
| Role of parasympathetic and sympathetic nervous systems | The sympathetic nervous system activates the fight or flight response during a threat or perceived danger, and the parasympathetic nervous system restores the body to a state of calm. Rest and Digest - Feed and Breed |
| insulin | -Cells respond quickly to insulin, which reduces food intake and makes cells feel starved of sugar. Lead to increased appetite, even when there's already enough glucose in the bloodstream. -binds to the insulin receptor (IR) on the plasma membrane (PM |
| glucagon | a peptide hormone secreted from the alpha cells of the pancreatic islets of Langerhans. Glucagon receptor (GCGR) is a secretin-like (class B) family of G-protein coupled receptors (GPCRs) |
| Anatomy of hunger and satiety | Area postrema and nucleus of the solitary tract (AP/NST) in the medulla receive taste signals, as well as information from the internal organs, and send information to regions of forebrain to help control food intake |
| Prt 2 | The ventromedial nuclei is the satiety center, and when stimulated, it causes the sensation of fullness. On the other hand, the lateral hypothalamic area is the feeding center and when stimulated, it causes the sensation of hunger. |
| Peripheral signals | signals that originate from the sequence of food's location, selection, ingestion, digestion, and absorption. |
| Ghrelin and glucose/lipid detectors for hunger | Ghrelin increases activity in orexinergic cells of the lateral hypothalamus -The orexin cells project to the arcuate nucleus to promote feeding behavior |
| Ghrelin and glucose/lipid detectors for hunger prt 2 | -The orexin cells also project to the ventral tegmental area and nucleus accumbens, to interact with the dopaminergic reward/motivation system. |
| Ghrelin and glucose/lipid detectors for hunger prt 3 | -Ghrelin signals hunger - Levels of ghrelin in the blood rise prior to meal initiation. -Ghrelin is released by the stomach when it is empty. -Low levels of sugar in the blood are detected by glucose detectors in the brainstem and liver. |
| Insulin, PYY and leptin for satiety | Insulin, leptin, and GLP-1 activate the POMC/CART neurons in the ARC nucleus of the hypothalamus, which are related to satiety. PYY, leptin, and dopamine inhibit the AgRP/NPY neurons in the ARC, which are related to hunger. |
| Leptin deficiency | can cause severe obesity, hyperphagia, and other symptoms. Leptin is a hormone that helps regulate appetite by signaling hunger satisfaction. When leptin levels are low, people may feel hungry constantly and gain weight quickly |
| Orexin | is a neuropeptide that regulates wakefulness, arousal, and appetite. It's produced in the lateral hypothalamus and perifornical areas of the brain. Orexin is an excitatory neuropeptide that keeps the organism awake and under stress. |
| dopamine | Dopamine is a chemical messenger and neurotransmitter that is produced in the brain's substantia nigra, ventral tegmental area, and hypothalamus. |
| Rat “cafeteria diet” study | Normal rat chow Restricted “cafeteria diet”-1hr per day Extended ”cafeteria diet”-23hr per day Extended access rats: Gained more weight Had higher reward thresholds Decreased D2 receptor expression in the striatum |
| Ways in which hunger regulation can go awry prt 1 | Stomach detects nutrients, slows down ghrelin release. The intestines release cholecystokinin (CCK) and peptide YY3-36 (PYY) into the blood. |
| prt 2 | As nutrients enter the blood, the liver also sends a satiety signal. Insulin, which is released after a large meal, crosses the BBB and inhibits hypothalamic feeding circuits. Long term: leptin is released from adipose tissue to inhibit food intake. |
| Anorexia nervosa w/ rat exercise study | Potential factors that may lead to the development of anorexia nervosa: Prone to anxiety Perfectionism Excessive concern with body image Exposure to ultra-thin individuals in the media (“thinspiration”) Compulsive exercise |
| prt 2 | Rats had their food access restricted (24 hr control group, 4 hr, 2 hr, and 1 hr access experimental groups), and were also denied or given access to a running wheel (no wheel control groups vs. wheel experimental groups) |
| prt 3 | Rats with unlimited access to food, and no running wheel, gained the most weight. Rats with 1 hr food access, and wheel access, weighed less the all other groups. |
| prt 4 | Interestingly, rats with 1 hr food access ran more than any other group! Rats that were food deprived (1 hr) had greater levels of NPY mRNA. Infusion of NPY in food restricted rats decreased food consumption and further increased wheel running. |
| Hunger = | Hypothalamus |
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