NSCI 175 - Injestive Behavior

Physiological signals for hunger (2)

- Glucoprivation: drop of blood glucose levels stimulates eating (even if you don't feel like eating/aren't hungry) - Lipoprivation: drop in fat signals (drop in signals from fat in body that go to brain) stimulates hunger

Type 2 Diabetes

- Happens when insulin receptors stop responding when insulin binds to them; a bunch of different types of receptors have this happen when they're in the presence of an agonist for a long time - means that when insulin is released, it goes to bind to the cell so that the cells can use glucose for energy and it doesn't work ( glucose can't be transported to be used or for short term storage), leads to high levels of glucose and insulin - can be treated with drugs that sensitize insulin receptors - if a person has type 2 long enough, it can cause a problem with beta cells where they stop releasing insulin altogether (so have both type 1 and 2)

Anabolism

Aka anabolic metabolism, making macromolecules like glycogen and triglycerides from simple precursors

Visceromotor Response

Aka autonomic motor response; how neurons in hypothalamus responds to sensory signals by changing the balance of the sympathetic and parasympathetic divisions of autonomic motor system (sympathetic system helps get energy out, while parasympathetic involves brining in food, feeding, and storage)

Catabolism

Aka catabolic metabolism, breaking down macromolecules

AgRP and alphaMSH are ________________ (how?)

Antagonist neurotransmitters; both bind to MC4 receptor on postsynaptic neurons in hypothalamus, but AgRP inhibits it and stimulates feeding while alphaMSH activates it and inhibits feeding

What happens if your blood glucose levels start getting low?

Glucagon gets made and secreted by the pancreas; causes cells in liver and muscles to take glycogen, break it down into glucose, and release that glucose the bloodstream to raise blood sugar levels

Humoral response

Hormonal response; stimulating or inhibiting pituitary hormone release into blood stream

Glucostatic hypothesis

Hunger and eating is driven by glucose homeostasis; when glucose levels are low, need to eat to get more glucose into blood stream so that levels go back up to set range

Somatic Motor Response

Hypothalamic neurons (lateral hypothalamus) respond to sensory signals by inciting an appropriate somatic motor behavioral response (ex: drive to eat, feed, hunger, etc.; changes in activity levels)

What is long term storage?

In adipose tissue (fat), stored energy that is tapped when the body has used up short term storage/mechanisms; have more mechanisms to start eating than to stop eating and fat stores are homeostatically maintained to have relative fixed levels; have multiple systems and redundancies, which ensure behavior/survival

What happens when leptin levels increase?

Increases in leptin --> alphaMSH and CART Neurons get activated --> inhibit lateral hypothalamus --> inhibits feeding behavior; activiting alphaMSH and CART neurons also causes activation of paraventricular nucleus --> stimulates release of ACTH and thyrotropin from anterior pituitary which allows you get make cortisol // also activates brain stem neurons and preganglionic neurons of sympathetic ANS (stress response that pulls energy out of storage and uses it)

Why is it adaptive to have long-term/fat stores?

More likely to survive harsh winters, periods of famine, and reproduction (which have high energy costs)

Result of leptin increase

More use of energy, inhibit feeding, more metabolism

What happens when leptin levels decrease?

NPY and AgRP neurons get activated --> stimulate lateral hypothalamus --> stimulate feeding behavior; also inhibits paraventricular nucleus which inhibits release of ACTH and TSH, which decreases metabolism; also activate parasympathetic division of ANS

All short term appetite signals converge at the __________ (_________)

Nucleus of the solitary tract (brain stem)

MCH and Orexin neurons

Stimulate appetite and reduce metabolic rate

Lipostatic hypothesis

The brain monitors the amount of body fat to "defend" it from any changes; if a rat is induced to lose body fat through restrictive diet, the fat will go back up to normal once its taken off that diet because it would want to overeat (+ vice versa with gaining body fat); energy homeostasis

What happens if your brain stops responding to ghrelin?

You're not being told that you're hungry and you may not eat; happens in anorexia nervosa -- those with this eating disorder actually release a lot of ghrelin from the stomach to try to stimulate their appetite, but over time the ghrelin receptors in the brain stop being responsive to ghrelin

ob gene

gene that makes the hormone leptin (which is involved in long-term regulation of feeding/eating); signal released is a long-term satiety (change depend on how much fat is in the body not by every meal you eat) ; mice that didn't have ob gene didn't make leptin, which caused them to eat a lottt of food since their brain thought that they didn't have any food/fat stored

Hormones from the body drive a ___________ appetite controller; a circuit within the _________ integrates peptide hormone signals from the body

hypothalamic, arcuate nucleus

What does the MCH neurotransmitter do? What happens when it's injected to or removed from the body?

innervate cerebral cortex and tell it about leptin levels in blood, making us search for food; when injected, stimulates feeding behavior but when not present, reduces feeding

Gastric distension

stomachs expand as we eat food and the walls of our stomachs have neurons that go to the brain through the vagus nerve. This activates neurons in nucleus of solitary tract in medulla and inhibits feeding behavior

Energy regulation involves shuttling off energy between ___________ and _________

stores (short term/long term), avaliable energy

db gene (db/db gene)

when deleted, causes insulin/leptin resistance of receptors; leptin insensitivity which leads to insulin insensitivity and therefore type 2 diabetes-- brain can't interpret leptin signal, so makes you eat more and slows your metabolism

Ghrelin

Appetite stimulant; synthesized and released by endocrine cells of stomach, reaches high levels before eating and drops off after eating; your expectations of a meal (like how many calories a food has) can influence whether or not ghrelin decreases after eating or doesn't (high calorie --> decrease ghrelin, making you feel more satiated while low calorie --> increase)

Cholecystokinin (CCK)

Appetite suppressant; released by intestinal cells; reaches high levels after eating, especially after eating fatty foods; peptide released by the gut after feeding and acts on the vagus nerve to inhibit appetite

Type 1 Diabetes

Autoimmune disease where body is attacking beta cells in pancreas (which make insulin), making them stop working which makes the body stop producing insulin; can't be fixed with some sort of diet, so ppl with this diabetes need to have some sort of insulin replacement therapy

3 areas of energy regulation

Available energy (blood glucose for cells to use as energy), short term storage sites (liver and muscles; after you've eaten and used what you needed from the food, anything left over can get stored for short term storage and get pulled out easily to use when you haven't eaten in a while, when blood sugar drop, or when you need to exercise), long term storage sites (fat; each fat cells contains thousands of kilojoules of energy, useful if haven't eaten in a while)

Both the ________ and the _______ contain detectors

Brain and liver

What happens if glucose gets too low?

Brain cells can't function leading to unconsciousness

What happens if glucose goes too high?

Damage to kidney, retina, peripheral nerves, cardiovascular system

Hormones involved in regulating blood glucose

Insulin (released into bloodstream by beta cells of pancreas; take glucose from available stores and converting it to storage; storage hormone), glucagon (use hormone; helps to get energy out and use it)

Hormones that report short term energy balance/ "orexigenic and satiety signals" (4)

Insulin, Ghrelin, Cholecystokinin, Gastric distension (not a hormone, but still a signal)

Leptin

Peptide released by adipose tissue, have receptors in hypothalamus (arcuate nucleus)

Orexigenic peptides

Peptides that stimulate feeding behavior

Neuropeptide Y (NPY) and AgRP neurons

Project to the MCH and orexin neurons and activates them, which stimulates appetite and reduces metabolic rate; leptin inhibits this

alphaMSH (POMC) and CART neurons

Project to the MCH and orexin neurons and inhibit them, inhibiting appetite and increasing metabolic rate; leptin activates this

What does the orexin neurotransmitter do? How does this relate to the MCH neurotransmitter?

Promotes meal initiation/stimulates feeding behavior; is complementary to MCH, which prolongs consumption

What happens if your blood glucose levels start getting high?

Receptors tell the pancreas that glucose levels are high so it releases insulin; insulin binds to receptors in cells on liver and muscles and allows them to take up the glucose to either use immediately or use as glycogen (short term storage molecule)... this lowers glucose levels as glucose is being absorbed

Satiation

Satisfaction regarding full (different than fullness; you can be full but not satiated)

Why do we eat? (4)

Social and environmental factors, need energy, taste of food, and dietary selection (prefer a varied diet)

True or False: Set points can change over time (explain)

True; in adult animals, body weight is generally stable around a set point but will change with long term changes in feeding (more likely to go upwards than downards) due to changes in metabolism and adipose tissue