Hunger and Thirst

Homeostasis & allostasis

-Homeostasis: temperature regulation and other processes that keep body variables within a fixed range. Mostly range is so narrow we use a set point: single value that the body works to maintain. -Negative feedback: processes that reduce inconsistency from set point. Something happens to cause a disturbance and behavior varies until it relieves the disturbance. -Allostasis: body maintains a higher temperature during day then at night.

Insulin & Glucagon

-Insulin: enables glucose to enter cell. Insulin levels high -> cells receive glucose easily. When you get ready for a meal, insulin levels rise, increases even more during and after a meal. High levels of insulin decrease appetite. -Glucagon: stimulates liver to convert stored glycogen to glucose to replenish low supplies in blood.

Salt concentrations solutions

-Isotonic: salt concentration that is the same as found in interstitial fluid and blood plasma (0,9% salt). -Hypertonic: a solution with a higher salt concentration (+0,9% salt) -Hypotonic: a solution with a lesser concentration in salt than usual (-0,9% salt)

Create full feeling

-Premeal hunger: energy reserves are balanced homeostatically right before mail. Becomes irregular if you eat, body tries to prevent this by going trough a cephalic phase right before meal. -Satiety: full feeling which makes you stop eating. Food in intestines and glucose of blood stimulate satiety levels. Depend on volume and nutritive density of food. -Appetizer effect: small amounts of food before a meal increases hunger.

Metabolic phases

Cells regulate import of glucose via glucose transporters that span cell membrane and bring glucose molecules from ouside to inside. Most of body requires insulin to make use of glucose. Mechanisms: -Cephalic phase: sensory stimuli evoke release of insulin in anticipation of glucose arrival in blood. -Digestive phase: food entering stomach and intestines causes them to release gut hormones, stimulate pancreas to release insulin. -Absorptive phase: cells in liver (gluco-detectors) detect glucose entering bloodstream and signal pancreas to release insulin.

Sodium-specific hunger

Develops automatically as the need exist. It depends party on hormones. When the body's sodium reserves are low, the adrenal glands produce the hormone aldosterone, which cause kidneys, salivary glands, and sweat glands to reabsorption of ions and water in the kidney, to cause the conservation of sodium.

Set-point assumptions

Eating is used to make the energy sources in the body optimal. After a meal, an energy source will come close to the set point. All set point systems are negative feedback systems.

Osmotic thirst

Eating salty food causes osmotic thirst. The solutes inside and outside a cell produce a osmotic pressure: the tendency of water to flow across the membrane to the area with a higher concentration. Osmotic pressure occurs when solutes are more concentrated on one side of the membrane than the other. Detection of osmotic thirst: brain gets info from receptors in stomach that detects high levels of sodium, enabling brain to anticipate an osmotic need before rest of the body actually experiences it.

Lipostatic theory

Every person has a set point for body weight. Abnormalities of this set point creates changes in eating behavior, so that the body's fat will come back to the set point.

Cholecystokinin CCK

Food in duodenum releases this hormone, limits meal size: -CCK closes sphincter muscle between stomach and duodenum causing stomach to hold its contant and fill more quickly than usual. -CCK stimulates vagus nerve, which sends a message to the hypothalamus, causing cells there to release a neurotransmitter that is a shorter version of CCK molecule.

Ghrelin

Hormone produced and released mainly by stomach, but also released by small intestine, pancreas and brain. Stimulates appetite, increases food intake and promotes fat storage. Levels are primarily regulated by food intake. Levels rise just before eating and when fasting. Rises being affected by our normal meal routine. Levels are lower in individuals with a higher body weight compared to lean individuals.

Orexin

More orexin receptor -> slimmer. Not just plays a role in regulating appetite, but in regulating weight and overall metabolism.

Energy storage

Most immediate souche of energy is the collection of complex carbohydrates that are rapidly broken down to sugar that cells can use as energy.

Lateral hypothalamus (LH)

Output from paraventricular nucleus acts on lateral hypothalamus, includes many neuron clusters and passing axons. THe lateral hypothalamus controls insulin secretion, alters taste responsiveness, and facilitates feeding in other ways. Damage causes aphagia, where someone refuses food and water.

Arcuate nucleus

Part of hypothalamus, has one set of neurons sensitive to hunger signals and a second set sensitive to satiety signals. Hunger-sensitive cells receive input from the taste pathway: good-tasting food stimulates hunger. Another input to the hunger-sensitive cells comes from axons releasing the neurotransmitter ghrelin, which triggers stomach contractions.

Positive-incentive theory

People and animals aren't motivated to eat due to internal energy deficiency, but due to the pleasure of eating. Eating is also controlled like sexual behavior. The presence of food is important.

Vasopressin

Posterior pituitary release a hormone called vasopressin when you don't drink enough. It conserves water by excreting more concentrated urine. It raises blood pressure by constricting the blood vessels. Increased pressure helps compensate from the decreased volume. Vasopressin also known as anti-diuretic hormone (ADH) because it enables the kidneys to reabsorb water from urine making it more concentrated.

Ventromedial hypothalamus (VMH)

Satiety. Damage causes overeating. Two phases: dynamic (gainin weight, overeating) and static (stable overweight). It increasus insulin levels which causes lipogenesis; production of body fat.

Leptin

Signals the brain about the body's fat reserve, providing a long-term indicator of whether meals have been too large or too small. Each meal also increases the release of leptin, so the amount of circulating leptin indicates something about short-term nutrition as well.

Osmosensory neuron

Specialized neuron that measures movement in water in and out of intracellular side. Neurons have no constant volume. They also have channels that open and close when membrane changes. The power that pulls water through membrane (high conc. to low conc.) is called osmotic pressure. Concentration of a solute is called osmolality.

Stomach and intestines

Stomach conveys satiety messages to the brain via the vagus nerve and the splanchnic nerves. -Vagus nerve: conveys information about the stretching of the stomach walls, providing a basis for satiety. -Splanchnic nerves: conveys information about the nutrient contents of stomach.

Settling point

The body's weight has a tendency to vary at a certain point; the level where many factors influence body weight to reach an equilibrium.

Hypovolemic thirst

Thirst based on loss of volume (menstruation, sweating, diarrhea). When blood volume drops, kidneys release the enzyme rennin, which splits a portion of angiotensinogen, a large protein in blood, to form angiotensin I, which other enzymes convert to angiotensin II, which constricts the blood vessels compensating for the drop in blood pressure. Also helps trigger thirst in conjunction with receptors that detect blood pressure in large vain. Need to restore salts, not just water.

Compartments

Two types of compartments in human body: -Intracellular compartment: fluid space of the body that is contained with cells. -Extracellular compartment: fluid space of the body that exist outside the cells.

Homeostatic regulation

We cannot maintain water in the extracellular compartment without solutes. In addition to its effects on thirst and vasopressin secretion, angiotensin II release aldosterone from adrenal glands. Aldosterone stimulates the kidneys to conserve sodium in order to aid water retention.

Glucostatic theory

When the glucose level goes below a certain level (set point), we become hungry. Eating makes sure that the level will come back to the set point.