Transcript Chapter 12
Chapter 12 Ingestive Behavior Introduction “The constancy of the internal milieu is a necessary component for a free life.” – Claude Bernard Animals have evolved from single cell organisms that live in the ocean. In order to “carry” this environment with us (i.e. water and solutes), our body and its cells must regulate their fluid balance This regulation is part of what is called homeostasis – process by which the body’s substances and characteristics (such as temp and glucose level) are maintained at their optimal level Mammals maintain homeostatic control of our body’s fluid and energy through our ingestive behavior – intake of food, water, and minerals such as sodium Physiological regulatory mechanisms A physiological regulatory mechanism is one that maintains the constancy of some internal characteristic of the organism in the face of external variability Four essential features: e.g. keeping body temp constant despite changes in ambient temp System variable – the characteristic to be regulated; e.g. temp Set point – the optimal value of the system variable; e.g. 78° Detector – monitors the value of the system variable; e.g. thermostat Correctional mechanism – restores the system variable to its set point; e.g. AC or heater Negative feedback – a process whereby the effect produced by an action serves to diminish or terminate that action; when AC or heater is turned on and successfully changes temp back to set point, the detector senses this and turns AC/heater off Satiation mechanism – a brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water Drinking Fluid balance Body contains 4 major fluid compartments: Intracellular and intravascular fluid must be kept in tight regulation Intracellular fluid controlled by conc. of solutes in interstitial fluid (normally isotonic, or same osmotic pressure, by process of diffusion) If ISF loses water (hypertonic), water will be pulled out of the cells If ISF gains water (hypotonic), water will move into the cells Blood plasma volume must be regulated in order to pump blood effectively 1 of intracellular fluid – 2/3 of body’s water 3 of extracellular fluid (intravascular fluid – blood plasma, cerebrospinal fluid, interstitial fluid – b/t cells) If blood volume too low (hypovolemia), lead to heart failure For 2 different types of regulation, need 2 types of receptors: one measuring blood volume, the other measuring cell volume Drinking 2 types of thirst Most times, we ingest more water or solutes than needed; these are then excreted by kidney When levels of either water or solutes are too low, corrective mechanisms are activated: thirst, or salt appetite (rare for modern humans) Our bodies lose water continuously, through sweating, breathing, urination, defecation, and in some circumstances through vomiting Osmometric (osmotic) thirst – occurs when the tonicity (solute conc.) of the ISF increases; e.g. when eat salty meal with no water Osmoreceptors – neuron that detects changes in the solute conc. of the ISF that surrounds it Hypertonicity of blood plasma (where salt is absorbed into) draws water from ISF, which then causes water to leave cells; when blood volume increases, the kidneys begin to excrete both water and solutes, allowing the blood plasma volume to remain constant Drinking 2 types of thirst Osmotic thirst (con’t) Osmoreceptors located in the anterior hypothalamus, one of the circumventricular organs (CVO’s) OVLT (organum vasculosum of the lamina terminalis) – CVO located on the blood side of the BBB, and thus substances dissolved in the blood are able to pass through to the ISF of this organ Volumetric thirst Produced when blood plasma volume is low Leads to both thirst and salt appetite 2 types of receptor systems: Renin-angiotensin system & atrial baroreceptors Renin-angiotensin system – hypovolemia activates kidneys to release an enzyme called renin, which then catalyzes the conversion of a blood protein called angiotensinogen into a hormone called angiotensin (AngII) AngII stimulates secretion of hormones by posterior pituitary and adrenal gland to conserve water and solutes, and stimulates drinking and salt appetite Drinking 2 types of thirst Volumetric thirst (con’t) Atrial baroreceptors The atria of the heart contains stretch receptors that detect when blood volume is low, which then stimulates thirst Neural mechanisms of thirst Sensory info from atria is conferred to the nucleus of the solitary tract (NTS) in the medulla AngII crosses weak BBB near CVO’s to provide thirst and salt appetite signal (esp. via subfornical organ (SFO)) Neurons in SFO project to MnPO (median preoptic nucleus) Eating Some facts about metabolism Food ingestive behaviors are more complex than those of water balance We must obtain adequate amounts of carbohydrates, fats, amino acids, vitamins, and minerals other than sodium Absorption, fasting, and the 2 nutrient reservoirs Our bodies need food for “building blocks” (i.e. to construct and maintain our organs and muscles) and “fuel” Fuel comes from food we have consumed that travels through the digestive tract, but those nutrients must be able to be stored for when the gut is empty 2 types of reservoirs: short-term (carbs) and long-term (fats) Nutrient reservoirs Short-term Located in cells of liver and muscles Cells filled with complex, insoluble carb called glycogen Cells in the liver convert glucose (obtained from diet) into glycogen and store it; this storage is stimulated by the presence of insulin, a peptide hormone produced by the pancreas When glucose enters the body, some is stored as glycogen and some is used as fuel When there are low levels of glucose in the blood, the pancreas begins to secrete glucagon, which stimulates the conversion of glycogen back into glucose This reservoir primarily serves to fuel the CNS Nutrient reservoirs Long-term Adipose tissue – filed with triglycerides (complex molecules that contain glycerol, a soluble carb, combined with 3 fatty acids) Found beneath the skin and in various locations in the abdominal cavity Cells can expand in size Reservoir for rest of body besides brain What keeps us alive when we are fasting; when body starts to use carb reservoir, fat cells start converting triglycerides into fuel that cells can use Fatty acids can be metabolized by cells in all of the body except the brain; glycerol can be converted to glucose in the liver for use in the brain So, why does brain get all the glucose? Insulin must be present at a cell in order for it to take up glucose into it However, neurons and glia do not require insulin to take up glucose Metabolism Fasting phase – the phase of metabolism during which nutrients are not available to from the digestive system; glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase Absorptive phase – the phase of metabolism during which nutrients are absorbed from the digestive system; glucose, and amino acids constitute the principle source of energy for cells during this phase, and excess nutrients are stored What starts a meal? Social and environmental factors Often we eat out of habit or because of some stimuli present in our env’t (e.g. clock, smell food) Meal schedule very important: rarely adjust times of meals, but can adjust size of meals If we have eaten recently or if a previous meal was large, we tend to eat a smaller meal However, due to other social factors, such as parental cues (“finish your plate”) or peer influence, satiety signals can be ignored DeCastro and DeCastro (1989) found that the amount of food eaten was directly proportional to the amount of other people who were present during a meal What starts a meal? Physiological hunger signals The amount of food that we eat is inversely related to the amount of nutrients left over from previous meals Fall in glucose level (hypoglycemia) is a potent stimulus for hunger Glucoprivation – a dramatic fall in the level of glucose available to cells Hunger can also be caused by lipoprivation ( fall in level of fatty acids available to cells) 2 sets of detectors for these metabolic fuels: one set located in the brain (sensitive to glucoprivation) and the other in the liver (sensitive to both glucoprivation and lipoprivation) What stops a meal? 2 types of satiety signals: short-term info from gastrointestinal tract, long-term from adipose tissue Head factors Receptors located in in head (e.g. eyes, nose, tongue, and throat) provide info about appearance, odor, taste, texture, and temp of food Most effects involve learning: taste and odor of foods can serve as stimuli that permit animals to learn about the caloric density of foods (e.g. sweet taste = glucose, fuel) Rats can learn to eat less of a food with a particular flavor when the eating of that food was paired with caloric infusion What stops a meal? Gastric factors Stomach not necessary for feelings of hunger? Not completely true: when stomach is empty, a peptide called ghrelin is secreted which activates a hunger signal The stomach also contains receptors that can detect the presence of nutrients Intestinal factors Afferent axons from the duodenum (first portion of small intestine) are sensitive to the presence of glucose, amino acids, and fatty acids Entry of food into the duodenum suppresses food intake in rats; rats fitted with a gastric fistula ( a tube that drains contents out of the stomach) continue to consume food (this method is called sham feeding) The duodenum controls the normal rate of stomach empyting by secreting a peptide called cholecystokinin (CCK), which also serves a a satiety signal in the brain What stops a meal? Liver factors Metabolic factors present in the blood The liver is the first organ to “learn” that food is being received by the intestines; when it does so it sends a satiety signal to the brain Insulin receptors in the brain may serve as a satiety signal Long-term satiety: signals from adipose tissue Signals from the long-term nutrient reservoir may either suppress hunger signals or augment short-term satiety signals Some variable related to body fat (as opposed to weight) may serve as the system variable Leptin – hormone secreted by adipose tissue; decreases food intake and increases metabolic rate Genetically obese mice (ob mouse) cannot produce leptin, thus become grossly obese Brain mechanisms Brain stem Ingestive behaviors are evolutionarily old; thus controlled by “older” parts of the brain (mid- and hindbrain) Decerebrate animals (animals in which the brain stem has been severed from the forebrain) can still perform basic ingestive behaviors (e.g. chewing, swallowing) but not more complex ingestive behaviors (e.g. foraging) Hypothalamus Lateral hypothalamus (LH) lesions produce anorectic effects (stop eating) Ventromedial hypothalamus (VMH) lesions produce increase in food intake and severe weight gain Brain mechanisms Hypothalamus (con’t) Role in hunger Two populations of neurons in LH secrete hormones that stimulate hunger and increase metabolic rate: melanin-concentrating hormone (MCH) and orexin Arcuate nucleus of the hypothalamus: secretes a NT called neuropeptide Y (NPY) and a peptide called agouti-related peptide (AGRP); these both act on the MCH and orexin neurons of the LH to induce hunger Also, ghrelin secreted from stomach induces hunger Role in satiety Arcuate nucleus also contains neurons that secrete both CART and α-MSH, which serve to induce satiety Eating disorders Obesity Evolutionarily old bodies living in a modern environment i.e. our bodies still act accordingly to possible times of famine; but in modern industrialized nation, this is obviously unnecessary Both genetic and environmental factors Treatments include: pharmacotherapy, behavior therapy, gastric surgery, combo Unfortunately very common in modern world Anorexia nervosa/bulimia nervosa Both exaggerated concern of body image AN is refusal to maintain above certain BMI by not eating BN concerns cycles of binge eating and purging behaviors (e.g. vomiting, laxative use) Not as common as obesity, ~2% of population