PHY2032: Exam notes - Endocrinology, Digestion, Sugar Metabolism

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Department
General Education Studies
Course
ATS1262
Professor
Various
Semester
Spring

Description
The Endocrine System ENDOCRINOLOGY 4 – ADRENAL GLAND - The secretion from the adrenal cortex of the glucocorticoid hormone cortisol increased - Activity of the sympathetic nervous system, including release of the hormone epinephrine from the adrenal medulla, also increases due to stress - The increased cortisol secretion during stress is mediated by the hypothalamo-anterior pituitary gland system - Neural input to the hypothalamus from portions of the nervous system responding to a particular stress induces secretion of CRH - This hormone is carried by the hypothalamo-pituitary portal vessels to the anterior pituitary gland, where it stimulates ACTH secretion - ACTH in turn circulates through the blood, reaches the adrenal cortex, and stimulates cortex release - The secretion of ACTH, and therefore of cortisol, is stimulated by several hormones in addition to hypothalamic CRH. These include vasopressin, which usually increases in response to stress - Some of the cytokines also stimulate ACTH secretion both directly and by stimulating the secretion of CRH. These cytokines provide a means for eliciting and endocrine stress response when the immune system is stimulated Physiological Functions of Cortisol: - Cortisol is always produced by the adrenal cortex and exerts many important actions even in non-stress situations - Basal levels of cortisol help maintain normal blood pressure - Basal levels of cortisol are required to maintain the cellular concentrations of certain enzymes involved in metabolic homeostasis - These enzymes are located primarily in the liver, and they act to increase hepatic glucose production between meals, thereby preventing plasma glucose levels from significant decreasing below normal - Two important systemic actions of cortisol are its anti-inflammatory and anti-immune functions - Cortisol inhibits the production of both leukotrienes and prostaglandins, both of which are involved in inflammation - Cortisol also stabilizes lysosomal membranes in damaged cells, preventing the release of their proteolytic contents - Cortisol reduces capillary permeability in injured areas and it suppresses the growth and function of certain key immune cells - Cortisol may serve as a ‘brake’ on the immune system, which might overreact to minor infections in the absence of cortisol. Effects of increased plasma cortisol concentration during stress: - Effects on organic metabolism: = stimulation of protein catabolism in bone, lymph, muscle and elsewhere = stimulation of liver uptake of amino acids and their conversion to glucose (gluconeogenesis) = maintenance of plasma glucose levels = stimulation of triglyceride catabolism in adipose tissue, with release of glycerol and fatty acids into the blood - Enhanced vascular reactivity (increased ability to maintain vasoconstriction in response to norepinephrine and other stimuli) - Unidentified protective effects against the damaging influences of stress - Inhibition of inflammation and specific immune responses - Inhibition of nonessential functions (reproduction and growth) Adrenal insufficiency and Cushing’s syndrome: - The complete absence of cortisol leads to the body’s inability to maintain homeostasis, particularly when confronted with a stress - The general term for any situation in which plasma levels of cortisol are chronically lower than normal is adrenal insufficiency Primary adrenal insufficiency: - Due to a loss of adrenal cortical function - The syndrome is due to autoimmune attack in which the immune system mistakenly recognizes some component of a person’s own adrenal own adrenal cells as foreign - This results in inflammation of the immune system and causes a destruction of many cells of the adrenal glands, thus all the zones of the adrenal cortex are affected - Not only cortisol but also aldosterone levels are decreased below normal - This decrease in aldosterone concentration creates the additional problem of an imbalance in Na+, K+, and water in the blood because aldosterone is a key regulator of those variables Cushing’s syndrome: - Usually due to an ACTH secreting tumor of the anterior pituitary gland - The increased blood levels of cortisol tend to promote uncontrollable catabolism of bone, muscle, skin, and other organs - The increased catabolism may produce such a large quantity of precursors for hepatic gluconeogenesis that blood sugar increases to levels observed in diabetes mellitus Hypertension: - High blood pressure - Not due to increased aldosterone production but instead to the pharmacological effects of cortisol, including cortisol’s ability to potentiate the effects of epinephrine and norepinephrine on the heart and blood vessels - At high concentrations, cortisol exerts aldosterone-like actions on the kidney, resulting in salt and water retention, which contributes to hypertension Other hormones released during stress: - Other hormones that are usually released during many kinds of stress are: = aldosterone = vasopressin (ADH) = growth hormone = glucagon = beta-endorphin (which is co-released from the anterior pituitary gland with ACTH) - Vasopressin and aldosterone act to retain water and Na+ within the body - Vasopressin also stimulates the secretion of ACTH - The overall effects of the changes in growth hormone, glucagon, and insulin are, like those of cortisol and epinephrine, to mobilize energy stores - The sympathetic nervous system plays a key role in the stress response - Activation of the sympathetic nervous system during stress is termed the fight-or-flight response Actions of the sympathetic nervous system, including epinephrine secreted by the adrenal medulla, during stress: - increased hepatic and muscle glycogenolysis (provides a quick source of glucose) - Increased breakdown of adipose tissue triglyceride (provides a supply of glycerol for gluconeogenesis and of fatty acids for oxidation) - Increased cardiac function (increased heart rate) - Diversion of blood from viscera to skeletal muscles by means of vasoconstriction in the former beds and vasodilation in the latter - Increased lung ventilation by stimulating brain breathing centres and dilating airways The Endocrine System ENDOCRINOLOGY 2 – THE PANCREAS Source of blood glucose: - The hydrolysis of glycogen stores to monomers of glucose 6- phosphate, occurs in the liver and skeletal muscle - In the liver, glucose 6-phosphate is enzymatically converted to glucose, which then enters the blood - It is the first line of defence in maintaining the plasma glucose concentration - Glycogenolysis also occurs in skeletal muscle, which contains approximately the same amount of glycogen as the liver - Muscles lack the enzyme necessary to form glucose from the glucose 6-phosphate formed during glyconeolysis; therefore, muscle glycogen is not a source of blood glucose - Instead, the glucose 6-phosphate undergoes glycolysis within muscle to yield ATP, pyruvate and lactate - The ATP and pyruvate are used directly by the muscle cell - Some of the lactate, however, enters the blood, circulates to the liver, and is converted into glucose, which can then leave the liver cells to enter the blood - Therefore, muscle glycogen contributes to the blood glucose indirectly via the liver - Synthesis of glucose from such precursors as amino acids and glycerol is known as gluconeogenesis – that is ‘creation of new glucose’ - The kidneys also perform gluconeogenesis, particularly during a prolonged fast Summary of nutrient metabolism during the post-absorptive period: - Glycogen, fat, and protein are curtailed, and net breakdown occurs - Glucose is formed in the liver both from the glycogen stored there and by gluconeogenesis from the blood-borne lactate, pyruvate, glycerol, and amino acids. The kidneys also perform gluconeogenesis during a prolonged fast - The glucose produced in the liver (and kidneys) is released into the blood, but its utilization for energy is greatly reduced in muscle and other nonneural tissues - Lipolysis released adipose tissue fatty acids into the blood, and the oxidation of these fatty acids by most cells and of ketones produced from them by the liver provides most of the body’s energy supply - The brain continues to use glucose but also starts using ketones as they build up in the blood Feasting to fasting hormones: - The two most important controls of these transitions from feasting to fasting are two pancreatic hormones – insulin and glucagon - Also playing a role are the adrenal glands and the sympathetic nerves to liver and adipose tissue - Insulin and glucagon are peptide hormones secreted by the islets of Langerhans, clusters of endocrine cells in the pancreas - The beta cells are the source of insulin - The alpha cells are the source of glucagon - One such molecule is somatostatin, secreted by cells called delta cells - Pancreatic somatostatin is the same peptide chemically as the hypothalamic somatostatin, which controls growth hormone secretion from the anterior pituitary glands Insulin: - The most important controller of organic metabolism - Its secretion – and, therefore, its plasma concentration – is increased during the absorptive state and decreased during the post absorptive state - The metabolic effects of insulin are exerted mainly on muscle cells (both cardiac and skeletal), adipose tissue cells, and liver cells - Like all peptide hormones, insulin induces its effects by binding to specific receptors on the plasma membrane of its target cells - This binding triggers signal transduction pathways that influence the plasma membrane transport proteins and intracellular enzymes of the target cells Control of insulin secretion: - The major controlling factor for insulin secretion is the plasma glucose concentration - An increase in plasma glucose concentration, as occurs after a meal, acts on the beta cells of the islets of Langerhans to stimulate insulin secretion, whereas a decrease in plasma glucose removes the stimulus for insulin secretion - Following a meal, the increase in plasma glucose concentration stimulates insulin secretion - The insulin stimulates the entry of glucose into muscle and adipose tissue, as well as net uptake rather than net output of glucose by the liver - These effects eventually reduce the blood concentration of glucose to its premeal level, thereby removing the stimulus for insulin secretion and causing it to return to its previous level - Increased amino acid concentrations stimulate insulin secretion. This is another negative feedback control; amino acid concentrations increase in the blood after ingestion of a protein-containing meal, and the increased plasma insulin stimulates the uptake of these amino acids by muscle and other cells, thereby lowering their concentrations - Incretins – secreted by endocrine cells in the GI tract in response to eating – amplify the insulin response to glucose - The actions of incretins provide a feedforward component to glucose regulation during the ingestion of a meal - Insulin secretion increases more than it would if plasma glucose were the only controller, thereby minimizing the absorptive peak in plasma glucose concentration - This mechanism minimizes the likelihood of large increases in plasma glucose after a meal, which among other things could exceed the capacity of the kidneys to completely reabsorb all of the glucose that appears in the filtrate in the renal nephrons - Decreases in incretins after absorption of a meal also allow insulin to decrease when plasma glucose is still above fasting levels; this prevents significant insulin-induced hypoglycemia after absorption of a meal - Input of the autonomic neurons to the islets of Langerhans, also influences insulin secretion - Activation of the parasympathetic neurons, which occurs during the ingestion of a meal, stimulates the secretion of insulin and constitutes a second type of feedforward regulation - Activation of the sympathetic neurons to the islets or an increase in the plasma concentration of epinephrine inhibits insulin secretion - Insulin plays the primary role in controlling the metabolic adjustments required for feasting or fasting - Other hormonal and neural factors, however, also play significant roles. They all oppose the action of insulin in one way or another and are known as glucose-counterregulatory controls Glucagon: - The major physiological effects of glucagon occur within the liver and oppose those of insulin - Thus, glucagon increases glycogen breakdown, increases gluconeogenesis, and increases the synthesis of ketones - The overall results are to increase the plasma concentrations of glucose and ketones, which are important for the postabsorptive period, and to prevent hypoglycemia - The major stimulus for glucagon secretion is a reduction in the circulating concentration of glucose (which also causes a reduction in insulin). - A decreasing plasma glucose concentration induces an increase in the secretion of glucagon into the blood, which, by its effects on the metabolism, serves to restore normal blood glucose concentration by glycogenolysis and gluconeogenesis - An increased plasma glucose concentration inhibits the secretion of glucagon, thereby helping to return the plasma glucose concentration toward normal - As a result, during the postabsorptive state, there is an increase in the glucagon/insulin ratio in the plasma, and this accounts almost entirely for the transition from the absorptive to the postabsorptive state - The secretion of glucagon, like that of insulin, is controlled not only by the plasma concentration of glucose and other nutrients but also by neural and hormonal inputs to the islets Epinephrine and sympathetic nerves to liver and adipose tissue: - Epinephrine and the sympathetic nerves to the pancreatic islets inhibit insulin secretion and stimulate glucagon secretion - Epinephrine also affects nutrient metabolism directly. Its major direct effects include stimulation of glycogenolysis in both the liver and skeletal muscle, gluconeogenesis in the liver, and lipolysis in adipocytes - Activation of the sympathetic nerves to the liver and adipose tissue elicits essentially the same responses from these organs as does circulating epinephrine - Low blood sugar leads to increases in both epinephrine in both epinephrine secretion and sympathetic nerve activity to the liver and adipose tissue - This is the same stimulus that leads to increased glucagon secretion, although the receptors and pathways are totally different - When the plasma glucose concentration decreases, glucose-sensitive cells in the CNS initiates the reflexes that lead to increased activity in the sympathetic pathways to the adrenal medulla, liver, and adipose tissue Cortisol: - The major glucocorticoid produced by the adrenal cortex, plays an essential permissive role in the adjustments to fasting - The plasma cortisol level does not need to increase much during fasting, but the presence of cortisol in the blood maintains the concentrations of the key liver and adipose tissue enzymes required for gluconeogenesis and lipolysis - Cortisol actually reduces the sensitivity of muscle and adipose cells to insulin, which helps to maintain plasma glucose levels during fasting, thereby providing a regular source of energy for the brain Growth hormone: - The primary physiological effects of growth hormone are to stimulate both growth and protein synthesis - Growth hormone renders adipocytes more responsive to lipolytic stimuli, increases gluconeogenesis by the liver, and reduces the ability of insulin to stimulate glucose uptake by muscle and adipose tissue Summary of hormonal controls: - Insulin’s secretion and plasma concentration are increased during the absorptive period and decreased during post-absorption - Glucagon and the sympathetic nervous system play a major role in prevent hypoglycemia - The rates of secretion of cortisol and growth hormone are not usually coupled to the absorptive post-absorptive pattern - Their presence in the blood at basal concentrations is necessary for normal adjustment of lipid and carbohydrate metabolism to the post- absorptive period, and excessive amounts of either hormone cause abnormally elevated plasma glucose concentrations Hypoglycemia: - Abnormally-low plasma glucose concentration - The plasma glucose concentration can decrease to very low values, usually during the post-absorptive state, in persons with several types of disorders - Fasting hypoglycemia include an excess of insulin due to an insulin- producing tumor, drugs that stimulate insulin secretion, or taking too much insulin; and a defect in one or more glucose counterregulatory controls Energy homeostasis in exercise and stress: - During exercise, large quantities of fuels must be mobilized to provide the energy required for muscle contraction. These include plasma glucose and fatty acids as well as the muscle’s own glycogen - The additional plasma glucose used during exercise is supplied by the liver, both by breakdown of its glycogen stores and by gluconeogenesis - Glycerol is made available to the liver by a large increase in adipose- tissue lipolysis, with a resultant release of glycerol and fatty acids into the blood, the fatty acids serving as an additional energy source for the exercising muscle - Glucose output by the liver increases approximately in proportion to increased glucose utilization during exercise, at least until the later stages of prolonged exercise when it begins to lag somewhat - Exercise is characterized by a decrease in insulin secretion and an increase in glucagon secretion, and the changes in the plasma concentrations of these two hormones are the major controls during exercise - In addition, activity of the sympathetic nervous system increases and cortisol and growth hormone secretion both increase as well - The increased sympathetic nervous system activity characteristic of exercise not only contributes directly to energy mobilization by acting on the liver and adipose tissue but contributes indirectly by inhibiting the secretion of insulin and stimulating that of glucagon - Glucose uptake and utilization by the muscles are increased, whereas during fasting they are markedly reduced - Even though exercising muscles require more glucose than do muscles at rest, less insulin is required to induce transport into muscle cells Digestion GASTROINTESTINAL TRACT (THE GUT): Functions of the GI tract: 1-. MOUTH: The GI tract begins at the mouth, where digestion starts with chewing, which breaks up large pieces of food into smaller particles 2. SALIVA: - Secreted by three pairs of salivary glands located in the head, drains into the mouth through a series of short ducts - Contains mucus, moistens and lubricates the food particles before swallowing - Also contains the enzyme, amylase, which partially digests polysaccharides - Dissolve some of the food molecules - Only in the dissolved state can these molecules react with chemoreceptors in the mouth, giving rise to the sensation of taste 3. PHARYNX & ESOPHAGUS: - They do not contribute to digestion but provide the pathway for ingested materials to reach the stomach - The muscles in the walls of these segments control swallowing 4. STOMACH: - Saclike organ between the esophagus and the small intestine - Store, dissolve, and partially digest the macromolecules in food and to regulate the rate at which the contents of the stomach empty into the small intestine - The glands lining the stomach wall secrete a strong acid, hydrochloric acid, and several protein-digesting enzymes, pepsin - A precursor of pepsin, pepsinogen, is secreted and converted to pepsin in the lumen of the stomach - The primary function of the HCl acid is to dissolve the particulate matter of food - The acidic environment in the gastric lumen alters the ionization of polar molecules, especially proteins, disrupting the extracellular network of connective-tissue proteins that form the structural framework of the tissues in the food - The proteins released by the dissolving action of HCl acid are partially digested in the stomach by pepsin - Polysaccharides and fat are major food components that are not dissolved to a significant extent by acid - HCl acid also kills most of the bacteria that enter along with the food. This process is not completely effective, and some bacteria survive to colonize and multiply in the GI tract, particularly in the large intestine - The digestive actions of the stomach reduce food particles to a solution, chyme, which contains molecular fragments of proteins and polysaccharides; droplets of fat; and salt, water and various other small molecules ingested in the food - None of these molecules, except water, can cross the epithelium of the gastric wall, and thus little absorption of organic nutrients occurs in the stomach 5. SMALL INTESTINE: - Most absorption and digestion occur here - Leads from the stomach to the large intestine - Hydrolytic enzymes in the small intestine break down molecules of intact or partially digested carbohydrates, fats, and proteins into monosaccharides, fatty acids, and amino acids - Some of these enzymes are on the luminal surface of the intestinal lining cells, whereas others are secreted by the pancreas and enter the intestinal lumen - The products of digestion are absorbed across the epithelial cells and enter the blood and/or lymph - Vitamins, minerals and water, which do not require enzymatic digestion, are also absorbed in the small intestine 6. LARGE INTESTINE: - Temporarily stores the undigested material and concentrates it by absorbing salts and water 7. RECTUM: - Contractions and relaxation of associated sphincter muscles expel the feces, defecation The small intestine: - Divided into 3 segments; an initial short segment, the duodenum, is followed by the jejunum and then by the longest segment, the ileum - Most of the chyme entering the stomach is digested and absorbed in the duodenum and jejunum - monosaccharides and amino acids are absorbed by specific transporter-mediated processes in the plasma membranes of the intestinal epithelial cells, whereas fatty acids enter these cells primarily by diffusion - Most mineral ions are actively absorbed by transporters, and water diffuses passively down osmotic gradients - The motility of the small intestine, brought about by the smooth muscles in its walls, mixes the luminal contents with the various secretions, brings the contents into contact with the epithelial surface where absorption takes place, and slowly advances the luminal material toward the large intestine Pancreas: - An elongated gland located behind the stomach - The exocrine portion of the pancreas secretes digestive enzymes and a fluid rich in HCO3- - The high acidity of the chyme coming from the stomach would inactivate the pancreatic enzymes in the small intestine if the acid were not neutralized by the HCO3- in the pancreatic fluid Liver: - A large organ located in the upper-right portion of the abdomen - Secretes bile Bile: - Contains HCO3-, cholesterol, phospholipids, bile pigments, a number of organic wastes, and bile salts - The HCO3-,
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