lecture 12: homeostasis and disorders of metabolism

- maintain fuel supply for cellular respiration to all cells regardless of metabolic state
- maintaining blood glucose concentration within normal range
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- ingested glucose is taken up by cells to be used as fuel for cellular resp.
- excess glucose is taken up and stored as glycogen (glycogenesis) in liver and muscle and excess converted into fat (lipogenesis) in adipose tissue and liver
- amino acids from protein digestion are taken up for protein synthesis. excess used as fuel for cellular resp. or lipogenesis
once in blood, insulin binds to its receptor on target cells and stimulates uptake, utilization, and storage of glucose by activating metabolic pathwayswhat is the insulins mechanism of action?facilitates entry of glucose into cardiac and skeletal muscle cells and adipocytes by stimulating insertion of GLUT-4 into membranesinsulin facilitates entry of glucose into what, by insertion of glucose transport proteins called what?- it is a protein transporter present in cytoplasmic vesicles, where the incapable of transporting glucose - binding of insulin to receptors on such cells leads rapidly to fusion of those vesicles with membrane and insertion of transporters, thereby giving the cell ability to efficiently take up glucose - when blood levels of insulin decrease and insulin receptors are no longer occupied, the transporters are recycled back into cytoplasmwhat are GLUT-4?1. increased glucose (stimulate) - a major stimulus for insulin release is plasma glucose concentration greater 5.5 mmol/L 2. increased amino acid (stimulate) - increased plasma amino acids following a meal also trigger insulin secretion 3. feed-forward effects of GI hormones 4. parasympathetic activity (stimulate) 5. sympathetic activity (inhibit)what 5 factors may stimulate, amplify or inhibit insulin secretion?incretin hormones produced by enteroendocrine cells in small intestine are released when glucose is present in intestinal lumen. - these hormones stimulate insulin secretion by the beta cells in pancreas before blood glucose levels risewhat is the feed- forward effects of GI hormones?parasympathetic stimulation of the GI tract and pancreas increases during and following a meal. - the input to beta cells also stimulates insulin secretionwhat is the parasympathetic influence?- insulin secretion is inhibited directly by sympathetic neurons in times of stress or physical exertion - this is reinforced by hormones released from the adrenal medulla, epinephrine and norepinephrine - metabolic drive switches to mobilizing energy stores. lipolysis and glycogenolysis dominatewhat is the sympathetic influence?in fasted state, blood glucose declines, this triggers release from alpha cellswhat is glucagon?- stimulates glycogenolysis and gluconeogenesis in liver - stimulates lipolysis in adipose tissue - fatty acids released by lipolysis will be used by body cells as an alternative fuel for cellular resp. leaving glucose available for the brain (glucose sparing)what 3 events are triggered with release of glucagon?- primary stimulus for glucagon secretion is falling blood glucose levels - sympathetic nervous system stimulation promotes glucagon release to liberate glucose for fight or flight - insulin inhibits the effects of glucagonwhat are 3 factors influencing glucagon secretion?abnormally elevated plasma glucose concentrations (hyperglycemia) resulting from inadequate insulin secretion or abnormal target cell responsivenesswhat is diabetes mellitus?- insulin deficiency resulting from beta cell destruction - quick onset (days to weeks) - acute severe symptomswhat is type 1 diabetes?- body cells become resistant to insulin (even when present in normal or even elevated amounts) - gradual onset (years) - symptoms more moderate and long to developwhat is type 2 diabetes?autoimmune disease in which the body fails to recognize the beta cells as "self" and destroys them with antibodies and white blood cells - with no beta cells present, insulin is no longer madediabetes type 1 is commonly known as an?- following a meal, nutrient absorption by intestines proceeds normally (not insulin independent). the blood becomes full of nutrients from digestion - nutrient uptake from blood and metabolism by liver, skeletal muscle, adipose tissue and many other tissue are insulin dependent - metabolic pathways stimulated by insulin do not occurhow does post-absorptive state dominates in untreated type 1 diabetics?- without glucose for energy and amino acid for protein synthesis, muscle break down their contractile proteins to provide a substrate for ATP production. amino acids also leave the muscles and are transported to liver - fat stores are broken down (lipolysis). fatty acids and glycerol enter blood for transport to liverhow does skeletal muscle and adipose tissue work with glucose?- glycogenolysis and gluconeogenesis dominate - glycogen stores are broken down - amino acids from protein hydrolysis and glycerol from lipolysis will be used to make new molecules of glucose - both processed contribute more glucose into the blood worsening hyperglycemiawhat happens in the liver?by B-oxidative and converted into acetyl-CoA - because hepatocytes are preoccupied with gluconeogenesis, acetyl-CoA is converted into ketone bodies and released into bloodhow are fatty acids from lipolysis broken down?1. increased appetite and consumption of food (polyphagia) 2. hyperglycemia and lipidemia - glucosuria - increased urine output (polyuria) - increased thirst (polydipsia) 3. metabolic acidosis - ketonemia and ketonuria - acetone breathe - kidney compensation - respiratory compensationwhat are 3 symptoms of type 1 diabetes?- most neurons in brain are not insulin dependent and carry out metabolism, but certain neurons in the hypothalamus which govern our sense of hunger versus satiety are insulin dependent - in the absence of insulin these cells promote feelings of hunger - this results in polyphagia (excessive eating)how does insulin control hunger in our brain?eating sugary food may increase blood glucose levels for short period of time, but untreated diabetes causes chronic hyperglycemiahow is hyperglycemia and lipidemia different for untreated diabetics?- osmotic diuresis - plasma glucose exceeds the renal threshold for glucose reabsorption in proximal tubules of kidneys - consequently, some filtered glucose is not reabsorbed, and it is excreted in the urine (glucosuria) - osmotic diuresis results as extra solute in collecting duct lumen prevents water reabsorption - this creates large volumes of urine (polyuria) and if unchecked dehydrationwhat is polyuria caused by?- dehydration leads to decreased blood volume and decreased blood pressurewhat can dehydration lead to?- secretion of ADH (attempting to increase water reabsorption in collecting ducts - thirst that causes constant drinking (polydipsia)what is the 2 homeostatic mechanisms for maintaining blood pressure?- ketone bodies (primary cause) - anaerobic metabolic occurring in muscle (secondary cause)what are 2 potential sources of metabolic acidosis?when blood pH is low due to ketoacidosis, the kidneys will attempt to compensate by - excreting ketone bodies - excreting H+ - reabsorbing and producing bicarbonate ionswhat is the renal compensation?- peripheral and central chemoreceptors respond to increases in H+ in arterial blood. they transmit stimulatory impulses to the respiratory centers in the medulla oblongata: respiratory rate and depth increase - drop in pCO2 results, but left in untreated, a diabetic will continue to have reduced blood pH due to ketone body productionwhat is the respiratory compensation?- broad spectrum immunosuppressants to slow B cell destruction - insulin injectionswhat are the treatment options for type 1?false: often goes undetected until secondary health issues resulttrue or false: diabetes type 2 is always recognized right away?- primary treatment for most type 2 and those at high risk for developing: weight loss through dietary changes and exercisewhat are the treatment options for type 2?it decreases hyperglycemia and lipidemia because exercising skeletal muscles does not require insulin for glucose uptakehow does exercise help with hyperglycemia?1. stimulate beta cells secretion of insulin 2. slow the digestion or absorption carbohydrates in the intestine 3. inhibit hepatic glucose output 4. make target tissues more responsive to insulinwhat are 4 things drugs used to treat type 2 diabetes may do?