EXSS 276 1st Edition Lecture 11 Outline of Last Lecture I. Hormone Regulation in Blood II. Hypothalamus and Pituitary Glands – Master GlandsIII. Targets and Functions of Pituitary HormonesIV. The Endocrine System: Stress, Metabolic, Water/Electrolyte Balance HormonesOutline of Current LectureI. Adrenal CortexII. Metabolic HormonesIII. Diabetes MellitusIV. Human Growth Hormone (hGH) and Insulin-like Growth Factors (IGF)Current LectureI. Adrenal Cortexa. Three zonesi. Middle layer – zona fasciculate = secretes glucocorticoidsb. Cortisoli. Most abundant of glucocorticoidsii. Secreted by adrenal cortex under control of hypothalamic-pituitary-axisiii. Stimuli for release:1. Emotional stress2. Physical stress/trauma3. Exercise4. Decreased blood glucose levelsiv. Metabolic effects:1. Breakdown of protein to amino acids in the muscle2. Hepatic gluconeogenesis3. Increased lipolysisv. Cardiovascular effects1. Increase blood vessel sensitivity to hormone induced vasoconstrictionvi. Immune system effects1. Inhibits WBC that participate in inflammatory responses2. Depresses other immune system responsesvii. Regulation of CortisolThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.1. Releasing hormone out of hypothalamus = corticotropin releasing hormone2. Pituitary releasing hormone = Adrenocorticotropin3. Stimulates adrenal cortex 4. Negative feedback loopviii. Medical Problems1. Cushing’s Syndromea. Hormonal disorder caused by prolonged exposure of body tissues to high levels of cortisolb. Mostly affects 20-50 year oldsc. Only 10-15 out of every million people affected (rare)d. Symptomsi. Upper body obesityii. Thin and fragile skin and fragile bonesiii. Weakness, fatigue, irritation, high blood glucose, high BPe. Treatmentsi. Taper doses of glucocorticoidsii. Removal of tumorsiii. Drugs in inhibit cortisol synthesis 2. Addison’s Disease – autoimmune disease a. Adrenal insufficiencyb. Opposite of Cushing’s c. Common symptoms:i. Chronic, worsening fatigueii. Muscle weaknessiii. Loss of appetiteiv. Weight lossv. Nausea, vomiting, diarrhea, low BP, irritability, depression, craving salty foods, hypoglycemia, headache, sweating, women-irregular periodsII. Metabolic Hormones: insulin, glucagon, growth hormone, thyroid and parathyroid hormonesa. Insulin: pancreatic beta cells (70%)b. Glucagon: pancreatic alpha cellsc. Physiological rolesi. Insulin1. Promotes glucose UPTAKE from blood to DECREASE blood glucosea. Increase uptake of amino acids and protein synthesisb. Increase glycogenesisc. Increase lipogenesisd. Decrease gluconeogenesise. Decrease glycogenolysisii. Glucagon1. Promotes RELEASE of glucose into blood to INCREASE blood glucosea. Increase glycogenolysisb. Increase gluconeogenesisc. Increase lipolysisiii. Stimulus for release: changes in blood glucose levels1. Low blood glucose stimulates release of glucagon2. High blood glucose stimulates release of insulind. Insulin-glucagoni. Blood glucose is affected by food we eatii. CHO in our food increases blood glucoseiii. Hormone levels in blood are constantly going up and down, changing to meet the need of more or less glucose in blood iv.v. High blood sugar stimulates beta cellsvi. Stimulates insulin to come into blood, take up glucose1. To get blood sugar levels lowere. Insulin: Anabolic Hormonei. Insulin promotes glucose uptake from bloodii. Also: amino acid uptake from blood1. Promotes protein synthesis2. Lipogenesis and glycogenesis3. Slows gluconeogenesis and glycogenolysis4. Important during youth/pubertyIII. Diabetes Mellitusa. Major medical problem in the USb. Estimated 17% of yearly health costs in US c. 26 million people have diabetesd. 79 million (1 in 3 Americans) have pre-diabetes (blood glucose levels high but notas high as diabetes levels)e. Affects young and oldi. One of fastest growing problems in US youthf. Major Typesi. Type I – Insulin Dependent DM1. Old name: Juvenile Onset2. Absolute deficiency of insulin3. Autoimmune disease, body destroys beta cellsii. Type II – Non-insulin Dependent DM1. Old name: Adult Onset2. Insulin produced, tissues insensitive, down-regulation of insulin receptors3. HISTORYa. As insulin resistance increases, blood glucose levels increases and insulin production decreases iii. Gestational DM1. DM that develops during pregnancy2. Usually goes away once baby is borniv. Physiological Effects1.v. Treatment Strategies1. Type I a. Insulin injection/treatmentb. Pancreatic beta-cell transplant2. Type IIa. May need insulinb. Diet modificationc. Weight lossi. Regular exerciseii. Caloric restrictionIV. Human Growth Hormone (hGH) and Insulin-like Growth Factors (IGF)a. hGH – most plentiful anterior pituitary hormoneb. Essential for normal growth during childhood and adolescencec. Promotes synthesis and secretion of small protein hormones called IGF’s i. IGF’s stimulate growth and regulate metabolismd. Major physiological effects of hGHi. Common target cells are liver, skeletal muscle, cartilage and boneii. Stimulation of growth:1. Increasing amino acid uptake and protein synthesis while decreasing breakdown of protein and amino acid use for ATP productioniii. Metabolic effects:1. Stimulate lipolysis, fatty acids used for ATP2. Spares use of glucose for ATP production, keeps blood glucose levels high enough to supply brainiv. Stimuli for release:1. Decreased glucose, fatty acid, and amino acid levels in blooda. Things we use for energy – when they are low, hGH activated2. Increased SNS activity, stress, exercise, other hormones a. Things that cause stress – increase hGH