PHIS 206 1st EditionLecture 34Outline of Last Lecture I. Adrenal GlandsII. Adrenal CortexIII. GlucocorticoidsIV. Function of AldosteroneV. CortisolVI. Sex Hormones―Dehydroepiandrosterone VII. Hypersecretion of AldosteroneVIII. Hypersecretion of GlucocorticoidsIX. DHEA HypersecretionX. ControlXI. Hyposecretion in Adrenal CortexXII. Adrenal MedullaXIII. Effects of Epinephrine + Norepinephrine in CirculationXIV. Disorder of Catecholamine-Secreting TumorOutline of Current Lecture I. DiagramII. Metabolism in the BrainIII. Hormones that are Major Players in Determining which StateIV. InsulinV. Diabetes MellitusVI. Glucagon VII. Fed v. Fasting StateCurrent LectureI. Diagram-Sugars Glycogen (liver + muscles; extremely limited) ↑↓ -Amino Acids Protein (storage is muscle mass) ↑↓ -Fatty Acids Fat (no limit to storage) ↑↓ II. Metabolism in the Brain-can only use glucose-blood glucose levels have to be regulated These 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. Normal plasma glucose levels: 1 mg/mL 100 mg/mL 100 mg/dL 100mg %-how to regulate use fats as fuels use other tissues-normal day: oscillate b/w 2 metabolic states1. absorptive: fed state (pouring nutrients from gut) metabolically take glucose to store as fat + glycogen2. post-absorptive: fasting state most cells use fat as fuels; break glycogen down to maintain plasma glucose levels-absorptive state: glucose as fuel; synthesize glycogen; glucose uptake increases-post-absorptive state: fatty acids as fuel; glycogen breakdown; glucose uptake decreasesIII. Hormones that are Major Players in Determining which State-insulin: secreted by beta cells-glucagon: secreted by alpha cells-insulin: maintains absorptive state-glucagon: maintains post-absorptive stateIV. Insulin-most important effect: promotes glucose intake by every cell; promotes storage and conversion of glucose into glucagon in liver and muscles-promotes fatty acids and amino acids to proteins and fats-reduces plasma glucose levels: net effect glucose out of plasma + into storage-when absorbing nutrients, liver gets it 1st and gets it in higher concentrations since the nutrients have not reached the general circulation yet-major stimulus: increased plasma levels-insulin secretion largely a direct response to elevated glucose levels in plasma so liver sees elevated insulin levels tooo in return, it increases rate of storing and reduces plasma glucose levels-neural influences sympathetic: decreases plasma glucose levels (increases insulin secretion) parasympathetic: increases plasma glucose levels by inhibiting insulin secretionV. Diabetes Mellitus-most common endocrine disorder-“diabetes” : large volume of urine-“mellitus”: honeylike-urine has lots of glucose b/c when plasma glucose levels get high enough, amount exceeds how much kidneys can absorb once 3 times above normal glucose in urine-2 Types of Diabetes Mellitus Type I: insulin deficiencyo unable to produce insulin Type II: insulin receptors in inadequate #so reduced responsiveness but normal secretion- Diabetes mellitus: “starvation in the midst of plenty” high metabolized nutrients but unable to get into cells- inadequate insulin or defective receptors hyperglycemia: glucose output from liver accelerates and plasma glucose increases glucose intake from cells diminishes proteins broken down in addition to hyperglycemiao muscle weakness, decrease in muscle mass rate of losing fluid at advanced rate: results in always being thirsty o drinks more fluid but does not compensate fluid levelso loss of plasma volume, decreased arterial pressure poor wound healing b/c arterial pressure decreased possible kidney failure b/c intracellular glucose decreases, feels hungry, eats a lot increased appetite + food intake but cannot bring food into cellso so lose weight obesity predisposes diabeteso diabetes consequence of obesity diabetics metabolize fat instead of glucose, so different end productso ketones: “sweetish” breathe has a ketone odoro organic acids reduced so become acidonic diabetic coma: result of acidosis Type I: treated w/ insulin since they don’t make insulin Type II: inadequate receptors; treated with pharmaceuticals that make receptors responsiveVI. Glucagon -stimulated by sympathetic + inhibited by parasympathetic-stimulated by low plasma glucose-decreases storage of glucose as glycogen-opposite of insulin-no common disorders relatedVII. Fed v. Fasting State-depends on ratio of insulin and glucagon-Fed state: insulin
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