PHIS 206 1st Edition Lecture 34 Outline of Last Lecture I Adrenal Glands II Adrenal Cortex III Glucocorticoids IV Function of Aldosterone V Cortisol VI Sex Hormones Dehydroepiandrosterone VII Hypersecretion of Aldosterone VIII Hypersecretion of Glucocorticoids IX DHEA Hypersecretion X Control XI Hyposecretion in Adrenal Cortex XII Adrenal Medulla XIII Effects of Epinephrine Norepinephrine in Circulation XIV Disorder of Catecholamine Secreting Tumor Outline of Current Lecture I Diagram II Metabolism in the Brain III Hormones that are Major Players in Determining which State IV Insulin V Diabetes Mellitus VI Glucagon VII Fed v Fasting State Current Lecture I II Diagram Sugars Amino Acids Fatty Acids Glycogen liver muscles extremely limited Protein storage is muscle mass Fat no limit to storage 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 states 1 absorptive fed state pouring nutrients from gut metabolically take glucose to store as fat glycogen 2 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 decreases III 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 state IV 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 too o 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 secretion V 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 deficiency o unable to produce insulin Type II insulin receptors in inadequate s o 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 hyperglycemia o 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 levels o 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 cells o so lose weight obesity predisposes diabetes o diabetes consequence of obesity diabetics metabolize fat instead of glucose so different end products o ketones sweetish breathe has a ketone odor o 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 responsive VI Glucagon stimulated by sympathetic inhibited by parasympathetic stimulated by low plasma glucose decreases storage of glucose as glycogen opposite of insulin no common disorders related VII Fed v Fasting State depends on ratio of insulin and glucagon Fed state insulin increases
View Full Document
Unlocking...