IPHY 4440 1st Edition Lecture 25Outline of Last Lecture II. Lipid MetabolismIII. Lipid transport IV. Lipoprotein structureV. Lipoprotein function VI. Fate of TAG and cholesterolVII. Protein MetabolismOutline of Current Lecture VIII. The endocrine pancreas IX. Adrenal MedullaX. Adrenal CortexXI. Thyroid Gland and GonadXII. DiabetesXIII. Appetite Resistance Interactions of hormones on metabolismCurrent LectureI. The endocrine pancreas A. Glucagon: produced by the alpha cell- Hyperglycemic Glycogenolytic (liver) (+) phosphorylase a- Lipolytic adipose (+) hormone depending lipase - Gluconeogenic (+) PEPCK elevates blood glucoseB. Main targets for glucagon: adipose and liver…NOT muscle II. Adrenal MedullaEpinephrine Hyperglycemic- Glycogenolytic increase phosphorylase a- Occurs IN liver and muscle A. Pituitary - GH hyperglycemic and lipolytic (+) HDL increase NEFAs for gluconeogenesis B. Protein anabolic AA to proteinThese 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.- GH not gluconeogenic from AA- Other actions blocked by insulin III. Adrenal CortexGlucocorticoids hyperglycemic, prevent glucose uptake but NOT in CNS1) Lipolytic: permissive, enhance actions of E, GH, and glucagon 2) Anti-protein anabolic: skeletal muscle increase protein catabolism and decrease protein synthesis “protein catabolic”3) Gluconeogenic: AA Liver; NEFAs liver; (+) PEPCK in LiverIV. Thyroid Gland and GonadA. Thyroid Hormones: permissive actions TH actions on metabolism depend on other hormones and are not direct effects THs increase metabolic rateC. Gonads: androgens protein anabolic, androgenic anabolic steroidsInduce liver cancer to decrease reproduction V. DiabetesA. Type 1 diabetes mellitus: juvenile onset, insulin-dependent (IDDM), ketosiscommon, autoimmune disease, small % may be due to infection all due to insulin shortage ketone bodies accumulate acidosis coma deathB. Type 2 most common type, maturity onset, non-insulin dependent (NIDDM), ketosis uncommon, related to obesity, genetic component all due to insulin resistance cardiovascular diseasesVI. Appetite Resistance A. Orexic factors: ghrelin discovery ghrelin binds to “orphan” receptor (GHS-R 1a) stimulates GH secretion- Ghrelin secreted by stomach endocrine cells and has positive effect on GH release, food intake, and insulin release but inhibitory effect on gastric emptying- Orexin A & B (hypocretins -1, -2) hypo= hypothalamus and cretin= secretin and orex= appetite B. Anorexic factors: leptin 167 AA lipostatic theory that body weight maintained by regulating body fat content- Product of obese mouse gene and produced by adipose cells suppresses appetite Leptin is very potent because of its many sites of action on
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