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Lecture

HORMONAL REGULATOIN

5 Pages
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Department
Biology
Course Code
BIOLOGY 2D03
Professor
Laura Parker

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Description
HORMONAL REGULATOIN OF BLOOD GLUCOSE Normal Levels: 5mM (80 mg/dL) fatty acids cannot cross blood-brain barrier (brain can only use ketones and glucose) RBC’s are totally dependent upon glucose for energy (no mitochondria) hypoglycemia: leads to fatigue, death hyperglycemia: dehydradion, tissue damage, protein glycosylation 4 sytems involved in glucose regulation: pancreas/intestive liver fat muscle Blood glucose levels are kept relatively constant (highly regulated) throughout day 1) FED STATE (up to 2 hours after a meal) 1. insulin released by pancrease 2. glucose to liver 3. some stored as glycogen, rest sent into bloodstream 4. glucose in fat cells is stored as TG’s 2) 4 hours after eating 1. GLUCAGON now released from pancreas 2. liver begins to breakdown glycogen 3. fat cells do not take up glucose, nor do they release it yet 3) FASTING (24 hours after eating) 1. more glucagon released fatty acid release (can be used in B-oxidation in muscle) FA  ketone bodies (for use in brain and muscle) 2. GLUCOCORTICOID release also ketogenesis neoglucogenesis (muscle protein  glucose for brain) 4) FASTING (3+ days) HGH: upregulation of ketogenesis (FA  KB  brain); spares muscle tiss. fatty acids for muscle (all KB’s sent to brain) muscle breakdown for brain glucose EPINEPHRINE made/secreted in CHROMAFFIN cells of adrenal medulla GLUCOCORTICOID made/secreted in adrenal CORTEX in response to CRH (corticotropin release hormone) from hypothalamus (affected by hyperglycemia, circadian rhythm, stress) stimulates gluconeogenesis muscle protein -> aa’s aa deamination (liver) fatty acid mobilization GROWTH HORMONE very sensitive to diet (triggered by HYPOglycemia) made and released from anterior pituitary **spares muscle protein during starvation ** - fatty acid mobilization - favors ketogenesis (liver/kidney) - saves glucose for brain and RBC’s PANCREATIC HORMONES GLUCAGON
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