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Four Major Tissues in Fuel Metabolism
Liver
Adipose TIssue
Muscle
Brain
Communication Tissues is mediated by:
Nervous system
Availability of substrates
Variation of plasma hormone levels
Integration of metabolism is controlled primarily by 2 peptide hormones
Insulin and Glucagon
Insulin
Peptide hormone produced by BETA cells
Most IMPORTANT hormone containing use of fuels
ANABOLIC metabolic effects = glycogen TAGs proteins
2 polypeptide chains if composed of 51 AA link by short half bridges
Has short half life
Regulation of insulin
In testimony of carb rich meal —> Rise of glucose —> Primary stimulus of insulin secretion
Ingestion of Fatty acids and amino acids enhance glucose stimulated secretion of insulin
Ingestion of food —> Release of INCRETIN hormones from small intestine = increase sensitivity of beta cells to glucose
INCRETINS
Glucagon-like protein-1 (GLP-1)
Glucose-dependent insulinotropic peptide OR gastric-inhibitory polypeptide (GIP)
Decrease of Synthesis and Release of INSULIN
Scarce dietary fuels and during periods of STRESS (Infection, hypoxia, and vigorous excercise)
Catecholamine Hormones
Norepinephrine and Epinephrine
mediates the synthesis and release of dietary fuels
Cause RAPID MOBILIZATION
Glycogen Breakdown/Proudction
Lipolysis
Glycogen Breakdown
Type of rapid mobilization
Glucose from liver break down glycogen
Lipolysis
Type of rapid mobilization
Fatty acids from adipose tissue via LIPOLYSIS
METABOLIC EFFECTS OF INSULIN
PROMOTES the STORAGE of nutrients as Glycogen TAG and Protein and inhibits mobilization
Muscle and Adipose increase
Decrease in glycogenogenesis and Glyconeogenesis
Carb Metabolism in Insulin
Promote storage in liver muscle and adipose tissue
In Liver and Muscle —> Stored as Glycogen via Glycogen synthesis (Glycogenesis)
Lipid Metabolism Effects in Insulin
Reduction in fatty acid RELEASE by inhibiting LIPASE
Increases transport and metabolism of glucose into ADIPOCYTES → FAs added to glycerol → Increase in TAG
Protein Metabolism Effects in Insulin
Stimulated entry of AAs into cells and increase protein synthesis
Glucagon
Peptide Hormone secreted by ALPHA cells of islets of Langerhans of endocrine pancrease
Acts to maintain blood glucose levels through glycogenolysis and gluconeogenesis
Short half life
COUNTERREGULATORY HORMONES
Oppose many actions of insulin consists of:
Glucagon
Epinephrine
Norepinephrine
Cortisol
Growth Hormone
Glucagon Regulation: Increase
increased by Hypoglycemia, AAs, and catecholamines
Primary stimulus
Some amino acids (e.g. Arginine)
Adrenal Medulla = catecholamines
Glucagon Regulation: Decrease
Elevated blood glucose and insulin
Glucagon Metabolic effects
Glucagon is a Catabolic hormone
binds to G-protein coupled receptor —> Activation of adenylyl cyclase —> increase in cAMP —> Activates PKA
Carbohydrate mechanism in Glucagon
Immediate rise in blood glucose
Increase in breakdown of liver glycogen and increase in hepatic gluconeogenesis
Lipid Metabolism in Glucagon
Inhibition of fatty acid SYNTHESIS and increase in fatty acid OXIDATION
The MAJOR activators of lipase are the CATECHOLAMINES
Free FAs released are taken up by the liver → Oxidized to acetyl-CoA → Used in KETONE synthesis
Protein Metabolism in Glucagon
Increases uptake by the liver of AAs supplied by muscle → Increase in availability of carbon skeletons for gluconeogenesis
Plasma levels of AAs are decreased