Metabolism
- Glycogenolysis
- Lipolysis
- Gluconeogenesis (aa, glycerol)
- Lipogenesis
- Post-absorptive state- > 4 hrs meal
- Catabolic state
Goal : maintain blood glucose via
- glycogenolysis (liver, skeletal muscle)
- lipolysis (liver, adipose)
- Protein catabolism (skeletal muscle)
- Hormonal & Neural Control
- Glucagon (+ other hyperglycemic hormones)
- sympathetic (epinephrine)lipolysis,glycogenolysis
- Absorptive State (just after/during a meal)
- Insulin directs all events
- glucose uptake (carrier-mediated transport)
- increases AA uptake--> protein synthesis
- inhibits glucogenogenesis (liver)
- enhances triglyceride synthesis (favors an anabolic state)
- parasympathetic, GI hormones stimulate pancreas
- Protein metabolism- essential
- AA deaminated (NH2 removed)
- Urea formed (removes ammonia)
- makes plasma proteins, clotting
- CHO metabolism
- gluconeogenesis factors
- Fructose--> glucose
- glucose --> fats (storage)
- glycogenolysis
- Fat metabolism
- Beta oxidation (fats-->acetyl CoA)
- Lipoproteins (fat transport in blood)
- Makes cholesterol from acetyl CoA
- Liver- main source of VLDL
- cholesterol, Triglyceride insoluble so need carrier
- VLDL - mostly lipid
- released to blood, lipase breaks down
- converted to LDL (major cholesterol carrier)(85%, 15% made in intestine)
- liver can take up chylomicron, LDL
- HDL -transports cholesterol to liver to make bile salts
- hypothalamus (satiety/ hunger centers)
- various theories regarding hunger stimulation
- Glucostatic theory - neurons sensitive to glucose levels
- Lipostatic Theory - adipose tissue release substance (FA, Glycerol?) to depress hunger
- Thermostatic Theory
- hi temp depress feeding while low body temp stimulates feeding
- Hormonal influences:
insulin may suppress hunger
- CCK depress hunger (may also be released & bound in brain)
- psychological factors:
- stress
- sight of food
- eating disorders
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