INTEGRATION OF METABOLISM

Well Fed State:

Glucose is the source of energy for the brain

AA to liver for protein

Excess AA used for energy - trans- and de-amination (­ urea synthesis)

Fats go to adipose tissue

CHO for NADPH production

Starvation:

Nothing coming for the diet

Sources of nutrients:

Fat (stored in adipose tissue)

Glycogen (liver & muscle)

Brain uses glucose, but not muscle

Early starvation, muscle uses ketone (FA, but limited number available)

Can only break down so much protein - only 25-30% of muscle an be broken down.

Brain can be eventually forced to used ketone bodies for energy 

 

Hormones

Insulin: Polypeptide (51 AA) - produced by b cells of Islets of Langerhans in Pancreas. Anabolic (synthesize glycogen, triglycerides, protein)

Regulation: of secretion (what stimulates secretion)

1. High blood glucose (hyperglycemia) after a meal

2. High blood amino acids after a meal

 

Metabolic effects - due to binding to receptors in liver, muscle, adipose tissue.

1. CHO Metabolism - Prevent hyperglycemia by ¯ blood glucose

a. Increase glucose transport into adipose and muscle cells

b. Increase glycolysis (glucose ® acetyl-CoA)

c. Decrease gluconeogenesis in the liver

d. Increase glycogen synthesis in liver and muscle

2. Lipid Metabolism Promotes lipogensis (triglyceride synthesis in adipose tissue)

a. Increase fatty acid synthesis: 1) Acetyl-CoA from glucose (glycolysis); 2) NADPH from glucose

b. Increase triglyceride synthesis

c. Increase triglyceride storage in adipose tissue

 3. Amino Acid Metabolism Reduce blood AA increasing synthesis

a. Increase entry of AA to liver and muscle cells

b. Increase protein synthesis

c. Increase degradation of surplus AA

d. ­ Urea cycle activity

Glucagon: Polypeptide (29 AA) produced by a cells of Islets of Langerhans in Pancreas. Catabolic - favors breakdown of glygogen in liver, mobilization of fatty acids, protein degradation, and gluconeogenesis (oppose the action of insulin)

Regulation: - Low blood glucose (hypoglycemia) after overnight or prolonged fast.

Metabolic Effects - due to binding to receptors in liver & adipose tissue ONLY!!

1. CHO Metabolism - Prevent hypoglycemia by ­ mobilization and synthesis of glucose

a. Increase glycogen breakdown in liver (NOT muscle = no receptors)

b. Increase gluconeogenesis by activating key gluconeogenic enzymes

2. Lipid Metabolism - promotes lipolysis (breakdown)

a. Increase triglyceride breakdown - release free FA

b. Increase mobilization of FA and uptake by the liver

c. Increase b -oxidationin liver - ­ Acetyl-CoA

d. Increase ketone body formation

3. Amino Acid Metabolism - lowers AA concentration in the blood

a. Increase uptake of AA by the liver for gluconeogenesis

b. Other hormones (cortisol) ­ degradation of muscle protein, release AA into blood