59. Hormonal Regulation of Metabolism in the Fed and Fasting State. Biochemical Mechanisms of Fasting, Starvation and Stress Starvation. Malnutrition.

Hormonal Regulation of Metabolism in the Fed State

• Occurs after a meal; blood glucose, amino acids, and triglycerides are elevated.
• Main hormone: Insulin
• Secreted by β-cells of the pancreas in response to high glucose.
• Stimulates glucose uptake in insulin-dependent tissues (muscle, adipose).
• Activates glycogenesis in liver and muscle.
• Promotes lipogenesis in liver and adipose tissue.
• Stimulates protein synthesis in muscle; inhibits proteolysis.
• Suppression of catabolic hormones:
• Glucagon, cortisol, and catecholamines are low.
• Glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis are inhibited.

Hormonal Regulation of Metabolism in the Fasting State

• Begins 4–6 hours after a meal; glucose starts to fall.
• Hormonal changes:
• Insulin decreases → reduced glucose uptake in muscle and adipose.
• Glucagon increases → stimulates glycogenolysis and gluconeogenesis in liver.
• Epinephrine → activates glycogenolysis and lipolysis in muscle/adipose tissue.
• Metabolic changes:
• Liver: glycogen → glucose; amino acids → gluconeogenesis; fatty acids → ketone bodies.
• Muscle: protein catabolism releases amino acids.
• Adipose: triglycerides → free fatty acids and glycerol (for energy and gluconeogenesis).

Biochemical Mechanisms of Starvation

• Prolonged fasting (>24–48 hours); glycogen stores are depleted.
• Hormones:
• Low insulin
• High glucagon, cortisol, and catecholamines
• Metabolic adaptations:
• Gluconeogenesis becomes the main source of glucose.
• Fatty acid oxidation increases → liver produces ketone bodies (acetoacetate, β-hydroxybutyrate) for brain and muscle energy.
• Protein sparing: after 3–5 days, ketones are used by brain → reduces need for muscle protein breakdown.
• Nitrogen balance:
• Initially negative due to amino acid catabolism.
• Later partially restored due to adaptation and increased ketone utilization.