Metabolic Regulation and Tissue Metabolism

Liver: Serves anabolic and catabolic roles simultaneously. It regulates blood chemistry, specifically carbohydrate and amino acid levels, and is responsible for the synthesis of plasma proteins and the metabolism of excess amino acids or foreign molecules.
Adipose Tissue: Primary storage site for triacylglycerols (TAG). Under high energy conditions, fatty acid synthesis and the pentose phosphate pathway (for $NADPH$ ) are active.
- White Adipose: Energy storage.
- Brown Adipose: High mitochondrial content and blood flow; produces heat through proton uncoupling via thermogenin.
Skeletal Muscle: Highly dependent on oxygen; consumes $30\%$ of body $O_2$ at rest. It utilizes glucose during activity and fatty acids during rest. Muscle protein is degraded during fasting to conserve energy.
Cardiac Muscle: Requires a constant supply of oxygen and energy. It uses glucose and fatty acids when well-fed, shifting to fatty acids and ketone bodies at other times.
Brain: Accounts for $2\%$ of body mass but uses $20\%$ of total energy to maintain membrane potentials. It lacks glycogen stores, relying on glucose or ketone bodies (during starvation) and does not export nutrients.

Energy Stores: Adipose tissue contains the bulk of body energy; glycogen supplies only a small portion. Total expenditure is approximately $2400$ to $7200\,kcal/day$ .
Sprinting (100 m): High rate of energy expenditure ( $200\,kJ/minute$ ). Relies on anaerobic metabolism (phosphocreatine and glucose). Fatigue is caused by an increase in intracellular proton concentration ( $H^+$ ) that lowers $pH$ (rest: $7.1$ , post-exercise: $6.3$ ).
Marathon (42.2 km): Moderate rate of energy expenditure ( $84\,kJ/minute$ ). Relies on aerobic metabolism (glucose, fatty acids, glycogen, and triacylglycerols). Fatigue is caused by the depletion of muscle glycogen.

Feeding Phase: Regulated by gastrin, secretin, and cholecystokinin. Pancreatic $\beta$ -cells release insulin.
- Metabolic Effects: Stimulates glucose uptake via $GLUT4$ , increases glycogen synthesis ( $Glycogen\,synthase$ ), and promotes fatty acid synthesis ( $Acetyl-CoA\,carboxylase$ ).
Fasting Phase: Pancreatic $\alpha$ -cells release glucagon; overnight fasts trigger norepinephrine release.
- Metabolic Effects: Stimulates liver glycogen breakdown ( $Glycogen\,phosphorylase$ ), gluconeogenesis (from amino acids, glycerol, and oxaloacetate), and fatty acid mobilization ( $Hormone-sensitive\,lipase$ ).
Prolonged Fasting/Starvation: Blood glucose is sustained initially by muscle breakdown. In extreme starvation, the brain utilizes ketone bodies as an alternative fuel to reduce the rate of muscle wasting.

General Action: A glucocorticoid produced by the adrenal gland that induces long-term changes in enzyme levels.
Metabolic Impact: Increases blood glucose by stimulating muscle protein breakdown and triacylglycerol mobilization in adipose tissue.
Side Effects of Long-term Exposure: Leads to decreased muscle and bone mass and a significantly impaired immune response.

Threonine and Tyrosine: Academic exercises track the conversion of specific amino acids into glucose (gluconeogenesis), calculating the requirements or production of $ATP$ , $NADH$ , and $FADH_2$ based on mitochondrial yields.