Glucose and Lipid Metabolism

Glucose and Lipid Metabolism

• Hormonal Regulation: Insulin, glucagon, somatostatin, epinephrine, growth hormone, and cortisol all regulate glucose, protein, and fat metabolism. Gut hormones (GI hormones) and nutrients also play a crucial role.

Hormonal Effects

• Pancreas: Insulin promotes glucose and lipid storage; Glucagon promotes glucose production; Somatostatin inhibits insulin and glucagon; Amylin inhibits glucagon.
• Pituitary: Growth hormone increases glucose production.
• Adrenal: Epinephrine and cortisol increase glucose production.
• GI Tract: GLP-1, GIP, gastrin, secretin, and CCK alter insulin secretion.
• Adipose Tissue: Leptin, adiponectin, and resistin influence satiety, glucose levels, and insulin resistance.
• Thyroid: T3 and T4 regulate metabolism and metabolic rate.

Metabolic Processes

• Glycogenesis: Formation of glycogen.
• Glycogenolysis: Breakdown of glycogen.
• Glycolysis: Breakdown of glucose to pyruvate or lactate.
• Gluconeogenesis: Synthesis of glucose from non-carbohydrate sources (e.g., lactate, glycerol, amino acids).
• Adipogenesis: Differentiation of pre-adipocytes into adipocytes (fat cells).
• Lipogenesis: Synthesis of fatty acids from acetyl-CoA.
• Lipolysis: Breakdown of fats into fatty acids.

Anabolic vs. Catabolic Hormones

• Anabolic Hormones: Insulin and growth hormone (especially for protein) build storage molecules (protein, fat, glycogen).
• Catabolic Hormones: Glucagon, epinephrine, and cortisol break down larger molecules to release glucose for energy.

Insulin Synthesis and Release

• Insulin is synthesized as proinsulin, processed into insulin and C-peptide.
• C-peptide is a marker for insulin secretion level (1:1 ratio).
• Released in response to increased blood glucose.
• Insulin is a peptide hormone and not a steroid hormone.

Insulin Action Mechanisms

• Rapid Actions: GLUT4 translocation, potassium uptake.
• Intermediate Actions: Protein synthesis, glycolysis activation, glycogen synthesis stimulation.
• Slow Actions: Inhibition of phosphorylase and gluconeogenic enzymes; increased mRNA for lipogenic enzymes.
• Insulin activates PI3 kinase, which causes GLUT4 translocation to the cell membrane for glucose uptake.

Insulin's Effects on Different Organs

• Liver: Increases glucose uptake, glycolysis, glycogen synthesis, lipid synthesis, and protein synthesis.
• Fat Tissue: Increases triglyceride synthesis (storage).
• Skeletal Muscle: Increases protein synthesis, glucose uptake, glycogen synthesis, decreases protein breakdown and gluconeogenesis.

Glucose Stimulated Insulin Secretion

• Glucose enters beta cells via GLUT-2, metabolized, producing ATP, inhibiting potassium channels, causing depolarization, calcium influx triggering insulin release.

Factors Affecting Insulin Secretion

• Stimulators: Glucose, amino acids, beta-keto acids, glucagon, acetylcholine, GIP, GLP-1, secretin, CCK, and beta-adrenergic stimulators.
• Inhibitors: Low potassium concentration, somatostatin, galanin, epinephrine, norepinephrine.

GI Hormones (Gut Hormones)

• GIP (Gastric Inhibitory Peptide): Released by K cells in response to fat and glucose; increases insulin secretion in the presence of glucose.
• GLP-1 (Glucagon-like peptide 1): Released by L cells; increases insulin secretion, reduces glucagon secretion, slows gastric emptying.
• Both GLP-1 and GIP promote beta-cell proliferation and have protective effects.

Cortisol Effects and Aging

• Excess/Deficiency: Can impact cardiovascular health and glucose homeostasis.
• Reduced Growth Hormone with Aging: Affects metabolism.

Meal, Fasting, and Hormone Regulation

• Hormone levels and effects change during meals, between meals, and during fasting, impacting metabolism dynamically.