Chapter 19 of Marks' Basic Medical Biochemistry: A Clinical Approach (5th Edition) explains how insulin, glucagon, and other hormones coordinate the regulation of fuel metabolism to maintain blood glucose homeostasis between 80–100 mg/dL. The chapter begins by emphasizing metabolic homeostasis—the balance between nutrient intake, oxidation, storage, and mobilization—which is achieved through nutrient concentrations in blood, hormonal signaling, and neural regulation. Insulin, secreted by pancreatic β-cells after carbohydrate ingestion, promotes anabolic processes: glucose uptake and storage as glycogen in liver and muscle, triacylglycerol synthesis and storage in adipose tissue, and protein synthesis in muscle and liver. Glucagon, secreted by α-cells during fasting, acts as the major fuel-mobilizing hormone by stimulating glycogenolysis, gluconeogenesis, and lipolysis, ensuring glucose and fatty acid availability. Counterregulatory hormones—including epinephrine, norepinephrine, and cortisol—oppose insulin to mobilize fuels during stress, fasting, and exercise. The chapter highlights clinical cases: Deborah S. with type 2 diabetes showing insulin resistance and hyperglycemia; Dianne A. with type 1 diabetes caused by autoimmune β-cell destruction; and Connie C. with insulinoma, presenting with hypoglycemia and neuroglycopenic symptoms. Signal transduction pathways differ: insulin acts via a receptor tyrosine kinase, IRS-1, and phosphorylation cascades to stimulate glucose transport, protein synthesis, and enzyme regulation, while glucagon acts through G-protein–coupled receptors, cAMP, and protein kinase A to phosphorylate key enzymes. Cortisol and thyroid hormone regulate gene expression through intracellular receptors, and catecholamines act via adrenergic receptors to enhance fuel mobilization in stress responses. Pathophysiologic states are explained: hyperglycemia causing osmotic diuresis, glycosylation of hemoglobin (HbA1c), and long-term diabetic complications (retinopathy, nephropathy, neuropathy, and cardiovascular disease). Hypoglycemia triggers adrenergic and neuroglycopenic symptoms, with epinephrine serving as a rapid emergency hormone. Rare conditions such as MODY (due to glucokinase mutations), neonatal diabetes (mutations in KCNJ11 or ABCC8), and insulinomas illustrate disruptions in insulin regulation. The chapter concludes that insulin and glucagon are the central regulators of metabolic homeostasis, with other hormones modulating their effects to balance storage and fuel mobilization for survival, growth, and adaptation.
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