Insulin and Glucagon: Glucose Regulation

Insulin Secretion Control

• Triggered by elevated blood glucose levels, facilitating glucose transport into cells.
• Glucagon secretion decreases with elevated blood glucose, preventing excessive insulin release.

Actions of Insulin on Glucose

• Increases glucose transport into skeletal muscle and adipose tissue.
• Promotes glycogen synthesis.
• Decreases gluconeogenesis.

Actions of Glucagon on Glucose

• Promotes glycogen breakdown.
• Increases gluconeogenesis.

Actions of Insulin on Protein

• Enhances active transport of amino acids into cells.
• Increases protein synthesis.
• Decreases protein breakdown, improving glucose and fatty acid utilization as fuel.

Actions of Glucagon on Proteins

• Increases amino acid transport into hepatic cells.
• Increases breakdown of proteins into amino acids for gluconeogenesis.
• Increases conversion of amino acids into glucose precursors.

Other Hormones Affecting Blood Glucose

• Catecholamines (epinephrine and norepinephrine) from the adrenal cortex and locus coeruleus increase glucose levels, aiding maintenance during stress.
• Glucocorticoids increase glucose, critical for survival during fasting and starvation, and stimulate hepatic gluconeogenesis.
• Growth hormone increases glucose, promotes protein synthesis, mobilizes fatty acids from adipose tissue, and antagonizes insulin effects.

Diabetes Mellitus

• A metabolic disorder affecting carbohydrate, protein, and fat metabolism.
• Results from an imbalance between insulin availability and need.
• Body cells may not respond to insulin or there may be insufficient insulin production.
• Cells are starved for fuel, leading to alternative fuel sources.

Potential Representations of Diabetes

• Absolute insulin deficiency.
• Impaired insulin release.
• Inadequate or defective insulin receptors.
• Production of inactive or destroyed insulin.

Causes of Beta Cell Dysfunction in Diabetes

• Initial decrease in beta cell mass.
• Decreased insulin production.
• Increased beta cell apoptosis or decreased regeneration.
• Long-standing insulin resistance leading to beta cell exhaustion.
• Chronic hyperglycemia (glucotoxicity) can induce beta cell desensitization.
• Chronic elevation of free fatty acids (lipotoxicity) can cause toxicity to beta cells.
• Amyloid deposition in beta cells can cause dysfunction.

Types of Diabetes

• Type 1 involves loss of beta cell function, resulting in an absolute insulin deficiency requiring lifelong insulin administration.
  • Causes are often unknown, autoimmune destruction of beta cells is likely.
  • Typically diagnosed from childhood to early adulthood.
• Type 2 involves impaired ability of tissues to use insulin, a relative lack of insulin, or impaired insulin release relative to blood glucose levels.
  • Increasingly diagnosed in children due to obesity.

"Sweet Diabetes" (Three Polys)

• Polydipsia: Increased thirst due to high blood glucose levels.
• Polyuria: Increased urine output via osmotic diuresis as kidneys struggle with high glucose levels, pulling water toward glucose.
• Polyphagia: Increased appetite due to body cells being starved for fuel.

Diabetes Symptoms

• Abrupt weight loss.
• Fatigue.
• Paresthesias.
• Recurrent blurred vision.
• Easy injury.
• Skin infections.

Type 1 Diabetes Management

• Nutrition therapy.
• Exercise/weight control.
• Glucose monitoring (frequent, at least 4x/day, before meals and at bedtime - ACHS).
• Healthcare provider follow-up.
• Insulin/insulin pump/pancreatic transplant.
• Includes short-acting, intermediate-acting, and long-acting options.

Explore the roles of insulin and glucagon in blood glucose control. Learn how insulin manages glucose transport, glycogen synthesis, and protein metabolism. Understand glucagon's impact on glycogen breakdown, gluconeogenesis, and amino acid conversion.