Focus: Blood glucose regulation and diabetes treatment.
Reference: Chapter 31 for detailed study material.
Key Hormones: Control blood glucose levels.
Insulin: Lowers blood glucose.
Released by pancreas after meals.
Facilitates glucose uptake in cells and stores as glycogen in liver and muscles.
Inhibits glucose production and promotes fat/protein storage.
Glucagon: Raises blood glucose.
Released during fasting to stimulate glycogen breakdown and gluconeogenesis.
Epinephrine (Adrenaline): Mobilizes glucose during stress.
Cortisol: Increases glucose levels under prolonged stress.
Growth Hormone: Reduces glucose uptake and promotes fat breakdown.
Binding to Receptors:
Insulin binds to insulin receptors on target cells (muscle/fat).
Triggers signaling cascade leading to increased glucose transport into cells (via GLUT4).
Immediate Effects:
Increased glucose uptake.
Stimulates glycogen synthesis and inhibits gluconeogenesis.
Long-term Actions:
Affects gene expression and intermediary metabolism through the Ras-MAP kinase pathway.
Secreted by alpha cells in the pancreas during hypoglycemia.
Effects:
Stimulates glycogenolysis (glycogen breakdown).
Promotes gluconeogenesis from non-carbohydrate sources.
Somatostatin: Inhibits insulin/glucagon secretion to fine-tune glucose regulation.
Diabetes Recognition:
Symptoms: Increased appetite (polyphagia), thirst (polydipsia), urination (polyuria), fruity breath (ketosis), fatigue, recurrent infections.
Diabetes prevalence in Australia: ~1.2 million people (~4.9% of the population).
Type 1:
Insulin deficiency.
Autoimmune destruction of beta cells.
Type 2:
Initially insulin resistance; may progress to insulin deficiency.
Most common (95% of diabetes cases).
Medications Categories: Injectable vs. Oral agents.
Insulin:
Essential for type 1; used in type 2 if oral agents fail.
GLP-1 Agonists: Mimic incretin hormones to enhance insulin release.
Benefits include weight loss.
Oral Medications:
Metformin: First-line treatment, improves insulin sensitivity, does not stimulate insulin production.
Sulfonylureas: Stimulate insulin release from pancreas; risk of hypoglycemia.
DPP-4 Inhibitors: Enhance incretin hormone action; low risk of hypoglycemia.
Alpha-Glucosidase Inhibitors (e.g., Acarbose): Slow carbohydrate absorption; side effects include gastrointestinal symptoms.
SGLT2 Inhibitors: Promote glucose excretion via urine; monitor for UTIs and dehydration.
Thiazolidinediones (Glitazones): Enhance insulin sensitivity; work at a genetic level but may take time for effects.
Metformin:
Mechanism: Lowers glucose production, improves insulin sensitivity; side effects: nausea, gastrointestinal upset.
Sulfonylureas:
Mechanism: Increase insulin secretion; side effects: hypoglycemia, weight gain.
DPP-4 Inhibitors:
Mechanism: Prevent DPP-4 degradation of incretins; side effects: mild GI discomfort.
SGLT2 Inhibitors:
Mechanism: Block glucose reabsorption in kidneys; side effects: dehydration, UTIs.
GLP-1 Agonists:
Mechanism: Stimulates insulin secretion and curbs appetite; side effects: nausea, risk of antibody formation.
Diabetes management is multifaceted, involving lifestyle changes, monitoring, and medication.
Treatment goals include maintaining glycemic control and preventing complications.
Understanding medication mechanisms and potential side effects is crucial for effective management.