Diabetes, Insulin, and Glucagon Notes
Diabetes, Insulin, and Glucagon
Insulin and Glucagon Overview
- Insulin and Glucagon are two hormones produced by the pancreas.
Insulin - Fed State (Storing Energy)
- Insulin is associated with the fed state, focusing on storing energy (sugars and fatty acids) for later use.
- Increases glucose entry into cells
- Increases glycogen formation: Glycogen is the storage form of glucose.
- Endurance athletes tend to have lower glycogen levels.
- Sprinters typically have high glycogen levels for short bursts of energy.
- Decreases lipolysis: Inhibits the breakdown of fats.
- Increases fatty acid storage
- Increases protein synthesis
- Decreases gluconeogenesis: Reduces glucose formation in the liver.
Hypoglycemia (Low Blood Sugar)
- Hypoglycemia is the condition of having low blood sugar.
- Some drugs can cause hypoglycemia, including:
- Ethanol
- ACE inhibitors
- Beta blockers
- Lithium
Hyperglycemia (High Blood Sugar)
- Hyperglycemia is the condition of having high blood sugar.
- Some drugs can cause hyperglycemia, including:
- Epinephrine
- T3 (Triiodothyronine, a thyroid hormone)
- Thyroxine (a thyroid hormone)
- Growth hormone
- Cortisol
- Corticosteroids
- NSAIDs (Nonsteroidal Anti-Inflammatory Drugs)
- Diuretics
Glucagon - Starve State (Releasing Sugar)
- Glucagon is associated with the starved state, triggering the release of sugar (not fats) into the blood.
Diabetes Type 1
- Insulin-dependent
- Signs and Symptoms:
- Hyperglycemia: High blood sugar.
- Fasting glucose + 160
- Polyuria: Excessive urination.
- Polyphagia: Excess hunger.
- Polydipsia: Excess thirst.
- Glucose in the urine (Glucosuria)
- Glucosuria has a prevalence of 1/100,000 people.
- Weight loss
- Fatigue
- Pathophysiology: No insulin production by the body, necessitating insulin administration.
- Diagnostic Criteria:
- HIAC (Glycosylated hemoglobin) > 6.5
- Treatment goal is to keep it below 6.5.
- Fasting oral glucose < 126 after 8 hours
- Oral glucose tolerance test ? 200Mg/ld
- Treatment:
- Insulin (both slow-acting and fast-acting formulations)
Diabetes Type 2
- Insulin-independent
- Insulin resistance: The body produces insulin, but it is not as effective at the cell level.
- Precursor: Metabolic syndrome, which leads to a pre-diabetic state.
- Treatments (Drug Classes):
- Sulfonylureas (Oral medication)
- Examples:
- Mechanism:
- Increase insulin secretion by the pancreas.
- Increase the sensitivity of insulin receptors to insulin.
- Side Effects:
- Hypoglycemia (low blood sugar)
- Biguanides
- Example:
- Mechanism:
- Decrease gluconeogenesis by the liver.
- Decrease insulin resistance.
- Does not alter pancreatic insulin secretion.
- Can decrease glucose in Type 1 patients.
- Major use is in treating Type 2 diabetes.
- Decreases triacylglycerols.
- Decrease LDL via a decrease in VLDL secretion
- Thiazolidinediones (TZDs)
- Example:
- Mechanism:
- Stimulate PPAR Alpha and PPAR Gamma, which control lipid synthesis and gluconeogenesis.
- Effects:
- Decrease in liver glucose secretion.
- Increase in insulin sensitivity.
- Incretin inhibitor
- Example:
- Mechanism:
- Stimulate GLP1 (glucagon-like peptide 1).
- Effects:
- Very expensive.
- Increase creatine.
- Stimulates fullness.
- Increase pancreas insulin secretion.
- Decrease glucagon.
Diabetic Ketoacidosis (DKA)
- Excessive use of lipids for energy.
- The liver shifts to making ketone bodies.
- Decrease blood PH – that is the acidosis part