Diabetes Mellitus results from failure of insulin to exert its normal metabolic effects.
Type 1 Diabetes:
Type 2 Diabetes:
Pharmacology only makes sense when viewed through mechanism.
Dr. O conceptualizes Type 2 Diabetes as:
This process disrupts the “8-Organ Model”:
Diabetes is not simply hyperglycemia — it is metabolic signaling failure.
Glucose delivered too rapidly:
Problem is not glucose alone — It is glucose delivered too fast, too often.
Low-quality fats:
Branched-chain amino acids:
Worst metabolic combination:
Maximal insulin resistance + maximal insulin demand.
Pancreatic beta cell:
Incretins amplify this:
Broken down by:
Insulin action:
Liver:
Muscle & Adipose:
Chronic overactivation → receptor downregulation → insulin resistance.
Acute damage:
Chronic damage:
End-organ damage:
In the proximal tubule:
When glucose exceeds transport maximum:
These agents increase insulin levels and carry hypoglycemia risk. Insulin Therapy
Rapid-Acting (Prandial)
Short-Acting
Intermediate-Acting
Long-Acting (Basal)
Ultra-Long Acting
These agents improve glycemia without directly increasing insulin secretion.
Dual GLP-1/GIP Incretin Agonists
Diabetes management now prioritizes:
High-impact classes:
By completing this module, you should be able to: