Diabetes Mellitus | Pathogenesis | Types | Clinical Features | Diagnosis | MedLive | Dr. Priyanka

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The pancreas is an intra-abdominal organ that appears as a single entity but is histologically divided into two distinct components. Its exocrine part releases digestive enzymes through ducts, while its endocrine portion, known as the islets of Langerhans, secretes hormones. Four major cell types reside in the islets: alpha cells that produce glucagon, beta cells that release insulin, delta cells that generate somatostatin, and cells that secrete pancreatic polypeptide. This detailed cellular architecture underpins the hormonal dynamics relevant to diabetes mellitus.

Balanced Glucose Homeostasis via Insulin and Glucagon In healthy metabolism, insulin directs glucose into liver, muscle, and adipose cells for storage as glycogen, while glucagon mobilizes stored glycogen back into the bloodstream during fasting. This precise hormonal interplay ensures blood sugar levels remain steady and cells receive the energy they need. The coordinated release of these hormones during feeding and fasting maintains overall metabolic balance.

Insulin Dysfunction in Diabetes: Hyperglycemia and Cellular Starvation Diabetes results when insulin is either absent or non-functional, preventing glucose from entering cells and causing elevated blood sugar levels. The surplus glucose damages vital organs such as the kidneys, eyes, and nerves, leading to complications like diabetic nephropathy, retinopathy, and neuropathy. Meanwhile, cells face an energy shortage despite the abundance of circulating glucose, encapsulating the dual impact of this metabolic disorder.

Diabetes is divided into two types: type 1 and type 2. Type 1 diabetes, representing about 10% of cases, typically emerges during adolescence and requires insulin replacement as the sole treatment. Type 2 diabetes, which accounts for 90% of cases, usually appears after the age of 40 or 50 and is initially managed with dietary modifications, lifestyle changes, and oral medications before moving to insulin if necessary.

After a meal, absorbed glucose elevates blood levels, prompting pancreatic beta cells to secrete insulin. Insulin then acts as a key, binding to receptors on the liver, skeletal muscle, and adipose tissue to trigger GLUT4 insertion which allows glucose to enter these cells. Once inside, glucose is stored as glycogen, illustrating a precise regulatory mechanism that links nutrient intake to energy storage.

In type 1 diabetes, autoimmune processes target and destroy pancreatic beta cells, which are responsible for insulin production. Cytotoxic T cells mistakenly attack these cells due to a loss of self-tolerance, leading to a complete absence of insulin. Without insulin, glucose cannot enter key organs, causing blood sugar levels to remain elevated and be stored as fatty acids in adipose tissue.

In type 2 diabetes, the pancreas produces an adequate amount of insulin because the beta cells are normal, but the insulin receptors in the liver, skeletal muscle, and adipose tissue are defective. This receptor malfunction prevents insulin from opening the cellular door necessary for glucose uptake, leaving glucose to accumulate in the blood. The ineffective action of insulin results in hyperglycemia, highlighting that the problem lies not in insulin secretion but in its inability to function properly in target organs.

Diabetes results either from insulin resistance, where liver, skeletal muscle, and adipose tissues fail to respond properly, or from an absolute insulin deficiency. Hyperglycemia causes a classic triad of increased hunger, excessive thirst, and frequent urination, accompanied by an unexpected weight loss despite overeating. Excess glucose remains in the blood, is excreted in the urine with water, and leads to dehydration and volume depletion. In the absence of sufficient insulin, adipose tissue breaks down into free fatty acids that oxidize into ketone bodies, raising the risk of diabetic ketoacidosis and hyperosmolar coma.

Diagnosis of type 1 diabetes centers on detecting ketonemia and ketoneuria. The method primarily relies on urine testing to identify metabolic imbalances, using the Benedict test for glucose through its magnetic reagent-induced color change and the Rothera test for ketones. This diagnostic approach builds on understanding the pathogenesis, clinical features, and complications of diabetes to effectively confirm the condition.

The video outlines the American Diabetes Association’s criteria for diagnosing diabetes using blood tests. It explains that a random blood glucose level above 200 mg/dL, a fasting level above 126 mg/dL, and a postprandial level above 200 mg/dL after a 75 g oral glucose load serve as diagnostic thresholds, while intermediate ranges indicate impaired conditions. The discussion further highlights glycosylated hemoglobin, which forms when excess blood glucose binds to hemoglobin, reflecting average glucose levels over the past 90 to 120 days.