Type II Diabetes is a chronic metabolic disorder characterized by sustained hyperglycemia resulting from a progressive loss of pancreatic beta-cell insulin secretion, often compounded by peripheral insulin resistance in muscle, liver, and adipose tissue. This condition is fundamentally a disease of hormonal signaling failure and energy dysregulation. It represents a severe, chronic failure of the body’s fuel sensing and glucose homeostatic machinery.
Origin
The term “diabetes” comes from the Greek word meaning “to pass through,” referring to the excessive urination, a primary symptom. The designation “Type II” distinguishes it from the autoimmune Type I form, recognizing its primary etiology in lifestyle and metabolic factors leading to insulin insensitivity. This condition has become a major global health crisis, intrinsically linked to modern dietary patterns.
Mechanism
The pathological process begins with chronic over-nutrition leading to hyperinsulinemia and subsequent downregulation of insulin receptors, causing insulin resistance. The pancreas initially compensates by increasing insulin output, but the sustained demand eventually exhausts the beta-cells, leading to relative insulin deficiency. The resulting impaired glucose uptake by peripheral tissues and excessive hepatic glucose production combine to produce chronic, damaging hyperglycemia.
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