The Glucose Dysregulation Cycle describes the self-perpetuating metabolic cascade often preceding Type 2 Diabetes, characterized by persistent hyperglycemia and compensatory hyperinsulinemia. This cycle reflects a failure in the normal glucose homeostasis orchestrated by pancreatic hormones and peripheral tissue sensitivity. Sustained elevation of blood glucose damages vascular and neural tissues over time.
Origin
This term is derived directly from longitudinal studies in diabetology and metabolic endocrinology tracking the progression from insulin resistance to overt hyperglycemia. It emphasizes the cyclical nature of the pathology, where initial compensation leads to later decompensation. Understanding this cycle is key to metabolic intervention.
Mechanism
Initially, peripheral tissues develop insulin resistance, requiring the beta cells to secrete excessive insulin to maintain normoglycemia. Over time, this chronic demand leads to beta-cell exhaustion and failure, resulting in uncontrolled glucose release from the liver and reduced peripheral uptake, thus closing the negative dysregulation loop. Glucagon regulation also often becomes inappropriately high in this state.
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