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Blood plasma glucose concentration denotes the quantity of glucose dissolved in blood plasma, tightly regulated for metabolic stability and cellular energy provision. It is a fundamental biomarker in the diagnosis, management, and prognosis of diabetes mellitus and a wide spectrum of metabolic disorders. Normal fasting levels in healthy adults range from approximately 70–100 mg/dL (3.9–5.5 mmol/L), and diagnostic thresholds for diabetes and prediabetes are defined by clinical guidelines. Therapeutic interventions focus on underlying molecular targets (such as insulin or its receptor, glucagon, and various transporters), with clinical blood glucose serving as a primary endpoint for efficacy and safety monitoring. Persistent deviations — hyperglycemia or hypoglycemia — are implicated in acute crises and progressive complications, especially in diabetes mellitus.
Mechanisms by which drugs affect blood plasma glucose concentration include increased insulin signaling (lowers plasma glucose); inhibited hepatic gluconeogenesis (lowers plasma glucose, e.g. metformin); increased renal glucose excretion (SGLT2 inhibition); insulin secretagogue effect (e.g. sulfonylureas, GLP-1 receptor agonists); inhibited carbohydrate digestion/absorption (e.g. alpha-glucosidase inhibitors); enhanced glucose uptake into peripheral tissues (insulin, thiazolidinediones); and raised plasma glucose via glycogen mobilization (glucagon injection).
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