METABOLIC AND FUNCTIONAL RESPONSES OF RAT LIVER TO ALLOXAN-INDUCED DIABETES ACROSS DISTINCT MICROSOMAL OXIDATION PHENOTYPES.
Abstract
Diabetes mellitus (DM) is a chronic metabolic disorder that disrupts carbohydrate, lipid, and protein metabolism due to insufficient insulin secretion or action. Among the primary organs affected, the liver plays a pivotal role in glucose homeostasis and energy balance. In experimental models, alloxan is frequently used to induce diabetes by selectively damaging pancreatic β-cells. Recent studies suggest that individual metabolic responses to diabetes may vary depending on the inherent microsomal oxidation activity of the organism. This activity, predominantly governed by cytochrome P450 enzymes, determines how endogenous and exogenous substrates are metabolized and detoxified. Phenotyping based on pentobarbital-induced sleep duration—a functional proxy for microsomal oxidation—enables stratification of rats into fast, moderate, and slow metabolizers. Our study investigates how these metabolic phenotypes respond differently to alloxan-induced diabetes, focusing on liver function parameters, glycemic control, and systemic physiological adaptations including body weight, food and water intake, and urine output.
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References
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