A high-sugar diet-induced animal model for insulin resistance, oxidative stress, and diabetic nephropathy: insights into empagliflozin's therapeutic potential
Abstract
BACKGROUND: Excessive sugar consumption has been implicated in the development of insulin resistance and diabetic nephropathy (DN). The present study aimed to establish a novel animal model of DN using a high-sugar diet (HSD) and evaluate the renoprotective effects of empagliflozin.
METHODS: Male Wistar rats were divided into four groups: Normal, Normal + Empagliflozin, Diabetic, and Diabetic + Empagliflozin. Diabetes was induced using a 35% sugar-water solution and a low-dose of streptozotocin. Empagliflozin (15 mg/kg/day) was administered via gavage. Biochemical parameters, renal function markers, oxidative stress indicators, and histopathological assessments were performed.
RESULTS: HSD significantly increased fasting blood glucose (FBS) (242.71 mg/dl in Diabetic vs. 96.6 mg/dl in Normal), insulin levels (0.63 vs. 0.288), and homeostatic model assessment for insulin resistance (HOMA-IR) (0.2716 vs. 0.0687), indicating severe insulin resistance. Empagliflozin treatment significantly reduced FBS (128 mg/dl), improved insulin sensitivity (insulin 0.2725, HOMA-IR 0.0854), and partially restored β-cell function (HOMA-B 1.5779). The diabetic group exhibited impaired renal function, with elevated blood urea nitrogen (BUN 38 mg/dl), creatinine (3.44 mg/dl), and proteinuria (2600 mg/24 h). Empagliflozin reduced these markers to near-normal levels (BUN 17 mg/dl, creatinine 0.44 mg/dl, proteinuria 135 mg/24 h). Oxidative stress parameters showed that empagliflozin increased…
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