Betanin Modulates the Leptin-Adiponectin Axis and Improves Glycemic Control in a High-Fat Diet and Streptozotocin-Induced Rat Model of Type 2 Diabetes

TL;DR

Betanin, a beetroot pigment, improves blood sugar and balances fat hormones in a rat model of type 2 diabetes.

Contribution

Betanin's novel role in modulating leptin and adiponectin to improve metabolic dysfunction in T2DM is demonstrated.

Findings

Betanin reduced fasting blood glucose and restored body weight in diabetic rats.

Betanin normalized leptin and adiponectin levels in a dose-dependent manner.

Metformin showed better glycemic control than betanin alone.

Abstract

Introduction

Type 2 diabetes mellitus (T2DM) is characterized by persistent hyperglycemia, insulin resistance, and chronic low-grade inflammation, accompanied by adipose tissue dysfunction and altered adipokine secretion. Elevated leptin and reduced adiponectin levels contribute significantly to metabolic deterioration and insulin resistance. Current antidiabetic therapies primarily target glycemic control but inadequately address underlying inflammatory and oxidative mechanisms. Betanin, a natural betalain pigment derived from beetroot, possesses potent antioxidant and anti-inflammatory properties and has shown metabolic benefits in experimental studies. The present study evaluated the effects of betanin on glycemic status and adipokine regulation in a high-fat diet (HFD) and streptozotocin (STZ)-induced rat model of T2DM.

Methodology

Thirty-six adult male Wistar rats were divided into six groups (n = 6): normal control, diabetic control, betanin (10 mg/kg), betanin (20 mg/kg), metformin (100 mg/kg), and metformin plus betanin. Type 2 diabetes was induced by HFD feeding followed by STZ (40 mg/kg). Treatments were administered orally for 28 days. Body weight, fasting blood glucose, and serum leptin and adiponectin levels were assessed. Data were analyzed using one-way ANOVA followed by Tukey’s post-hoc test.

Results

HFD-STZ induction produced significant hyperglycemia, body weight loss, hyperleptinemia, and reduced adiponectin levels compared to normal controls (p < 0.001). Betanin treatment produced dose-dependent improvements, including partial restoration of body weight and a significant reduction in fasting blood glucose. Betanin (20 mg/kg) reduced glucose levels from approximately 302 mg/dL to 188 mg/dL and significantly normalized leptin and adiponectin concentrations (p < 0.001). Metformin showed greater glycemic control and adipokine normalization, while combination therapy did not confer additional benefit over metformin alone.

Conclusion

Betanin significantly ameliorates metabolic dysfunction in an experimental model of T2DM by improving glycemic control and restoring adipokine balance. Its ability to reduce hyperleptinemia and enhance adiponectin secretion supports its potential as a preclinical adjunct strategy targeting metabolic and inflammatory pathways.

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