Differential Effects of High Methionine Diet on Biochemical Parameters in Normal and Diabetic Rat Models

TL;DR

A high methionine diet reduces liver fat in diabetic rats but worsens kidney damage, highlighting the need for targeted nutritional approaches in diabetes.

Contribution

The study reveals organ-specific metabolic effects of high methionine diets in diabetes, showing hepatic benefits and renal risks.

Findings

High methionine diet reduced liver triglycerides and activated AMPK in diabetic rats.

The same diet worsened kidney damage, increasing albuminuria and glomerulosclerosis.

Hyperhomocysteinemia occurred without changes in folate or vitamin B12 levels.

Abstract

This study investigated the organ-specific effects of a high-methionine (HM) diet
in streptozotocin (STZ)-induced diabetic rats, focusing on hepatic and renal
metabolic adaptations. Male Wistar rats were divided into four groups
(n=8/group): normal control, HM (2% methionine), STZ-diabetic, and HM+STZ. Over
12 weeks, HM supplementation in diabetic rats significantly reduced hepatic
triglyceride accumulation (42.00±7.71 vs. 20.76±3.63 mg/g tissue, P<0.01),
coinciding with AMP-activated protein kinase (AMPK) activation (1.96-fold,
P<0.05) and downregulation of lipogenic genes (sterol regulatory
element-binding protein 1c ↓63.2%, P<0.05). Conversely, HM exacerbated
diabetic nephropathy, elevating urinary albumin-creatinine ratio (411.90±88.86
vs. 238.41±62.52 mg/g, P<0.05) and glomerulosclerosis index (2.5±0.5 vs.
1.8±0.4, P<0.001). Hyperhomocysteinemia (105.69±33.81 μmol/L) persisted
across HM groups without altering folate/vitamin B12 levels (P>0.05). These
findings demonstrate a striking dichotomy: HM diet ameliorates hepatic steatosis
through AMPK-mediated lipid modulation while accelerating renal injury via
homocysteine-dependent pathways. The results highlight the need for
organ-specific nutritional strategies in diabetes management.

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