# 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.

## Key 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.