# The Biochemical Role of Bitter Melon (Momordica charantia L.) Aqueous Extract in Regulating Hepatic Gluconeogenesis in Rats Fed Ketogenic Diet

## TL;DR

Bitter melon extract helps counteract the negative metabolic effects of a ketogenic diet in rats, improving glucose and lipid balance.

## Contribution

This study demonstrates bitter melon's potential as a safe supplement to mitigate long-term metabolic issues caused by a ketogenic diet.

## Key findings

- Bitter melon extract partially restored glucose, insulin, and enzyme activity in rats on a ketogenic diet.
- Supplementation reduced cholesterol, lactate, and ketone bodies in KD-fed rats.
- Histological analysis showed improved liver architecture in bitter melon-treated groups.

## Abstract

The ketogenic diet (KD) has been suggested as a useful lifestyle intervention for metabolic syndrome; however, its long‐term metabolic effects remain debated. This study evaluated the biochemical impact of supplementing KD‐fed rats with a diluted aqueous extract of Bitter Melon (BM) on the regulation of hepatic gluconeogenesis. Thirty‐two male rats were divided into four groups: G1 (Control), G2 (KD), G3 (BM extract, 1.5 g/kg body weight), and G4 (KD + BM extract, 1.5 g/kg body weight). Serum and liver samples were analyzed for biochemical parameters. KD reduced glucose, insulin, triglycerides (TG), Free Fatty Acids (FFA), glycogen, pyruvate carboxylase, and PEPCK, while elevating cholesterol (+34%), lactate, and ketone bodies (p < 0.05). BM supplementation partially restored glucose (+15%), insulin, TG, FFA, glycogen, and enzyme activity, while lowering cholesterol (−14%), lactate (−16%), and ketone bodies (−27%) (p < 0.05). Histological analysis confirmed improved liver architecture in BM‐treated groups. BM aqueous extract counteracts KD‐induced metabolic disturbances, improving glucose and lipid homeostasis and supporting its role as a safe adjunct to KD for long‐term metabolic management.

Metabolic effects of a ketogenic diet and bitter melon extract on hepatic gluconeogenesis and glucose–lipid homeostasis.