The anti-adiposity effect of bitter melon seed oil is solely attributed to its fatty acid components.

Background: Obesity is the leading chronic disease affecting people of all ages. The objective of this study was to optimize composition of a bitter melon seed oil (BMSO) product to maximize its anti-adiposity effect.

Methods: Bleaching oil, saponifiables and non-saponifiables were prepared from BMSO, with α-eleostearic acid (α-ESA) content in BMSO maintained in bleaching oil and saponifiables.

A conjugated fatty acid present at high levels in bitter melon seed favorably affects lipid metabolism in hepatocytes by increasing NAD(+)/NADH ratio and activating PPARα, AMPK and SIRT1 signaling pathway.

α-Eleostearic acid (α-ESA), or the cis-9, trans-11, trans-13 isomer of conjugated linolenic acid, is a special fatty acid present at high levels in bitter melon seed oil. The aim of this study was to examine the effect of α-ESA on hepatic lipid metabolism. Using H4IIEC3 hepatoma cell line, we showed that α-ESA significantly lowered intracellular triglyceride accumulation compared to α-linolenic acid (LN), used as a fatty acid control, in a dose- and time-dependent manner.

Altered white adipose tissue protein profile in C57BL/6J mice displaying delipidative, inflammatory, and browning characteristics after bitter melon seed oil treatment.

Objective: We have previously shown that bitter melon seed oil (BMSO), which is rich in cis-9, trans-11, trans-13 conjugated linolenic acid, is more potent than soybean oil in attenuating body fat deposition in high-fat diet-induced obese C57BL/6J mice. The aim of this study was to obtain a comprehensive insight into how white adipose tissue (WAT) is affected by BMSO administration and to explore the underlying mechanisms of the anti-adiposity effect of BMSO.

Methods And Results: A proteomic approach was used to identify proteins differentially expressed in the WAT of mice fed diets with or without BMSO for 11 wks.

Bitter melon seed oil-attenuated body fat accumulation in diet-induced obese mice is associated with cAMP-dependent protein kinase activation and cell death in white adipose tissue.

The aim of this study was to investigate the antiadiposity effect of bitter melon seed oil (BMSO), which is rich in the cis-9, trans-11, trans-13 isomer of conjugated linolenic acid. In Expt. 1, C57BL/6J mice were fed a butter-based, high-fat diet [HB; 29% butter + 1% soybean oil (SBO)] for 10 wk to induce obesity.

Upregulation of lipogenesis and protein tyrosine phosphatase-1B expression in the liver of Wistar rats with metabolic syndrome chronically induced by drinking sucrose water.

Background: Establishing animal models with metabolic disorders similar to human metabolic syndrome (MS) is important. In terms of eliciting a full array of MS, we have previously shown that Wistar rats are more responsive to sucrose water drinking than are C57BL/6J mice. This study was aimed at investigating the underlying molecular mechanism of sucrose water-induced MS in Wistar rats.

Two unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, on inducing metabolic syndrome in Wistar rats and C57BL/6J mice.

To establish animal models with diet-induced metabolic disorders similar to human metabolic syndrome, 2 unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, were tested on Wistar rats and C57BL/6J mice. The 2 dietary habits were, respectively, simulated by feeding a high-fat diet (regimen A) or additionally providing 30% sucrose (wt/vol) in the drinking water (regimen B). Using a 2 x 2 factorial design, 4 groups of animals were fed chow diet plus plain water (group C), high-fat diet (30% [wt/wt] fat) plus plain water (group A), chow diet plus sucrose in drinking water (group B), and high-fat diet plus sucrose in drinking water (group AB) for 26 weeks.

The functional assessment of Alpinia pricei on metabolic syndrome induced by sucrose-containing drinking water in mice.

This study was designed to test whether Alpinia pricei (AP), a member of the ginger family indigenous to Taiwan, reduced metabolic syndrome induced by sucrose-containing drinking water in C57BL/6J mice. Mice given a chow diet were divided into a control group (C) or a test group given 30% sucrose water (SW) to drink ad libitum. After 22 weeks, mice in the SW group were subdivided into SW and SW + AP groups, the latter receiving a chow diet with an ethanol extract of AP (1500 mg/kg dosage).