ArticleNutrients2016
Roles of Peroxisome Proliferator-Activated Receptor α in Bitter Melon Seed Oil-Corrected Lipid Disorders and Conversion of α-Eleostearic Acid into Rumenic Acid in C57BL/6J Mice.
Article in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Diet-Induced Browning of White Adipose Tissue: Molecular Targets, Mechanisms, and Therapeutic Potential.Current issues in molecular biology · 2026Review
- Preparation, Characterization, and Safety Evaluation of a Submicron Emulsion Processed Using High-Pressure Homogenization to Protect Bitter Melon Seed Oil.Foods (Basel, Switzerland) · 2025Article
- Huayu Qutan Recipe promotes lipophagy and cholesterol efflux through the mTORC1/TFEB/ABCA1-SCARB1 signal axis.Journal of cellular and molecular medicine · 2024Article
- Combating Obesity With Thermogenic Fat: Current Challenges and Advancements.Frontiers in endocrinology · 2020Review
- Deficiency or activation of peroxisome proliferator-activated receptor α reduces the tissue concentrations of endogenously synthesized docosahexaenoic acid in C57BL/6J mice.Nutrition research and practice · 2019Article
- The anti-adiposity effect of bitter melon seed oil is solely attributed to its fatty acid components.Lipids in health and disease · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that bitter melon seed oil (BMSO) was an effective anti-steatosis and antiobesity agent. Since the major fatty acid α-eleostearic acid (α-ESA) in BMSO is a peroxisome proliferator-activated receptor α (PPARα) activator, the objective was to investigate the role of PPARα in BMSO-modulated lipid disorders and α-ESA metabolism. C57BL/6J wild (WD) and PPARα knockout (KO) mice were fed a high-fat diet containing BMSO (15% soybean oil + 15% BMSO, HB) or not (30% soybean oil, HS) for 5 weeks. The HB diet significantly reduced hepatic triglyceride concentrations and increased acyl-CoA oxidase activity in WD, but not in KO mice. However, regardless of genotype, body fat percentage was lowered along with upregulated protein levels of uncoupling protein 1 (UCP1) and tyrosine hydroxylase, as well as signaling pathway of cAMP-dependent protein kinase and AMP-activated protein kinase in the white adipose tissue of HB-treated groups compared to HS cohorts. In WD-HB and KO-HB groups, white adipose tissue had autophagy, apoptosis, inflammation, and browning characteristics. Without PPARα, in vivo reduction of α-ESA into rumenic acid was slightly but significantly lowered, along with remarkable reduction of hepatic retinol saturase (
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