The anti-adiposity effect of bitter melon seed oil is solely attributed to its fatty acid components
Authors:
Open Access
- 29 September 2017
- journal article
- research article
- Published by Springer Nature in Lipids in Health and Disease
- Vol. 16 (1) , 186
Abstract
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. 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. C57BL/6 J mice were allocated into five groups (n = 10/group) to receive diet C [30% soybean oil (SBO)], BM [25% SBO + 5% BMSO], BMS, BMNS or BMD. For the three latter diets, saponifiables (hydrolyzed fatty acids from BMSO), non-saponifiables (excluding fatty acids from BMSO) or bleaching oil (excluding pigments from BMSO), respectively, were added in amount equivalent to their content in 5% BMSO and SBO was added to bring total fat to 30%. After 14 wk., indices associated with adiposity and safety, as well as lipid metabolic signaling in white adipose tissue (WAT), were measured. The body fat percentage of mice in group BM, BMS, BMNS, and BMD were 90 ± 26, 76 ± 21, 115 ± 30 and 95 ± 17% of that in group C. Based on body fat percentage and plasma leptin concentrations, an anti-adiposity effect was evident in groups BM, BMS and BMD (greatest effect in BMS). Histologically, inguinal fat had smaller adipocytes in groups BM, BMS and BMD (P < 0.05), but not in group BMNS, relative to group C. There were no differences among groups in blood pressure or heart rate. Moreover, Sirt1 mRNA levels in inguinal fat were significantly greater in groups BM, BMS and BMD than group C. We concluded that the anti-adiposity function of BMSO was solely attributed to the fatty acid fraction, with the free fatty acid form having the greatest effect.Keywords
Funding Information
- Ministry of Science and Technology, R. O. C. (MOST 104-2622-B-039 -004 -CC2)
This publication has 39 references indexed in Scilit:
- Altered White Adipose Tissue Protein Profile in C57BL/6J Mice Displaying Delipidative, Inflammatory, and Browning Characteristics after Bitter Melon Seed Oil TreatmentPLOS ONE, 2013
- AMPK Phosphorylates and Inhibits SREBP Activity to Attenuate Hepatic Steatosis and Atherosclerosis in Diet-Induced Insulin-Resistant MiceCell Metabolism, 2011
- SIRT1 Deacetylates and Inhibits SREBP-1C Activity in Regulation of Hepatic Lipid Metabolism*Journal of Biological Chemistry, 2010
- Enzymes in the NAD+ Salvage Pathway Regulate SIRT1 Activity at Target Gene PromotersJournal of Biological Chemistry, 2009
- AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activityNature, 2009
- SIRT1 Modulation of the Acetylation Status, Cytosolic Localization, and Activity of LKB1Journal of Biological Chemistry, 2008
- SIRT1 Regulates Hepatocyte Lipid Metabolism through Activating AMP-activated Protein KinaseJournal of Biological Chemistry, 2008
- AMP-activated protein kinase signaling in metabolic regulationJournal of Clinical Investigation, 2006
- Functions of AMP‐activated protein kinase in adipose tissueThe Journal of Physiology, 2006
- Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-γNature, 2004