title: Reduced adiposity in bitter melon (Momordica charantia)-fed rats is associated with increased lipid oxidative enzyme activities and uncoupling protein expression.
abstract: To further explore the antiobesity effect of freeze-dried bitter melon (BM) juice, activities of mitochondrial lipid oxidative enzymes as well as the expression of uncoupling proteins and their transcription coactivator peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1alpha) were determined in diet-induced obese (DIO) rats. Rats were fed high-fat (HF) diets to induce obesity, and the effect of BM was assessed at doses of 0.75, 1.0, or 1.25% (wt:wt). In a dose-response experiment, BM-supplemented rats had lower energy efficiency (g weight gained/kJ consumed), visceral fat mass, serum glucose, and insulin resistance index, but higher plasma norepinephrine than unsupplemented rats (P < 0.05). Hepatic and skeletal muscle triglyceride concentrations were lower in supplemented HF diet-fed rats than in unsupplemented HF diet-fed rats (P < 0.05). An HF diet supplemented with BM elevated activities of hepatic and muscle mitochondrial carnitine palmitoyl transferase-I (CPT-I) and acyl-CoA dehydrogenase (AD) (P < 0.05). In another experiment, BM (1.0 g/100 g) lowered visceral fat mass but increased serum adiponectin concentration in HF diet-fed rats (P < 0.05). In the final study, rats were fed the HF diet with 0, 1.0 or 1.25% BM. Both groups of BM-supplemented rats had higher uncoupling protein 1 in brown adipose tissue (P < 0.05) and uncoupling protein 3 in red gastrocnemius muscle (P < 0.05), measured by Western blotting and RT-PCR, than the controls. The expression of the transcription coactivator PGC-1alpha in both tissues was also significantly elevated in the BM-supplemented rats (P < 0.05). The present results suggest that decreased adiposity in BM-supplemented rats may result from lower metabolic efficiency, a consequence of increased lipid oxidation and mitochondrial uncoupling.
authors.affiliation: Food and Nutritional Science Program, Department of Zoology, The University of Hong Kong, Hong Kong, The People's Republic of China.
authors.forename: Laureen L Y
authors.initials: LL
authors.lastname: Chan
authors.forename: Qixuan
authors.initials: Q
authors.lastname: Chen
authors.forename: Adi G G
authors.initials: AG
authors.lastname: Go
authors.forename: Emily K Y
authors.initials: EK
authors.lastname: Lam
authors.forename: Edmund T S
authors.initials: ET
authors.lastname: Li
mesh_terms: D042964:Acyl-CoA Dehydrogenase / Q000378:metabolism; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics*; D004032:Diet; D004041:Dietary Fats / Q000008:administration & dosage; D004734:Energy Metabolism; D050556:Fatty Acid-Binding Proteins / Q000032:analysis; D005638:Fruit; D015870:Gene Expression; D007328:Insulin / Q000097:blood; D007473:Ion Channels; D015227:Lipid Peroxidation / Q000502:physiology*; D008099:Liver / Q000737:chemistry; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D024101:Mitochondrial Proteins; D029777:Momordica charantia; D018482:Muscle, Skeletal / Q000737:chemistry; D009638:Norepinephrine / Q000097:blood; D009765:Obesity / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000032:analysis; D000071256:Uncoupling Protein 1; D000071247:Uncoupling Protein 3; D015430:Weight Gain
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D002352:Carrier Proteins; D004041:Dietary Fats; D050556:Fatty Acid-Binding Proteins; D007328:Insulin; D007473:Ion Channels; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D014280:Triglycerides; C000604373:Ucp1 protein, rat; C000604394:Ucp3 protein, rat; D000071256:Uncoupling Protein 1; D000071247:Uncoupling Protein 3; D042964:Acyl-CoA Dehydrogenase; D002334:Carnitine O-Palmitoyltransferase; D009638:Norepinephrine