Dietary diacylglycerol suppresses high fat and high sucrose diet-induced body fat accumulation in C57BL/6J mice.
Diacylglycerol (DG) comprises up to approximately 10% of various edible oils. In the present study, we examined the effects of dietary DG consisting mainly of 1,3-species on body weight, body fat accumulation, and mRNA levels of various genes involved in energy homeostasis in obesity-prone C57BL/6J mice. Five-month feeding with the high triacylglycerol (TG) diet (30% TG + 13% sucrose) resulted in significant increases in body weight, visceral fat accumulation, and circulating insulin and leptin levels compared with mice fed the control diet (5% TG). Compared with mice fed the high TG diet, body weight gain and visceral fat weight were reduced by 70% and 79%, respectively, in those fed the high DG diet (30% DG + 13% sucrose). In addition, circulating leptin and insulin levels were reduced to the respective control levels. Compared with high TG feeding, high DG feeding suppressed the elevation of leptin mRNA expression in adipose tissue, and up-regulated acyl-coenzyme (Co)A oxidase and acyl-CoA synthase mRNA expression in the liver. These results indicate that dietary DG is beneficial for suppression of high fat diet-induced body fat accumulation. Furthermore, it is suggested that structural differences in DG and TG, but not the composition of fatty acid, markedly affect nutritional behavior of lipids. -- Murase, T., T. Mizuno, T. Omachi, K. Onizawa, Y. Komine, H. Kondo, T. Hase, and I. Tokimitsu. Dietary diacylglycerol suppresses high fat and high sucrose diet-induced body fat accumulation in C57BL/6J mice. J. Lipid Res. 2001. 42: 372--378.
Murase
T
T
Biological Science Laboratories, Kao Corporation, 2606, Akabane, Ichikaimachi, Hagagun, Tochigi 321-3497, Japan.
Mizuno
T
T
Omachi
T
T
Onizawa
K
K
Komine
Y
Y
Kondo
H
H
Hase
T
T
Tokimitsu
I
I
D042962:Acyl-CoA Oxidase; D000273:Adipose Tissue / Q000737:chemistry / Q000502:physiology*; D000818:Animals; D001823:Body Composition / Q000187:drug effects*; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics; D002784:Cholesterol / Q000032:analysis; D003066:Coenzyme A Ligases / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D004041:Dietary Fats / Q000008:administration & dosage*; D004042:Dietary Fats, Unsaturated / Q000494:pharmacology*; D019422:Dietary Sucrose / Q000008:administration & dosage*; D004075:Diglycerides / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000032:analysis; D008099:Liver / Q000737:chemistry / Q000201:enzymology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010088:Oxidoreductases / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; D014280:Triglycerides / Q000008:administration & dosage / Q000032:analysis; D015430:Weight Gain
D022762:CCAAT-Enhancer-Binding Proteins; D004268:DNA-Binding Proteins; D004041:Dietary Fats; D004042:Dietary Fats, Unsaturated; D019422:Dietary Sucrose; D004075:Diglycerides; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; C497388:Srebf1 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; D014157:Transcription Factors; D014280:Triglycerides; D002784:Cholesterol; D010088:Oxidoreductases; D042962:Acyl-CoA Oxidase; D003066:Coenzyme A Ligases