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Volume 21, Issue 9, Pages 933-939 (September 2005)


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Dietary diacylglycerol reduces postprandial hyperlipidemia and ameliorates glucose intolerance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats

Yutaka Mori, M.D., Ph.D.aCorresponding Author Informationemail address, Hideaki Nakagiri, M.S.b, Hidehiko Kondo, Ph.D.b, Takatoshi Murase, Ph.D.b, Ichiro Tokimitsu, Ph.D.b, Naoko Tajima, M.D., Ph.D.c

Received 15 October 2004; accepted 11 January 2005. published online 14 July 2005.

Abstract 

Objective

The aim of the present study was to determine the effects of dietary diacylglycerol (DG) on the metabolism of lipids and glucose in type II diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats.

Methods

In experiment 1, the rats were orally administered 10 mL/kg of a triacylglycerol (TG) or DG emulsion (15% [w/v] oil), and the subsequent changes in the serum lipid levels were compared. In experiment 2, the rats were fed diets containing 15% DG or TG oil. After 22 weeks, the serum levels of lipids, glucose, and cytokines were determined. In addition, an oral glucose tolerance test (OGTT) was performed on the rats.

Results

Administration of an oral fat load caused marked hypertriglyceridemia with a peak at 2 h. Oral DG loading reduced the serum TG increase; the difference between the groups was significant at 4 and 6 h (P < 0.05). Diacylglycerol also markedly reduced the serum free fatty acid concentration increase due to the fat load. After 22 weeks of feeding, dietary DG reduced serum TG levels in the non-fasting state. Moreover, an OGTT revealed enhanced glucose disposal in the DG-fed rats compared with the TG-fed rats. Serum levels of adiponectin, an important insulin-sensitizing adipocytokine, were higher in the DG-fed rats than in the TG-fed rats (P < 0.05). In addition, DG-feeding reduced serum levels of C-reactive protein, a cardiovascular risk factor (P < 0.05).

Conclusion

These results suggested that dietary DG improves lipid metabolism and glucose tolerance, and retards the progress of diabetes mellitus in OLETF rats.

a Department of Internal Medicine, National Hospital Organization, Utsumomiya National Hospital, Tochigi, Japan

b Biological Science Laboratories, Kao Corporation, Tochigi, Japan

c Division of Diabetes and Endocrinology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan

Corresponding Author InformationCorresponding author. Tel.: +81-28-673-2111; fax: +81-28-673-6148.

PII: S0899-9007(05)00169-3

doi:10.1016/j.nut.2005.01.009


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