British Journal of Nutrition

Full Papers

Metabolism and Metabolic Studies

Supplementation with EPA or fish oil for 11 months lowers circulating lipids, but does not delay the onset of diabetes in UC Davis-type 2 diabetes mellitus rats

Bethany P. Cummingsa1a2, Kimber L. Stanhopea1a2, James L. Grahama1a2, Steven C. Griffena3 and Peter J. Havela1a2 c1

a1 Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA

a2 Department of Nutrition, University of California, Davis, Davis, CA, USA

a3 Department of Internal Medicine, University of California, Davis, Sacramento, CA, USA

Abstract

EPA or fish oil supplementation has been suggested as treatments for the prevention of type 2 diabetes mellitus (T2DM) due to their lipid-lowering and potential insulin-sensitising effects. We investigated the effects of supplementation with EPA (1 g/kg body weight per d) or fish oil (3 g/kg body weight per d) on the age of onset of T2DM and circulating glucose, insulin, lipids, leptin and adiponectin in UC Davis (UCD)-T2DM rats. Animals were divided into three groups starting at 1 month of age: control, EPA and fish oil. All the animals were followed until diabetes onset or for up to 12 months of age. Monthly fasting blood samples were collected for the measurement of glucose, lipids, hormones and C-reactive protein (CRP). Neither EPA nor fish oil delayed the onset of T2DM or altered fasting plasma glucose, insulin, CRP, adiponectin or leptin concentrations. The groups did not differ in energy intake or body weight. Fish oil treatment lowered fasting plasma TAG concentrations by 39 (sd 7) % (P < 0·001) and EPA lowered fasting plasma NEFA concentrations by 23 (sd 5) % (P < 0·05) at 4 months of age compared with the control group. EPA and fish oil lowered fasting plasma cholesterol concentrations at 4 months of age by 19 (sd 4) and 22 (sd 4) % compared with the control group, respectively (both P < 0·01). In conclusion, EPA and fish oil supplementation lowers circulating lipid concentrations, but does not delay the onset of T2DM in UCD-T2DM rats.

(Received January 20 2010)

(Revised May 28 2010)

(Accepted June 01 2010)

(Online publication August 24 2010)

Correspondence:

c1 Corresponding author: P. J. Havel, fax +1 530 752 4698, email pjhavel@ucdavis.edu

Footnotes

Abbreviations: CRP, C-reactive protein; T2DM, type 2 diabetes mellitus; UCD, UC Davis