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Department of Medicine, Division of Endocrinology (S.E.K., B.S., S.K.), and the Department of Nutrition and Food Science (K.-L.C.J., S.B.), Wayne State University Detroit, Michigan 48202
The Veterans Administration Medical Center (P.M.) Allen Park, Michigan 48101
Address requests for reprints to: Dr. Sidika Kasim, M.D., Division of Endocrinology, Wayne State University, University Health Center 4H, 4201 St. Antoine, Detroit, Michigan 48201.
We investigated the effects of
-3 fish oil (FO) supplementation on lipid metabolism, glycemic control, and blood pressure (BP) in patients with type II diabetes mellitus. In 22 diabetic patients without overt hyperlipidemia, serum triglyceride, total cholesterol, high density lipoprotein (HDL)- cholesterol, HDL2-cholesterol, HDL3-cholesterol, and apolipoprotein A-I (apo A-I) levels did not change during
-3 FO supplementation for 8 weeks. The mean serum apo B concentration increased significantly [baseline, 2.56 ± 0.11 (±SEM) mmol/L; 4 weeks, 2.82 ± 0.13 mmol/L; 8 weeks, 2.80 ± 0.13 mmol/L; P < 0.01]. The mean plasma postheparin lipoprotein lipase activity increased transiently during the fourth week (baseline, 168 ± 17 U/mL; 4 weeks, 182 ± 18 U/mL; P < 0.05), whereas postheparin hepatic triglyceride lipase activity did not change. Glycemic control worsened transiently during the fourth week, (baseline, 7.7 ± 0.4%; 4 weeks, 8.4 ± 0.3%; P < 0.05). Both systolic and diastolic BP decreased significantly throughout the study (systolic BP: baseline, 142 ± 5 mm Hg; 8 weeks, 128 ± 5 mm Hg; diastolic BP: baseline, 88 ± 4 mm Hg; 8 weeks, 80 ± 3 mm Hg; P < 0.01).
These findings suggest that in type II diabetics without overt hype dipidemia,
-3 FO supplementation does not improve either the glycemic control or serum lipids, and it is associated with a potentially detrimental rise in serum apo B concentrations. Until more information is available, use of such supplementation should be discouraged.
* This work was supported in part by a grant from Diabetes Treatment Centers of America Foundation and in part by NIH Grant 05384- 24. Presented at the National Meetings of American Heart Association, November 1987, Anaheim, CA.
Received July 27, 1987.
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