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Adverse Metabolic Effect of Omega-3 Fatty Acids in Non-Insulin-Dependent Diabetes Mellitus

HARRY GLAUBER, M.D.; PENNY WALLACE, R.N., M.S.N.; KAY GRIVER, R.D.; and GINGER BRECHTEL, R.N.
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Grant Support: in part by the Medical Research Service of the Veteran's Administration; by grant AM33649 from the National Institute of Arthritis, Metabolism and Digestive Diseases; and by grant #PHS RR-00827 from the General Clinical Research Branch, Division of Research Resources, National Institutes of Health.

Presented in part on 1-4 May 1987, at the meeting of the American Federation for Clinical Research, San Diego, California.

▸Requests for reprints should be addressed to Harry S. Glauber, M.D.; Northwest Permanente P.C., 4855 S.W. Western Avenue; Beaverton, OR 97005.


La Jolla and San Diego, California


Ann Intern Med. 1988;108(5):663-668. doi:10.7326/0003-4819-108-5-663
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Increased interest in using omega-3 fatty acids led us to examine their metabolic effects in six men with type II (non-insulin-dependent) diabetes mellitus. After 1 month of a diet supplemented with these fatty acids, the patients' fasting glucose rose from 13.1 ± 1.3 to 15.3 ± 1.3 mmol/L (P = 0.03) and glucose area during a mixed meal profile rose by 22% (P = 0.04). Basal hepatic glucose output rose from 97 ± 9 to 122 ± 8 mg/m2 · min (P = 0.004) but glucose disposal rates measured by euglycemic glucose clamp were unchanged. Fasting insulin levels were similar; peak insulin levels stimulated by meals or intravenous glucagon fell by 30% and 39%, respectively. Plasma and erythrocyte content of omega-3 fatty acid rose significantly. After omega-3 fatty acid withdrawal, fasting glucose returned to baseline. Omega-3 fatty acid treatment in type II diabetes leads to rapid but reversible metabolic deterioration, with elevated basal hepatic glucose output and impaired insulin secretion but unchanged glucose disposal rates. Caution should be used when recommending omega-3 fatty acids in type II diabetic persons.

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