Effects of n‐3 pufas on fasting plasma glucose and insulin resistance in patients with impaired fasting glucose or impaired glucose tolerance

Author:

Derosa Giuseppe123,Cicero Arrigo F.G.34,D'Angelo Angela1,Borghi Claudio4,Maffioli Pamela15

Affiliation:

1. Department of Internal Medicine and Therapeutics University of Pavia, Fondazione IRCCS Policlinico S. Matteo PAVIA Italy

2. Center for the Study of Endocrine‐Metabolic Pathophysiology and Clinical Research, University of Pavia PAVIA Italy

3. Center for Prevention, Surveillance, Diagnosis and Treatment of Rare Diseases, Fondazione IRCCS Policlinico S. Matteo Pavia Italy

4. Internal Medicine, Aging and Kidney Disease Department, University of Bologna BOLOGNA Italy

5. PhD School in Experimental Medicine University of Pavia PAVIA Italy

Abstract

AbstractAim: to evaluate if a supplementation with n‐3 PUFAs at high doses could give a regression of the condition of impaired glycemia. Methods: we enrolled 281 overweight/obese patients with impaired fasting glucose (IFG) or impaired glucose tolerance (IGT); 138 subjects were randomized to n‐3 PUFAs group, 1 g three times a day, and 143 to placebo for 18 months. We assessed at baseline, and after 9, and 18 months: circumferences, body mass index (BMI), fasting plasma glucose (FPG), fasting plasma insulin (FPI), HOMA‐index, lipid profile. At baseline and at the end of the study, all patients underwent an oral glucose tolerance test (OGTT). Results: we observed a decrease of glycemia and HOMA‐IR with n‐3 PUFAs, compared to baseline, and to placebo. Fasting plasma insulin decreased with n‐3 PUFAs and increased with placebo. HDL‐cholesterol increased after 18 months of n‐3 PUFAs, while triglycerides decreased compared to baseline and to placebo. After OGTT performed at the end of the study, more patients returned to a condition of euglycemia with n‐3 PUFAs compared to placebo. Conclusions: n‐3 PUFAs were effective in reducing glycemia in patients affected by IFG or IGT and seem to be helpful to slow the development of type 2 diabetes mellitus. © 2016 BioFactors, 42(3):316–322, 2016

Publisher

Wiley

Subject

Clinical Biochemistry,Molecular Medicine,General Medicine,Biochemistry

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