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Gli acidi grassi omega-3 non migliorano il metabolismo glucidico

In modelli animali gli acidi grassi omega-3 hanno dimostrato effetti positivi su alcuni aspetti della patologia aterosclerotica e del diabete. Aumento della sensibilità all'insulina, azione anti-infiammatoria, miglioramento della funzione mitocondriale, diminuzione dei trigliceridi e delle LDL piccole e dense sono tra le azioni più interessanti, ma che non sono state sufficientemente documentate che avvenissero anche nell'uomo. Gli studi nell'uomo hanno dato risultati contrastanti, tanto che è sempre rimasto in dubbio che gli omega-3 avessero un'azione veramente preventiva nei confronti del diabete e più in generale della patologia cardiovascolare. In questo studio, la supplementazione con 3.9 g al giorno per sei mesi di acido eicosapentaenoico e docosaesaenoico non ha mostrato alcun effetto rilevante sulla sensibilità insulinica in un gruppo di soggetti insulino-resistenti non diabetici.

Effects of Dietary n-3 Fatty Acids on Hepatic and Peripheral Insulin Sensitivity in Insulin-Resistant Humans

Lalia AZ, Johnson ML, Jensen MD, Hames KC, Port JD2, Lanza IR

Diabetes Care. 2015;38:1228-37

OBJECTIVE: Dietary n-3 polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), prevent insulin resistance and stimulate mitochondrial biogenesis in rodents, but the findings of translational studies in humans are thus far ambiguous. The aim of this study was to evaluate the influence of EPA and DHA on insulin sensitivity, insulin secretion, and muscle mitochondrial function in insulin-resistant, nondiabetic humans using a robust study design and gold-standard measurements.
RESEARCH DESIGN AND METHODS: Thirty-one insulin-resistant adults received 3.9 g/day EPA+DHA or placebo for 6 months in a randomized double-blind study. Hyperinsulinemic-euglycemic clamp with somatostatin was used to assess hepatic and peripheral insulin sensitivity. Postprandial glucose disposal and insulin secretion were measured after a meal. Measurements were performed at baseline and after 6 months of treatment. Abdominal fat distribution was evaluated by MRI. Muscle oxidative capacity was measured in isolated mitochondria using high-resolution respirometry and noninvasively by magnetic resonance spectroscopy.
RESULTS: Compared with placebo, EPA+DHA did not alter peripheral insulin sensitivity, postprandial glucose disposal, or insulin secretion. Hepatic insulin sensitivity, determined from the suppression of endogenous glucose production by insulin, exhibited a small but significant improvement with EPA+DHA compared with placebo. Muscle mitochondrial function was unchanged by EPA+DHA or placebo.
CONCLUSIONS: This study demonstrates that dietary EPA+DHA does not improve peripheral glucose disposal, insulin secretion, or skeletal muscle mitochondrial function in insulin-resistant nondiabetic humans. There was a modest improvement in hepatic insulin sensitivity with EPA+DHA, but this was not associated with any improvements in clinically meaningful outcomes.

Diabetes Care. 2015;38:1228-37