Journal Name:
Prog. Lipid Res.
Article Title:
Dietary fats and prevention of type 2 diabetes.
Date Written:
2009
Volume:
48
Number:
1
Page:
44
Author(s):
Risérus, U.; Willett, W.C.; Hu, F.B.
Article:
Although type 2 diabetes is determined primarily by lifestyle and genes, dietary composition may affect both its development and complications. Dietary fat is of particular interest because fatty acids influence glucose metabolism by altering cell membrane function, enzyme activity, insulin signaling, and gene expression. This paper focuses on the prevention of type 2 diabetes and summarizes the epidemiologic literature on associations between types of dietary fat, fatty acids (FA) and diabetes risk.
No long-term randomized controlled studies on the relation between the quality of dietary fat and diabetes risk exist. Short-term studies on the effects of dietary FAs on surrogate endpoints, e.g., insulin sensitivity, insulin secretion, or glycemic control are described. Overall results from studies to date have shown no significant effect of SFA, MUFA, or PUFA on insulin sensitivity. Problems inherent in these trials however included short duration, poor dietary compositions and few subjects. Several additional studies have been conducted in the past few years which have shown more positive results, possibly because of their greater statistical power. With regard to monounsaturated fatty acid (oleic acid), the main finding was that substitution of MUFA for SFA improves insulin sensitivity, which was impaired on the SFA diet. In another controlled crossover study in insulin resistant (n = 11) offspring of obese diabetic patients, the results indicated that a diet rich in MUFA improved insulin sensitivity compared with a diet rich in SFA. These effects were observed despite the short intervention period (28 days) and the relatively high intake of total fat.
Results following high P/S (PUFA to SAT ratio) diets, generally report that insulin-mediated glucose disposal at physiologic insulinemia increase significantly (32%) compared with the low P/S diet. However, at higher insulin infusion rates, the MCRs of glucose were not significantly different between diets. Since the total fat content was high (38%), it is possible that a beneficial effect of the high P/S-diet was underestimated. These findings however, are important since they suggest a potential long-term benefit from the substitution of SFA with omega 6 and omega 3 PUFA.
Animal experiments indicate that intake of fatty acids from the n-3 family (especially fish oils) have a beneficial effect on insulin sensitivity in rats, but not in healthy humans or in subjects with type 2 diabetes. These results are consistent with those from a recent study in which omega 3 supplementation (3.5% energy) for 14 weeks had no effect on high-molecular weight adiponectin concentrations in moderately obese subjects. Insulin sensitivity, however, was not measured in that study. The few available studies on the omega 6/ omega 3 FA ratio suggest that it does not play a major role in the development of insulin resistance and type 2 diabetes. In particular, controlled intervention studies show that the ratio has no impact on insulin action.
With regards to mechanism of action in diabetes, SFA and MUFA have minimal effects on lipogenic gene expression, while PUFA (arachidonic acid > eicosapentaenoic acid > docosahexaenoic acid > linoleic acid) suppress lipogenic expression in vitro, partly by binding to and activating nuclear receptors, such as PPAR. SFA also affects enzyme activities, inflammatory gene expression, and transcription factors that may contribute to its effects on glucose metabolism. Diets high in unsaturated long-chain omega 6 and omega 3 FA may inhibit hepatic lipogenesis and stimulate hepatic FA oxidation, which may improve hepatic insulin sensitivity. In vitro studies and animal experiments suggest that FAs could act directly on insulin-sensitive tissues. In several experiments, PUFAs (e.g., linoleic acid and omega 3 FAs) have suppressed lipogenic gene expression and enhanced oxidative metabolism. Conversely, SFAs—palmitic acid, in particular—have had an opposite effect.
Available data from controlled intervention studies suggest beneficial effects on insulin sensitivity when SFA and trans FA are replaced with MUFA or PUFA. Outcomes from observational studies using serum biomarkers of dietary fat intake or dietary questionnaires are consistent with those from controlled studies of insulin sensitivity; both suggest that replacing SFA and TFA with PUFA will lower the risk of type 2 diabetes. More controlled long-term studies with sufficient power are needed to identify the optimal dietary FA composition to reduce risk of type 2 diabetes.
Improving fat quality should be considered part of a dietary lifestyle strategy to prevent or manage type 2 diabetes. Replacing fats from red meats and butter with non-hydrogenated vegetable oils and margarines rich in MUFA and/or PUFA such as canola oil, should be encouraged to improve insulin sensitivity and reduce diabetes risk. Such dietary fat composition also lowers cardiovascular risk by reducing the serum LDL/HDL ratio and triacylglycerols. Few data are available on the effects of dietary fat quality in individuals with diabetes, and the optimal proportion of SFA, MUFA, and PUFA remains uncertain. The authors conclude that future studies are needed to investigate the interaction between dietary fat quantity and quality regard to insulin action and metabolic control.
Back to New research paper