Review
Dietary fats and prevention of type 2 diabetes

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Abstract

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 and diabetes risk. It also summarizes controlled feeding studies on the effects of dietary fats on metabolic mediators, such as insulin resistance. Taken together, the evidence suggests that replacing saturated fats and trans fatty acids with unsaturated (polyunsaturated and/or monounsaturated) fats has beneficial effects on insulin sensitivity and is likely to reduce risk of type 2 diabetes. Among polyunsaturated fats, linoleic acid from the n-6 series improves insulin sensitivity. On the other hand, long-chain n-3 fatty acids do not appear to improve insulin sensitivity or glucose metabolism. In dietary practice, foods rich in vegetable oils, including non-hydrogenated margarines, nuts, and seeds, should replace foods rich in saturated fats from meats and fat-rich dairy products. Consumption of partially hydrogenated fats should be minimized. Additional controlled, long-term studies are needed to improve our knowledge on the optimal proportion of different types of fats to prevent diabetes.

Introduction

Dietary composition could play a significant role in improving insulin sensitivity and reducing risk of diabetes and its complications [1]. The role of dietary fat in type 2 diabetes has been of clinical interest for many decades. Kinsell et al. were probably the first to report that type of fat consumed could influence insulin action in humans [2]. In a case report, a patient with type 1 diabetes required less exogenous insulin after substituting safflower oil rich in n-6 FA for triglycerides rich in saturated fatty acids (SFA) and oleic acid. Through our daily dietary intake, we ingest a variety of fatty acids (FAs) with different chain-length and numbers of double bonds. The most abundant dietary FAs are oleic acid, linoleic acid, palmitic acid, and stearic acid. These are reflected in plasma and tissue lipids. Thus, dietary fatty acid composition, to a large extent, determines the relative availability and storage of FAs in tissues [3].

The aim of this paper is to review the role of different types of dietary fat on insulin sensitivity and diabetes risk, and to update previous reviews on this topic [4], [5], [6]. Since there are no long-term randomized trials on the effect of dietary fat quality on diabetes risk, this review will focus on the effect of dietary FAs on surrogate endpoints, e.g., insulin sensitivity in randomized controlled interventions, and the relation of dietary fats to diabetes incidence in epidemiologic studies. In controlled feeding studies, test diets are typically isocaloric and differ only in dietary fat quality. However, such studies are usually small and of short duration, and thus, can only evaluate intermediate endpoints, e.g., insulin sensitivity.

Epidemiologic studies, on the other hand, are typically large, with long follow-up periods. Some of these studies have used objective methodology to assess dietary fat quality with biomarkers of FA intake, e.g., serum FA composition. Other studies have assessed dietary fat quality using food records or questionnaires. Both types of studies will be discussed, but the latter have previously been reviewed in detail [5], and therefore, will only be briefly updated here.

Section snippets

Assessment of dietary FA intake

In that the composition of several FAs in serum lipids or tissues reflects the composition of dietary FAs, they can be used as objective and reliable biomarkers of the relative FA content of the diet [7], [8], [9], [10]. FAs that cannot be synthesized endogenously from carbohydrates are the best biomarkers of FA intake. These include polyunsaturated fatty acids (PUFA), such as linoleic acid (n-6) and α-linolenic acid (n-3), trans fatty acids (TFA), and odd numbered FAs, e.g., 15:0 and 17:0 [11]

Overview

No long-term randomized controlled studies on the relation between the quality of dietary fat and diabetes risk exist. Thus, we have to rely on short-term studies on the effects of dietary FAs on surrogate endpoints, e.g., insulin sensitivity, insulin secretion, or glycemic control. FAs may not only act through alterations of cell-membrane FA composition and function, but also through short-term alterations of gene expression and enzyme activities. Vessby reviewed several randomized controlled

Dietary fats and diabetes: potential mechanisms

Mechanisms underlying the relation between dietary FAs and incidence of diabetes are still unclear, but the traditional view has been that dietary fat quality mainly affects cell-membrane FA composition and, consequently, cell membrane function [70]. The FA composition of cell membranes is thought to alter several cellular functions, including membrane fluidity, ion permeability, and insulin receptor binding/affinity; functions affected by translocation of glucose transporters interacting with

Conclusions

Available data from controlled intervention studies suggest beneficial effects on insulin sensitivity when SFA and TFA 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

Acknowledgments

Dr. Risérus is supported by the Swedish Research Council and The Heart and Lung Foundation, and has also received a grant from NordForsk within the Nordic Centre of Excellence in Food, Nutrition and Health (SYSDIET). Dr Frank Hu’s work is supported by Grant DK48845 from National Institute of Health (NIH).

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