Although many epidemiological and human experimental studies have investigated the role of dietary fatty acids in coronary heart disease (CHD), and on cardiovascular risk biomarkers such as cholesterol, there are only a limited number of human studies that have investigated the role of dietary fat, specifically, in the development of insulin resistance.
A number of prospective studies have focused on associations between dietary fatty acid intakes or plasma and tissue fatty acid compositions in relation to either insulin action or risk of type 2 diabetes. In the Nurses' Study, intakes of dietary SFA or MUFA were neutral, but intakes of PUFA were negatively, and trans fatty acids were positively, related to increased risk of type 2 diabetes (Salmeron et al., 2001). Other prospective studies have shown that risk of type 2 diabetes is greatest in subjects showing relatively high proportions of SFA and low proportions of unsaturated fatty acids in blood lipids at baseline (Vessby et al., 1994), and that increased serum levels of linoleic acid (18:2), linolenic acid (18:3), total PUFA and PUFA: SFA were associated with a more favourable insulin outcome (Laaksonen et al., 2002b). In addition Pelikanova et al. (2001) demonstrated that serum phospholipid SFA and PUFA were negatively and positively associated with insulin sensitivity, respectively. Furthermore, higher proportions of oleic and linoleic acids and lower SFA in plasma phospholipids were associated with increased insulin sensitivity at baseline (Louheranta et al., 2002).
In general these studies support the hypothesis that unsaturated fats are protective and saturated fats are harmful with respect to risk of type 2 diabetes. This is supported by a recent review of the epidemiological evidence by Parillo & Riccardi (2004), which concluded that saturated fat from animal sources results in adverse effects on risk of type 2 diabetes, compared with unsaturated fat from vegetable sources. It was surmised that total dietary fat intake did not seem to predict the development of type 2 diabetes, although it was recognised that total fat intake may influence the development of type 2 diabetes indirectly, via excess body weight. However, it must be recognised that observational studies that measure associations between dietary intakes (or biomarkers such as serum fatty acids) and disease risk are limited in the extent to which they can provide evidence of causal relationships between measured variables, even when confounding factors are considered. Controlled intervention studies provide firmer evidence for causal associations but such studies are limited in number.
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