Research from the University of Maryland utilizing a primate model (Barnard et al 1990) is suggestive of an adverse effect on insulin receptors and insulin binding. A report from Kuller (1993) at the University of Pittsburg indicates that frequent users of partially hydrogenated vegetable fats in the form of margarine had higher insulin levels in response to glucose load.

At the National Obesity and Weight Control Symposium in New York in April 1993, it was reported that increases in dietary trans fatty acids affect muscle membranes in a manner that could trigger diabetes and which could be worsened if the person was obese.

Simopolous (1994) cited the need for clinical investigations to evaluate the effect of trans fatty acids in the diet on insulin resistance. Mann (1994) predicted the development of insulin resistance from dietary intake of trans fatty acids.

Salmeron et al (2001) (Harvard University) reported "... the relations between dietary fat intakes and the risk of type 2 diabetes... [They] prospectively followed 84,204 women aged 34-59 y with no diabetes, cardiovascular disease, or cancer in 1980. Detailed dietary information was assessed at baseline and updated in 1984, 1986, and 1990 by using validated questionnaires. Relative risks of type 2 diabetes were obtained from pooled logistic models adjusted for nondietary and dietary covariates.... During 14 y of follow-up, 2,507 incident cases of type 2 diabetes were documented. Total fat intake, compared with equivalent energy intake from carbohydrates, was not associated with risk of type 2 diabetes; for a 5% increase in total energy from fat, the relative risk (RR) was 0.98 (95% CI: 0.94, 1.02). Intakes of saturated or monounsaturated fatty acids were also not significantly associated with the risk of diabetes. However, for a 5% increase in energy from polyunsaturated fat, the RR was 0.63 (0.53, 0.76; P < 0.0001) and for a 2% increase in energy from trans fatty acids the RR was 1.39 (1.15, 1.67; P = 0.0006). We estimated that replacing 2% of energy from trans fatty acids isoenergetically with polyunsaturated fat would lead to a 40% lower risk (RR: 0.60; 95% CI: 0.48, 0.75)." These researchers concluded that these data suggest that total fat and saturated and monounsaturated fatty acid intakes are not associated with risk of type 2 diabetes in women, but that trans fatty acids increase and polyunsaturated fatty acids reduce risk. Substituting nonhydrogenated polyunsaturated fatty acids for trans fatty acids would likely reduce the risk of type 2 diabetes substantially.

References

D.E. Barnard, J. Sampugna, E. Berlin, S.J. Bhathena and J.J. Knapka (1990) Dietary Trans Fatty Acids Modulate Erythrocyte Membrane Fatty Acyl Composition and Insulin Binding in Monkeys. Journal of Nutritional Biochemistry 1:190-195.

Kuller (1993) Trans Fatty Acids and Dieting (Letter) The Lancet 341:1093-1094.

A.P Simopolous (1994) Is Insulin Resistance Influenced by Dietary Linoleic Acid and Trans Fatty Acids? Free Radicals in Biology and Medicine 17:367-372.

B.V. Mann (1994) Metabolic Consequences of Dietary Trans Fatty Acids The Lancet 343:1268-1271.

Salmeron J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB, Willett WC (2001) Dietary fat intake and risk of type 2 diabetes in women. American Journal of Clinical Nutrition 73 (6):1019-26.

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