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Dietary fat has long been implicated as a driver of insulin resistance. Studies on animals have observed significant insulin resistance in rats after just 3 weeks on a high-fat diet (59% fat, 20% carb.)[10] Large quantities of saturated, monounsaturated, and polyunsaturated (omega-6) fats all appear to be harmful to rats to some degree, compared to large amounts of starch, but saturated fat appears to be the most effective at producing IR.[11] This is partly caused by direct effects of a high-fat diet on blood markers, but, more significantly, ad libitum high-fat diet has the tendency to result in caloric intake that's far in excess of animals' energy needs, resulting in rapid weight gain. In humans, statistical evidence is more equivocal. Being insensitive to insulin is still positively correlated with fat intake, and negatively correlated with dietary fiber intake,[12] but both these factors are also correlated with excess body weight.

The effect of dietary fat is largely or completely overridden if the high-fat diet is modified to contain nontrivial quantities (in excess of 5–10% of total fat intake) of polyunsaturated omega-3 fatty acids.[11][13][14] This protective effect is most established with regard to the so-called "marine long-chain omega-3 fatty acids", EPA and DHA, found in fish oil; evidence in favor of other omega-3's, in particular, the most common vegetable-based omega-3 fatty acid, ALA, also exists,[15] but it is more limited; some studies find ALA only effective among people with insufficient long-chain omega-3 intake,[16] and some studies fail to find any effect at all[17] (ALA can be partially converted into EPA and DHA by the human body, but the conversion rate is thought to be 10% or less, depending on diet and gender). The effect is thought to explain relatively low incidence of IR, type 2 diabetes, and obesity in polar foragers such as Alaskan Eskimos consuming their ancestral diet (which is very high in fat, but contains substantial amounts of omega-3).[18][19] However, it is not strong enough to prevent IR in the typical modern Western diet. Unlike their omega-6 counterparts (which can be cheaply produced from a variety of sources, such as corn and soybeans), major sources of omega-3 fatty acids remain relatively rare and expensive. Consequently, the recommended average intake of omega-3 for adult men in the United States is only 1.6?grams/day, or less than 2% of total fat; the actual average consumption of omega-3 in the United States is around 1.3?grams/day, almost all of it in the form of ALA; EPA and DHA contributed less than 0.1?grams/day.[20]

Elevated levels of free fatty acids and triglycerides in the blood stream and tissues have been found in many studies to contribute to diminished insulin sensitivity.[11][21][22][23] Triglyceride levels are driven by a variety of dietary factors. They are correlated with excess body weight.[24] They tend to rise due to overeating and fall during fat loss.[25] At constant energy intake, triglyceride levels are positively correlated with trans fat intake and strongly inversely correlated with omega-3 intake. High-carbohydrate, low-fat diets were found by many studies to result in elevated triglycerides,[26] in part due to higher production of VLDL from fructose and sucrose, and in part because increased carbohydrate intake tends to displace some omega-3 from the diet.

Several recent authors suggested that the intake of simple sugars, and particularly fructose, is also a factor that contributes to insulin resistance.[27][28] Fructose is metabolized by the liver into triglycerides, and, as mentioned above, tends to raise their levels in the blood stream. Therefore, it may contribute to insulin resistance through the same mechanisms as the dietary fat. Just like fat, high levels of fructose and/or sucrose induce insulin resistance in rats,[29][30] and, just like with fat, this insulin resistance is ameliorated by fish oil supplementation.[31] One study observed that a low-fat diet high in simple sugars (but not in complex carbohydrates and starches) significantly stimulates fatty acid synthesis, primarily of the saturated fatty acid palmitate, therefore, paradoxically, resulting in the plasma fatty acid pattern that is similar to that produced by a high-saturated-fat diet.[32] It should be pointed out that virtually all evidence of deleterious effects of simple sugars so far is limited to their concentrated formulations and sweetened beverages. In particular, very little is known about effects of simple sugars in whole fruit and vegetables. If anything, epidemiological studies suggest that their high consumption is associated with somewhat lower risk of IR and/or metabolic syndrome.[33][34]