Insulin resistance is a metabolic abnormality that is thought to lead to obesity, abdominal weight gain, cardiovascular disease and type 2 diabetes. The cause of insulin resistance is unknown, but evidence suggests that fatty acids play a role in its development. The role of dietary fat in the development of insulin resistance is contentious, but the role of sugar, in particular fructose, is more well established. High dietary intakes of fructose may cause insulin resistance because fructose can be metabolised to fatty acids by the liver through de novo lipogensis. These fatty acids may then accumulate in muscle tissue before spilling over into the blood, thus raising circulating fatty acid levels. The accumulated fatty acids in muscle tissue, then increase concentrations of various signal molecules such as sphingolipids, eicosanoids and phospholipids which somehow desensitise the insulin receptor.
Some evidence from both epidemiological and animal studies suggests that fish oils may be protective of the development of insulin resistance. Insulin resistance can be induced in rat models by using diets high in sucrose, and researchers1 have used such rats to study the effects of dietary long chain polyunsaturated fatty acids on the development of insulin resistance. Rats were fed a casein based diet which contained 100g/kg of fat for 12 weeks, after which insulin resistance were induced by replacing starch for sucrose. These changes resulted in an increase in plasma insulin, insulin area under the curve and plasma triglyceride concentrations following a glucose load, suggesting insulin resistance had developed. Adipocytes from rats fed sucrose had lower glucose transport rates, but had a higher rate of lipolysis that was insensitive to the inhibitory effect of insulin.
The researchers assessed the effects of fish oils on insulin insensitive rats by decreasing the n-6 to n-3 fatty acid ratio in the diet through replacement of linoleic acid (LA, C18:2 (n-6)) with eicosapentanoic acid (EPA, C20:5 (n-3)) and docosahexanoic acid (DHA, C22:6 (n-3)). The ratios of n-6 to n-3 were 210, 50 10, or 5 and a control group continued to be fed starch with a n-6 to n-3 ratio of 210. Decreasing the ratio n-6 to n-3 fatty acids to 50 normalised the plasma triglycerides in response to a glucose load, but normalisation the of plasma insulin levels and insulin area under the curve were not seen until the ratio was below 10. Low ratios of n-6 to n-3 fatty acids also partially reversed alterations adipocyte metabolism. The authors concluded that long chain polyunsaturated fatty acids at a level of 2.6 g/kg bodyweight (0.56% of energy, n-6 to n-3 ratio of ≤10) may prevent sucrose induced insulin resistance.
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