Inactivating PKC theta isoforms, blocking mitochondrial fatty acid oxidation, blocking fat entry into myocytes, overexpressing lipoprotein lipase in muscle, or overexpressing UCP3 in muscle can protect against diet-induced insulin resistance in animal models.

“we've been able to inactivate isoforms npkc theta you get protection we've been able to block mito oxidation and you make these animals prone to that buildup insulin resistance we block fat entry into the myocyte inactivate fat4 they're protected you overexpress lipoprotein lipase in the muscle more fatty acid delivery muscle specific and some resistance and then finally if you rev up mitochondrial fat oxidation let's say through uncoupling overexpress ucp3 in the muscle you get protection from insulin resistance and all these track with dags going up or down with the insulin resistance or protection from insulin resistance”