Diabetes effects fatty acid oxidation

In a placebo-controlled study in six patients with type 2 diabetes mellitus thalidomide 150 mg/day for 3 weeks reduced insulin-stimulated glucose uptake by 31% and glycogen synthesis by 48% (1115). However, it had no effect on rates of glycolysis, carbohydrate oxidation, non-oxidative glycolysis, lipolysis, free fatty acid oxidation, or re-esterification. The authors concluded that thalidomide increases insulin resistance in obese patients with type 2 diabetes. 

The hypolipidaemic effect of metformin has not been elucidated satisfactorily. The reduction of serum triglycerides and to a smaller extent total plasma cholesterol, however, is very welcome in the treatment of the metabolic syndrome in Type-II diabetes. The inhibitory effect of metformin on fatty acid oxidation (Schonborn et al., 1975) has been regarded as pivotal in its mechanism of antidiabetic action, because of the interrelations between fatty acid and carbohydrate metabolism. 

The clinical efficacy of fatty acid oxidation inhibitors has not yet been proven. Some beneficial effects have been noted in insulin-dependent diabetics, but no controlled clinical trials in non-insulin-dependent diabetics have been reported. Although the inhibition of fatty acid oxidation causes hypoglycaemia in the fasted state, it is unclear whether these compounds will be effective in an individual with normal eating habits. The safety and efficacy of this class of compounds can be determined only by further studies. 

It was found that the simple Vw complex with A,A -ethylenediaminediacetate (EDDA) had insulin-enhancing properties. 05 The corresponding complex with A,A -ethylene bis(5)-methionine was found to have a lesser effect with regard to inhibition of the free fatty acid release from diabetic rat adipocytes.605 The kinetics of the oxidation of YIV complexes in solution with... 

In comparison to the n-6 series, much less attention has been paid to the involvement of n-3 fatty acids in diabetic neuropathy, although the beneficial effects offish-oil supplements, a rich source of these fatty acids, in the prevention of atherosclerosis and hypertension in animal models and patients with vascular complications is well known (Lands et al. 1992). Proposals for the mechanisms by which n-3 fatty acids act include serving as precursors of vasoactive prostanoids and acting as shmulants for production of relaxing factors, such as nitric oxide (Lands etal. 1992 Boulanger 1990 McVeigh etal. 1993). 

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