Dietary fish oil augments nitric oxide production or release in patients with Type 2 (non-insulin-dependent) diabetes mellitus

Abstract

Decreased release of nitric oxide from damaged endothelium is responsible for the impaired endothelium-dependent vasodilator responses found in animal models of vascular disease. Dietary supplementation with fish oils has been shown to augment endothelium-dependent relaxations, principally by improving the release of nitric oxide from injured endothelium. Using forearm venous occlusion plethysmography we studied vascular responses to 60, 120, 180 and 240 nmol/min of acetylcholine (an endothelium-dependent vasodilator) and 3, 6 and 9 nmol/min of glyceryl trinitrate (an endothelium-independent vasodilator) infused into the brachial artery in 23 patients with Type 2 (non-insulin-dependent) diabetes mellitus. NG monomethyl-L-arginine was employed to inhibit stimulated and basal release of nitric oxide from the endothelium. On completion of the baseline studies patients randomly received either fish oil or matching olive oil capsules in a double-blind crossover fashion for 6 weeks followed by a 6-week washout period and a final 6-week treatment phase. Studies, identical to the initial baseline studies, were performed at the end of the active treatment periods at 6 and 18 weeks. Fish oil supplementation significantly improved forearm blood flow responses to each dose of acetylcholine when compared to the vasodilator responses recorded at baseline and after olive oil administration (p < 0.01). Neither fish oil nor olive oil supplementation produced any significant changes in forearm blood flow to the incremental infusions of glyceryl trinitrate when compared with responses recorded during the baseline studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Meta-analysis of the effects of n-3 polyunsaturated fatty acids on lipoproteins and other emerging lipid cardiovascular risk markers in patients with type 2 diabetes

“…The trials included in the pooled analyses were small, with a median of 23 patients. Seventeen of the published papers were duplicate publications of six trials [22, 27, 33, 34, 36-38, 40, 42-46, 48, 51, 54, 55]; multiple papers for each trial are indicated by the following grouping of references: [22,38], [27,34,36,37], [40,54,55], [42,48,51], [43,46], [44,45]. There was sufficient information on only 12 of the 98 outcomes to allow data to be pooled, the results of which are shown in Fig.…”

Long-chain polyunsaturated fatty acids interact with nitric oxide, superoxide anion, and transforming growth factor-β to prevent human essential hypertension

“…LCPUFAs not only enhance the formation of the beneficial PGs but also inhibit ACE activity (Kumar & Das, 1997;Das, 1997;Das, 2001a) and augment the synthesis of eNO (McVeigh et al, 1993). On the other hand, there is evidence to suggest that the L-arginine-NO system could upregulate the metabolism of LCPUFAs in experimental animals (Mohan & Das, 2000.…”

Essential fatty acids and their metabolites in the context of hypertension

“…[18][19][20][21] Dihomo-GLA, AA, EPA and DHA not only form precursors to vasodilator and platelet anti-aggregator factors PGE 1 , PGI 2 and PGI 3 , but also inhibit ACE activity and augment the synthesis of endothelial NO. [22][23][24][25] Therefore, PUFA deficiency leads to increased ACE activity, which causes an increase in the levels of angiotensin II that, in turn, augment superoxide anion generation by activating NADPH oxidase, events that lead to a decrease in NO levels. 26 As the brain contains all components of the renin-angiotensin system, it is likely that low brain levels of DHA and EPA could enhance the level of angiotensin II, increasing the generation of free radicals and thereby accelerating the development of hypertension.…”