DHA can delay the development of diabetic nephropathy
Diabetic nephropathy (DN), one of the microvascular complications of diabetes, is a major cause of death among patients with type 1 diabetes, while in those with type 2 diabetes (DT2) it is just below atherosclerotic injuries to coronary and brain arteries. DN, whose prevalence is increasing, has a negative impact on the quality of life of diabetics. Among the factors thought to be involved in the pathogenesis of the disorder are advanced glycation end-product (AGE) generation, activation of the C-reactive protein polyol pathways, inflammation and oxidative stress. Interactions with AGEs and their receptors are present in abnormal cellular reactions such as inflammation, autophagy and apoptosis. Evidence shows that low AGE formation and inactivation of their receptors can lead to an improvement in kidney function. Nuclear factor κ-light chain-enhancer of activated B cells (NF-kB) is one of the regulators of AGE receptor expression, favouring it and leading to an increase in interactions involved in the inflammatory process. Tumour necrosis factor-α (TNF-α), a proinflammatory cytokine, is an NF-kB agonist and activating its signalling pathway worsens muscle oxidative metabolism. Infiltration of inflammatory cells in the glomeruli is an important event in the development of DN. Fractalkine works as an adhesion and chemotactic molecule, which plays a regulatory role in protein overload and ischaemic kidney lesion. To determine the association between serum concentration of docosahexaenoic acid (DHA) and inflammatory factors in patients with DN, 100 patients with DT2 were divided into three groups according to whether they presented with DN, and whether it was in an initial or clinical stag. They were then assessed for various parameters: glycated haemoglobin, biochemical markers, β2 microglobulin, 24-h urinary albumin, DHA serum concentrations, AGE, fractalkine, superoxide dismutase (SOD) and TNF-α. The drop in DHA serum levels was different in patients with initial and clinical DN, while serum DHA correlated significantly with SOD and negatively with fractalkine and TNF-α in patients with DN (at any stage). Based on these results, the authors concluded that DHA can reduce/eliminate fractalkine expression and secretion by inhibiting TNF-α signalling pathways in patients with DN, thereby improving inflammation and oxidative stress in the kidney and delaying its development.