Abstract
To develop novel therapeutic methods for both diabetic and renal disorders, scientists had initially focused on elucidating the molecular mechanisms of taurine in established cell lines and mouse models. Although a large amount of data have been revealed, taurine has been confirmed to be the next step of novel promising therapeutic interventions against diabetic disorders. Taurine appears to ameliorate diabetes 1-related complications in various organs through its antioxidant, anti-inflammatory and anti-hormonal actions. In type 2 diabetes, taurine has been positively implicated in glucose homeostasis, exerting potent hypoglycemic, anti-obesity, hypotensive and hypolipidemic effects. Of particular interest is that taurine provides protection against renal dysfunction, including hypertension and proteinuria, specific glomerular and tubular disorders, acute and chronic renal conditions, and diabetic nephropathy. The ameliorative effects of taurine against renal disorders are based on its osmoregulatory properties, its association with signaling pathways and its association with the renin-angiotensin-aldosterone system (RAAS). Further clinical studies are required to ensure the importance of research findings.
Highlights
BALIOU et al: TAURINE AGAINST DIABETIC AND RENAL DISORDERS in insulin secretion, insulin action, or both [1]
Hyperglycemia‐induced superoxide anions and hyperglycemia induce the flux of mitochondrial electron transport chain through four damaging pathways [generation of advanced glycation end‐products (AGEs), protein kinase C (PKC) activation, polyol formation and hexosamine pathway stimulation], supporting the hypothesis that mitochondrial‐derived reactive oxygen species (ROS) is the missing link to the glucose disturbance observed in diabetes [7]
Cerebral cells isolated from strepto‐ zotocin (STZ)‐treated rats are characterized by increased levels of malondialdehyde (MDA), increased lipid peroxidation (LPO) and a concomitant reduction in antioxidant enzyme activity and in the glutathione‐to‐glutathione disulfide (GSH/GSSG) ratio [9]
Summary
The first line of evidence that taurine exerted a positive effect on glucose tolerance in diabetic patients, through the activation of glycolysis and glycogenesis, was provided in 1976 [12]. Taurine has been shown to exhibit neuroprotective and antioxidant activity by reducing LPO and increasing GSH levels, thereby providing protection to rat cerebral cells subjected to injury from D‐galactose‐related stress [42]. Another study demonstrated that the mRNA levels of MafA, neurogenin 3 (Ngn3) and NeuroD1 transcription factors appeared to increase in mice following the administration of taurine [49] Those findings were important considering that Pdx‐1, NeuroD1 and MafA are the crucial transcription factors that bind to the upstream regions of the insulin gene promoter, thereby deter‐ mining the rate of insulin synthesis [50], with NeuroD1 being essential for the survival and normal functioning of pancreatic cells [51]. It has been shown that taurine decreases hyper‐ glycemia, insulin loss and mitochondrial oxidative stress, as well as hormone‐associated changes through the inhibition of the hypothalamic‐pituitary‐gonadal axis [62]
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