Amino Acids (2004) 27: 187–191 DOI 10.1007/s00726-004-0108-2 Long-term taurine supplementation reduces mortality rate in streptozotocin-induced diabetic rats M. A. S. Di Leo 1 , S. A. Santini 2 , N. Gentiloni Silveri 1 , B. Giardina 2 , F. Franconi 3 , and G. Ghirlanda 4 1 Departments of Emergency Medicine, Catholic University, Rome, Italy 2 Institute of Biochemistry and Clinical Biochemistry, Catholic University, Rome, Italy 3 Department of Pharmacology and Center for Biotechnology Development and Biodiversity Research, University of Sassari, Italy and Gio.I.A Foundation, Pisa, Italy 4 Department of Internal and Geriatric Medicine, Catholic University, Rome, Italy Received May 5, 2004 Accepted June 13, 2004 Published online August 11, 2004; # Springer-Verlag 2004 Summary. Oxidative stress is implicated in the pathogenesis of diabetes mellitus. Taurine and vitamin E þ selenium supplementation has some benefits in experimental models of diabetes mellitus. This study evaluates whether taurine and vitamin E þ selenium supplementations reduce a hard end-point such as mortality due to diabetes. Streptozotocin-induced dia- betic rats were fed with standard diet or taurine (5%, w=w) or vitamin E (500 UI=Kg) þ selenium (8 mg=Kg) enriched diets. Taurine significantly decreased mortality rate (p < 0.04), while vitamin E failed to increase survival. In the late phase of the disease, taurine significantly decreased glycaemia, being vitamin E ineffective. No correlation between glycaemia and survival was found. None of supplementations modified body weight. Thus, only taurine decreases the mortality rate and glycaemia. These results encourage new research in the field, since classical hypoglycaemic agents are unable to decrease mortality in diabetic patients. Keywords: Taurine – Streptozotocin – Diabetes mellitus – Selenium – Vitamin E – Survival – Glycaemia Introduction In the last years, diabetes mellitus has reached epidemic proportion and is now becoming cause of premature mor- tality and morbidity (Zimmet, 2002). Indeed, the use of intensive hypoglycaemic therapies such as insulin, sulfo- nylureas appears unsuccessful UK Prospective Diabetes Study (UKPDS) Group (1998) in reducing mortality. Antioxidants has been proposed in the therapy of dia- betic patients (Devaraj and Jialal, 2000) because this metabolic disease is characterised by an increased pro- duction of oxidative species and by a decrease in anti- oxidant defences (Baynes and Thorpe, 1999; Lipinski, 2001; Santini et al., 1997; Seghieri et al., 1998; Marra et al., 2002). Consequently, the correction of oxidative stress may have important implications in preventing diabetes-induced complications and in reducing diabetic mortality. Taurine is a scavenger of hypochlorite and of carbonyl radicals with ancillary properties (Huxtable, 1992; Eppler and Dawson, 2001; Franconi et al., 2004). This amino acid seems also to have indirect antioxidant effects (Nonaka et al., 2001; Keys and Zimmerman, 1999; Schaffer et al., 2000). In addition, in vivo and in vitro, taurine is anti- hypoxic (Franconi et al., 1985; Malcangio et al., 1989). Taurine treatment shows beneficial effects in experimental diabetes mellitus models (Hansen, 2001; Franconi et al., 2004; Mozafari et al., 2003) and in clinical short study (Hansen, 2001; Franconi et al., 2004). On the other hand, in a double-blind trial of one-year duration, taurine failed to prevent kidney complications associated with type 2 diabetes mellitus (Odetti et al., 2002), and 4 months of taurine supplementation, in 2 type diabetic patients with bad metabolic control, failed to decrease glycosilated hae- moglobin and glucose (Chauncey et al., 2003). Vitamin E is a fat soluble vitamin known to be one of the most potent antioxidant that breaks the propagation of the free radical chain reaction in the lipid molecules (Sies et al., 1992). Selenium is essential for glutathione peroxidase activity. Previously, it has been shown that the vitamin E þ selenium supplementation in relatively short-term stud- ies delays retinal and renal alterations in streptozotocin