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- Title
Taurine supplementation enhances nutrient-induced insulin secretion in pancreatic mice islets.
- Authors
Ribeiro, Rosane A.; Bonfleur, Maria L.; Amaral, Andressa G.; Vanzela, Emerielle C.; Rocco, Silvana A.; Boschero, Antonio C.; Carneiro, Everardo M.
- Abstract
Background Taurine (TAU), a naturally occurring sulfur-containing amino acid, is found at high concentrations in plasma and mammalian tissues and regulates osmolarity, ion channel activity, and glucose homeostasis. Several reports have shown that physiological plasma TAU levels seem to be important for adequate beta (β)-cell function and insulin action, since low concentrations of TAU in the plasma have been reported in the pre-diabetic and diabetic states. Methods Glucose tolerance and insulin sensitivity were investigated in mice supplemented with 2% (w/v) TAU in their drinking water for 30 days, as well as the insulin secretion from isolated islets stimulated by glucose or L-leucine. Results TAU-supplemented mice demonstrated improved glucose tolerance and higher insulin sensitivity, compared to controls (CTL). In addition, their islets secreted more insulin in response to high concentrations of glucose and L-leucine. L-[U-14C]leucine oxidation was higher in TAU than in CTL islets, whereas D-[U-14C]glucose oxidation, ATP levels, glucose transporter (GLUT) 2 and glucokinase (GCK) protein expressions were similar in both types of islets. The L-type β2 subunit voltage-sensitive Ca2+ channel protein, as well as 45Ca uptake, were significantly higher in TAU-supplemented than CTL islets. In addition, islets from TAU-supplemented mice secreted more glucagon than CTL islets at low glucose. Conclusions TAU supplementation improves glucose tolerance and insulin sensitivity in mice, as well as insulin secretion from isolated islets. The latter effect seems to be, at least in part, dependent on a better Ca2+ handling by the islets. Copyright © 2009 John Wiley & Sons, Ltd.
- Publication
Diabetes/Metabolism Research & Reviews, 2009, Vol 25, Issue 4, p370
- ISSN
1520-7552
- Publication type
Article
- DOI
10.1002/dmrr.959