NDLI: Taurine supplementation ameliorates glucose homeostasis, prevents insulin and glucagon hypersecretion, and controls β, α, and δ-cell masses in genetic obese mice

Content Provider	Springer Nature Link
Author	Santos Silva, Junia C. Ribeiro, Rosane Aparecida Vettorazzi, Jean F. Irles, Esperanza Rickli, Sarah Borck, Patrícia C. Porciuncula, Patricia M. Quesada, Ivan Nadal, Angel Boschero, Antonio C. Carneiro, Everardo M.
Copyright Year	2015
Abstract	Taurine (Tau) regulates β-cell function and glucose homeostasis under normal and diabetic conditions. Here, we assessed the effects of Tau supplementation upon glucose homeostasis and the morphophysiology of endocrine pancreas, in leptin-deficient obese (ob) mice. From weaning until 90-day-old, C57Bl/6 and ob mice received, or not, 5 % Tau in drinking water (C, CT, ob and obT). Obese mice were hyperglycemic, glucose intolerant, insulin resistant, and exhibited higher hepatic glucose output. Tau supplementation did not prevent obesity, but ameliorated glucose homeostasis in obT. Islets from ob mice presented a higher glucose-induced intracellular Ca2+ influx, NAD(P)H production and insulin release. Furthermore, α-cells from ob islets displayed a higher oscillatory Ca2+ profile at low glucose concentrations, in association with glucagon hypersecretion. In Tau-supplemented ob mice, insulin and glucagon secretion was attenuated, while Ca2+ influx tended to be normalized in β-cells and Ca2+ oscillations were increased in α-cells. Tau normalized the inhibitory action of somatostatin (SST) upon insulin release in the obT group. In these islets, expression of the glucagon, GLUT-2 and TRPM5 genes was also restored. Tau also enhanced MafA, Ngn3 and NeuroD mRNA levels in obT islets. Morphometric analysis demonstrated that the hypertrophy of ob islets tends to be normalized by Tau with reductions in islet and β-cell masses, but enhanced δ-cell mass in obT. Our results indicate that Tau improves glucose homeostasis, regulating β-, α-, and δ-cell morphophysiology in ob mice, indicating that Tau may be a potential therapeutic tool for the preservation of endocrine pancreatic function in obesity and diabetes.
Starting Page	1533
Ending Page	1548
Page Count	16
File Format	PDF
ISSN	09394451
Journal	Amino Acids
Volume Number	47
Issue Number	8
e-ISSN	14382199
Language	English
Publisher	Springer Vienna
Publisher Date	2015-05-05
Publisher Place	Vienna
Access Restriction	Subscribed
Subject Keyword	Glucagon secretion Insulin secretion Obesity Somatostatin Taurine supplementation Biochemistry Analytical Chemistry Biochemical Engineering Life Sciences Proteomics Neurobiology
Content Type	Text
Resource Type	Article
Subject	Organic Chemistry Biochemistry Clinical Biochemistry

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