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

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• 作者：Junia C. Santos-Silva ; Rosane Aparecida Ribeiro ; Jean F. Vettorazzi…
• 关键词：Glucagon secretion ; Insulin secretion ; Obesity ; Somatostatin ; Taurine supplementation
• 刊名：Amino Acids
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：47
• 期：8
• 页码：1533-1548
• 全文大小：1,698 KB
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• 作者单位：Junia C. Santos-Silva (1)
  Rosane Aparecida Ribeiro (2)
  Jean F. Vettorazzi (1)
  Esperanza Irles (3)
  Sarah Rickli (1)
  Patrícia C. Borck (1)
  Patricia M. Porciuncula (1)
  Ivan Quesada (3)
  Angel Nadal (3)
  Antonio C. Boschero (1)
  Everardo M. Carneiro (1)
  
  1. Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, e Centro de Pesquisa em Obesidade e Comorbidades, Universidade Estadual de Campinas (UNICAMP), C.P. 6109, Campinas, SP, CEP 13083-970, Brazil
  2. Universidade Federal do Rio de Janeiro, NUPEM, Campus UFRJ-Macaé, Avenida S?o José do Barreto, 764, Barreto, Macaé, RJ, CEP 27965-045, Brazil
  3. Instituto de Bioingeniería y Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, CIBERDEM, Universidad Miguel Hernández de Elche, Elche, Alicante, Spain
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Analytical Chemistry
  Biochemical Engineering
  Life Sciences
  Proteomics
  Neurobiology
  
• 出版者：Springer Wien
• ISSN：1438-2199

文摘

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.