Amino Acids. 2015 Aug;47(8):1533-48. doi: 10.1007/s00726-015-1988-z. Epub 2015 May 5.
Taurine supplementation ameliorates glucose homeostasis, prevents insulin and glucagon hypersecretion, and controls β, α, and δ-cell masses in genetic obese mice.
Santos-Silva JC1, Ribeiro RA, Vettorazzi JF, Irles E, Rickli S, Borck PC, Porciuncula PM, Quesada I, Nadal A, Boschero AC, Carneiro EM.
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 Ca(2+) influx, NAD(P)H production
and insulin release.
Furthermore, α-cells from ob islets displayed a higher oscillatory Ca(2+) profile at low glucose concentrations, in association with glucagon hypersecretion. In Tau-supplemented ob mice, insulin and glucagon secretion was attenuated, while Ca(2+) influx tended to be normalized in β-cells and Ca(2+) 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.
Furthermore, α-cells from ob islets displayed a higher oscillatory Ca(2+) profile at low glucose concentrations, in association with glucagon hypersecretion. In Tau-supplemented ob mice, insulin and glucagon secretion was attenuated, while Ca(2+) influx tended to be normalized in β-cells and Ca(2+) 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.
- PMID:
- 25940922
- DOI:
- 10.1007/s00726-015-1988-z
- [PubMed - indexed for MEDLINE]
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