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Glycine treatment decreases proinflammatory cytokines and increases interferon-gamma in patients with type 2 diabetes

Authors :
Jesús Kumate
G. Carvajal-Sandoval
C. Maldonado-Bernal
Miguel Cruz
Rafael Mondragón-González
R. Sanchez-Barrera
Niels H. Wacher
Source :
Scopus-Elsevier
Publication Year :
2008

Abstract

Background: Amino acids have been shown to stimulate insulin secretion and decrease glycated hemoglobin (A1C) in patients with Type 2 diabetes. In vitro, glycine reduces tumor necrosis factor (TNF)-α secretion and increases interleukin-10 secretion in human monocytes stimulated with lipopolysaccharide. The aim of this study was to determine whether glycine modifies the proinflammatory profiles of patients with Type 2 diabetes. Materials/subjects and methods: Seventy-four patients, with Type 2 diabetes were enrolled in the study. The mean age was 58.5 yr, average age of diagnosis was 5 yr, the mean body mass index was 28.5 kg/m2, the mean fasting glucose level was 175.5 mg/dl and the mean A1C level was 8%. They were allocated to one of two treatments, 5 g/d glycine or 5 g/d placebo, po tid, for 3 months. Results: A1 C levels of patients given glycine were significantly lower after 3 months of treatment than those of the placebo group. A significant reduction in TNF-receptor I levels was observed in patients given glycine compared with placebo. There was a decrease of 38% in the interferon (IFN)-γ level of the group treated with placebo, whereas that of the group treated with glycine increased up to 43%. These data showed that patients treated with glycine had a significant decrease in A1C and in proinflammatory cytokines and also an important increase of IFN-γ. Conclusion: Treatment with glycine is likely to have a beneficial effect on innate and adaptive immune responses and may help prevent tissue damage caused by chronic inflammation in patients with Type 2 diabetes.

Details

ISSN :
17208386
Volume :
31
Issue :
8
Database :
OpenAIRE
Journal :
Journal of endocrinological investigation
Accession number :
edsair.doi.dedup.....0210cbd8f1f398681f71339bc4a6c32d