Glycine treatment decreases proinflammatory cytokines and increases interferon-gamma in patients with type 2 diabetes.
M Cruz, C Maldonado-Bernal, R Mondragón-Gonzalez, R Sanchez-Barrera, N H Wacher, G Carvajal-Sandoval, J Kumate
Author Information
M Cruz: Biochemistry Medical Research Unit, Hospital de Especialidades, Centro Medico Nacional Siglo XXI. IMSS, Col. Doctores. México DF, Mexico City, México. mcruzl@yahoo.com
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)-alpha 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: A1C 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)-gamma 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-gamma. 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.
References
Proc West Pharmacol Soc. 1999;42:35-6
[PMID: 10697682]
