Share This Article:

Effects of Metformin and Pioglitazone on impaired glucose tolerance patients—An open level prospective study

Abstract Full-Text HTML Download Download as PDF (Size:179KB) PP. 316-320
DOI: 10.4236/jdm.2012.23049    2,815 Downloads   4,868 Views   Citations

ABSTRACT

Introduction: impaired glucose tolerance (IGT) often leads to type 2 diabetes (T2DM) and macro vascular disease; and usually associated with insulin resistance. Pioglitazone and metformin are commonly used insulin sensitizers (IS); and can prevent or delay the development T2DM and macro vascular disease. This study was deployed to search the better IS between these two in relation to plasma glucose and lipid control; and physical parameter altering effect. Materials and methods: 100 IGT patients selected randomly from outpatients department following prefixed inclusion and exclusion criteria. Pioglitazone and metformin were administered sequentially. Washout period was 2 weeks. Total follow up period was 24 weeks. Results: 70 IGT patients had completed the study. Metformin had reduced plasma glucose (fasting & postprandial), lipids and physical parameters significantly (p < 0.05) more than Pioglitazone. Discussion: Metformin, a hepatic insulin sensitizer, is more effective than PPAR-□ agonist Pioglitazone in the treatment of IGT; and this is due to the expression of PPAR-□ is more in adipose tissue but postprandial utilization of plasma glucose is more in muscle tissue.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

Mazumdar, G. , Chakraborty, I. and Swaika, B. (2012) Effects of Metformin and Pioglitazone on impaired glucose tolerance patients—An open level prospective study. Journal of Diabetes Mellitus, 2, 316-320. doi: 10.4236/jdm.2012.23049.

References

[1] Bennett, P.H. and Knowler, W.C. (2010) Definition, diagnosis, and classification of diabetes mellitus and glucose homeostasis. In: Kahn, C.R., King, G.L., Moses, A.C., Weir, G.C., Jacobson, A.M. and Smith, R.J., Eds., Joslin’s Diabetes Mellitus, 14th Edition, Walter Kluwer Pvt. Ltd., New Delhi, 331-339.
[2] Gavin, J.R., III, Albert, K.G.M.M., Davidson, M.B. et al. (1997) Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care, 20, 1183-1197.
[3] Edelstein, S.L., Knowler, W.C., Bain, R.P., et al. (1997) Predictors of progression from impaired glucose tolerance to NIDDM: An analysis of six prospective studies. Diabetes, 46, 701-710. doi:10.2337/diabetes.46.4.701
[4] The DECODE Study Group, European Diabetes Epidemiological Group. Diabetes epidemiology: collaborative analysis of diagnostic criteria in Europe. (1999) Glucose tolerance and mortality: Comparison of WHO and American Diabetes association diagnostic criteria. Lancet, 354, 617-621. doi:10.1016/S0140-6736(98)12131-1
[5] Buchanon, T.A., Xiang, A.H., Peters, R.K., et al. (2001) Protection from type 2 diabetes persists in the TRIPOD cohort eight months after stopping trogitazone. Diabetes, 50, 327.
[6] Isommaa, B., Almgren, P., Hericson, M., et al. (1999) Chronic complications in patients with slowly progressing autoimmune type 1 diabetes (LADA). Diabetes Care, 22, 137-1353. doi:10.2337/diacare.22.8.1347
[7] Knowler, W.C., Barret-Connor, E., Fowler, S.E., et al., Diabtes Prevention Program Group (2002) Reduction in the incidence of type 2 diabetes with life style intervention or metformin. The New England Journal of Medicine, 346, 393-403.
[8] The Diabetes Prevention Progression Research Group (2002) Reduction in the incidence of type 2 diabetes with life style intervention of metformin. The New England Journal of Medicine, 346, 393-403. doi:10.1056/NEJMoa012512
[9] Groop, L. (2000) Genetics of the metabolic syndrome. British Journal of Nutrition, 83, S39-S48.
[10] Olefsky, J.M., Revers, R.R., Prince, M., et al. (1985) Insulin resistance in non-insulin dependent (type II) and insulin dependent (type I) diabetes mellitus. Advances in Experimental Medicine and Biology, 189, 176-205.
[11] Ratzmann, K.P., Ruhnke, R. and Kohnert, K.D. (1983) Effect of pharmacological suppression of insulin secretion on tissue sensitivity to insulin in subjects with moderate obesity. International Journal of Obesity, 7, 453-458.
[12] Buse, J.B., Polonsky, K.S. and Burant, C.F. (2008) Type 2 diabetes mellitus. In: Kronenberg, H.M., Melmed, S., Polanski, K.S. and Larsen, P.R., Eds., Williams Textbook of ENDOCRINOLOGY, 11th Edition, Volume 1, Elsevier Inc., Saunders, 1330-1389.
[13] Long, Y.C. and Zierath, J.R. (2006) AMP—Activated protein kinase signaling in metabolic regulation. Journal of Clinical Investigation, 116, 1776-1783. doi:10.1172/JCI29044
[14] Powers, A.C. (2011) Diabetes Mellitus. In: Longo, D.N., Kasper, D.L., Jameson, J.L., Fauci, A.S., Hauser, S.L. and Loscalzo, J., Eds., Harrison’s Principles of Internal Medicine, 18th Edition, Volume 2, McGraw-Hill Companies, Inc., New York, 2968-3009
[15] Powers, A.C. and D’Alessio, D. Endocrine pancreas and pharmacotherapy of diabetes mellitus and hypoglicemia. In: Brunton, L.L., Chabner, B.A. and Knollmann, B.C., Eds., Goodman & Gillman’s the Pharmacological Basis of Therapeutics, 12th Edition, McGraw-Hill Companies, Inc., New York, 1237-1273.
[16] Musi, N., Hirshman, M.F., Nygren, J. et al. (2002) Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. Diabetes, 51, 2074-2081. doi:10.2337/diabetes.51.7.2074

  
comments powered by Disqus

Copyright © 2019 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.