EFFECT OF SITAGLIPTIN ON LIPID PROFILE OF TYPE 2 DIABETES MELLITUS PATIENTS
Abstract
Background: Sitagliptin is a dipeptidyl-peptidase inhibitor (DPP-4 inhibitor) Like other DPP-4 inhibitors its action is mediated by increasing levels of the incretin hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP). The study was aimed to evaluate the effect of sitagliptin on lipid profile in patients with type-2 Diabetes Mellitus at 0 level and after 16 weeks of treatment with sitagliptin.
Material and Methods: A prospective study comprising 70 diagnosed cases of type 2 diabetes mellitus was carried out. These patients were put on sitagliptin 100 mg OD for 16 weeks and venous blood samples were taken at 0 level and after 16 weeks.
Results The decrease in mean serum cholesterol levels at 0 week and 16 weeks was 17.84mg/dl (6.64%) . The change in mean serum triglycerides level was 42.30mg/ dl (18.75%). On Statistical analysis, the reduction in serum cholesterol levels and in serum triglycerides levels in total number of patients was highly significant (p<0.001). The mean increase in serum high density lipoprotein cholesterol (HDL-C) level was 0.08 mg/dl and mean% increase in HDL-C level was 0.25% at 4 months from baseline. On statistical analysis the increase in mean serum HDL-C level in study group was non-significant (p 0.223).
Conclusions: The study concludes that Sitagliptin represents a substantial advance in antidiabetic therapy and it helps in improving the lipid profile of type 2 diabetes patients.
Keywords
Full Text:
PDFReferences
. Gaede P, Lund-Andersen H, Parving HH, et al. Effect of a multifactorial intervention on mortality in type 2 diabetes. N Engl J Med 2008;358:580–591. [PubMed] [Google Scholar]
Tan CE, Chew LS, Chio LF, et al. Cardiovascular risk factors and LDL subfraction profile in Type 2 diabetes mellitus subjects with good glycaemic control. Diabetes Res Clin Pract 2001; 51:107–114. [PubMed] [Google Scholar]
Chehade JM, Gladysz M, Mooradian AD. Dyslipidemia in type 2 diabetes: prevalence, pathophysiology, and management. Drugs 2013; 73:327–339.
The IDF Diabetes Atlas 5th Edition. Available at : http://www.idf.org/sites/default/files/The%20IDF%20Diabetes%20 Atlas%205th_Ed.ppt
Brunner Y, Schvartz D, Priego-Capote F, Couté Y, Sanchez JC. Glucotoxicity and pancreatic proteomics.c J Proteomics. 2009;71(6):576-91.
Nauck MA, Baller B, Meier JJ. Gastric inhibitory polypeptide and glucagon-like peptide-1 in the pathogenesis of type 2 diabetes. Diabetes. 2004;53 Suppl 3:S190-6.
Drucker DJ. The biology of incretin hormones. Cell Metab. 2006;3(3):153-65.
McIntosh CHS. Incretin-based therapies for type 2 diabetes. Canadian Journal of Diabetes 2008; 32(2):131-139.
Deacon CF. Incretin-based treatment of type 2 diabetes: glucagon like peptide-1 receptor agonists and dipeptidyl peptidase inhibitors. Diabetes Obes Metab. 2007;9 (Suppl 1):23-31.
Drucker DJ and Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet. 2006;368(9548):1696-705.
Deacon CF, Nauck MA, Toft-Nielsen M, Pridal L, Willms B, Holst JJ. Both subcutaneously and intravenously administered glucagon-like peptide I are rapidly degraded from the NH2-terminus in type II diabetic patients and in healthy subjects. Diabetes. 1995;44(9):1126-31.
Ahrén B, Landin-Olsson M, Jansson PA, Svensson M, Holmes D, Schweizer A. Inhibition of dipeptidyl peptidase-4 reduces glycemia, sustains insulin levels, and reduces glucagon levels in type 2 diabetes. J Clin Endocrinol Metab 2004;89(5):2078-84.
Deacon CF and Holst JJ. Dipeptidyl peptidase IV inhibition as an approach to the treatment and prevention of type 2 diabetes: a historical perspective. Biochem Biophys Res Commun 2002;294(1): 1-4.
Cobble M. DPP-4 Inhibitors: A New Therapeutic Class for the Treatment of Type 2 Diabetes. The Journal of Family Practice 2009;58(10).
Ahrén B. What mediates the benefits associated with dipeptidyl peptidase-IV inhibition? Diabetologia. 2005;48(4):605-7
Gallwitz B. Therapies for the treatment of type 2 diabetes mellitus based on incretin action. Minerva Endocrinol. 2006;31(2):133-47.
Allain CC, Poon LS, Chan CS, Richmond W, Fu PC. Enzymatic determination of total serum cholesterol. Clin Chem 1974;20(4):470-5.
McGowan MW, Artiss JD, Strandbergh DR, Zak B. A peroxidase-coupled method for the colorimetric determination of serum triglycerides. Clin Chem 1983;29(3):538-42.
Burstein M, Schalnick H R, Morfin R. Rapid Method for the isolation of Lipoproteins from human serum by precipitation with polyanions. J Lipid Res 1970;11(6):583-95.
Friedewald WT, Levy RJ, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin Chem 1972;18(6):499-502
Horton JD, Goldstein JL, Brown MS. SREBPs: activators of the complete program of cholesterol and fatty acid synthesis in the liver. J Clin Invest 2002;109:1125-31.
DeFronzo RA and Ferrannini E. Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991;14(3):173-94.
Krone W, Müller-Wieland D, Wirth H. Dyslipoproteinemia and metabolic syndrome. Effects of insulin resistance and hyperinsulinemia on lipid metabolism. Fortschr Med 1992;110(34): 645-48.
Gylling H, Hallikainen M, Pihlajamäki J, Simonen P, Kuusisto J, Laakso M et al. Insulin sensitivity regulates cholesterol metabolism to a greater extent than obesity: lessons from the METSIM Study. J Lipid Res 2010;51(8):2422-7.
Refbacks
- There are currently no refbacks.