sitagliptin-phosphate and Cardiomyopathies

sitagliptin-phosphate has been researched along with Cardiomyopathies* in 4 studies

Other Studies

4 other study(ies) available for sitagliptin-phosphate and Cardiomyopathies

ArticleYear
Gliptin therapy reduces hepatic and myocardial fat in type 2 diabetic patients.
    European journal of clinical investigation, 2017, Volume: 47, Issue:11

    Increased hepatic fat and cardiac fat are common in patients with type 2 diabetes mellitus (T2DM) and are associated with a greater risk of liver fibrosis and cardiovascular (CV) events. Sex-specific differences of dipeptidyl peptidase-four (DPP-4) inhibitor effects on hepatic (HCL) and myocardial fat content (MYCL) have not yet been evaluated.. Forty-one T2DM patients (20 male, 21 female) received a gliptin add-on therapy if HbA1c goals were not reached under metformin monotherapy. They underwent cardiac and liver magnetic resonance tomography and spectroscopy before and 6 months after therapy initiation. Plasma samples were analysed for the growth differentiation factor 15 (GDF-15), a novel marker for cardiovascular risk.. Thirty-eight patients on gliptin therapy completed the study. We observed a positive correlation between MYCL and HCL before therapy (R = 0·41, P = 0·05). After 6 months of therapy, we noticed a significant weight reduction in women only (P = 0·02) whereas waist circumference decreased similarly in both sexes. HbA1c sunk significantly in both sexes (P = 0·002). HCL decreased significantly (P = 0·0004), with women featuring higher basal HCL (P < 0·05). MYCL decreased in women only (P = 0·01) and GDF-15 comparably in both sexes (P < 0·05).. 6 months of DPP-4-therapy led to a significant overall decrease in HCL and body weight such as a reduction of MYCL only in women. This preliminary data set could implicate that gliptin may be a feasible therapy option in fatty liver patients with diabetes potentially including positive effects on cardiovascular function particularly in women.

    Topics: Adamantane; Adipose Tissue; Adult; Aged; Cardiomyopathies; Diabetes Complications; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Drug Therapy, Combination; Fatty Liver; Female; Humans; Hypoglycemic Agents; Male; Metformin; Middle Aged; Nitriles; Pyrrolidines; Sitagliptin Phosphate; Treatment Outcome; Vildagliptin

2017
Sitagliptin attenuates cardiomyopathy by modulating the JAK/STAT signaling pathway in experimental diabetic rats.
    Drug design, development and therapy, 2016, Volume: 10

    Sitagliptin, a dipeptidyl peptidase-4 inhibitor, has been reported to promote cardioprotection in diabetic hearts by limiting hyperglycemia and hyperlipidemia. However, little is known about the involvement of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway modulation in the cardioprotective effects of sitagliptin. The current study aimed to investigate the protective effects of sitagliptin against diabetic cardiomyopathy (DCM), focusing on the modulation of the JAK/STAT pathway. Diabetes was induced by streptozotocin injection, and rats received sitagliptin orally and daily for 90 days. Diabetic rats exhibited hyperglycemia, hyperlipidemia, and a significant increase in heart-to-body weight (HW/BW) ratio. Serum troponin I and creatine kinase MB, cardiac interleukin-6 (IL-6), lipid peroxidation, and nitric oxide levels showed significant increase in diabetic rats. In contrast, both enzymatic and nonenzymatic antioxidant defenses were significantly declined in the heart of diabetic rats. Histopathological study revealed degenerations, increased collagen deposition in the heart of diabetic rats. Sitagliptin alleviated hyperglycemia, hyperlipidemia, HW/BW ratio, histological architecture, oxidative stress, and inflammation, and rejuvenated the antioxidant defenses. In addition, cardiac levels of pJAK2 and pSTAT3 were increased in diabetic rats, an effect which was remarkably decreased after sitagliptin treatment. In conclusion, these results confer an evidence that sitagliptin has great therapeutic potential on DCM through down-regulation of the JAK/STAT signaling pathway.

    Topics: Animals; Cardiomyopathies; Creatine Kinase, MB Form; Diabetes Mellitus, Experimental; Enzyme Inhibitors; Interleukin-6; Janus Kinases; Rats; Rats, Wistar; Signal Transduction; Sitagliptin Phosphate; Streptozocin; Troponin I

2016
First treatment of a child suffering from severe ischemic cardiomyopathy with G-CSF and sitagliptin.
    International journal of cardiology, 2013, Dec-10, Volume: 170, Issue:2

    Topics: Cardiomyopathies; Combined Modality Therapy; Dipeptidyl-Peptidase IV Inhibitors; Granulocyte Colony-Stimulating Factor; Hematopoietic Stem Cell Transplantation; Humans; Infant; Male; Myocardial Ischemia; Pyrazines; Severity of Illness Index; Sitagliptin Phosphate; Treatment Outcome; Triazoles

2013
Effects of DPP-4 inhibitors on the heart in a rat model of uremic cardiomyopathy.
    PloS one, 2011, Volume: 6, Issue:11

    Uremic cardiomyopathy contributes substantially to mortality in chronic kidney disease (CKD) patients. Glucagon-like peptide-1 (GLP-1) may improve cardiac function, but is mainly degraded by dipeptidyl peptidase-4 (DPP-4).. In a rat model of chronic renal failure, 5/6-nephrectomized [5/6N] rats were treated orally with DPP-4 inhibitors (linagliptin, sitagliptin, alogliptin) or placebo once daily for 4 days from 8 weeks after surgery, to identify the most appropriate treatment for cardiac dysfunction associated with CKD. Linagliptin showed no significant change in blood level AUC(0-∞) in 5/6N rats, but sitagliptin and alogliptin had significantly higher AUC(0-∞) values; 41% and 28% (p = 0.0001 and p = 0.0324), respectively. No correlation of markers of renal tubular and glomerular function with AUC was observed for linagliptin, which required no dose adjustment in uremic rats. Linagliptin 7 µmol/kg caused a 2-fold increase in GLP-1 (AUC 201.0 ng/l*h) in 5/6N rats compared with sham-treated rats (AUC 108.6 ng/l*h) (p = 0.01). The mRNA levels of heart tissue fibrosis markers were all significantly increased in 5/6N vs control rats and reduced/normalized by linagliptin.. DPP-4 inhibition increases plasma GLP-1 levels, particularly in uremia, and reduces expression of cardiac mRNA levels of matrix proteins and B-type natriuretic peptides (BNP). Linagliptin may offer a unique approach for treating uremic cardiomyopathy in CKD patients, with no need for dose-adjustment.

    Topics: Animals; Area Under Curve; Cardiomyopathies; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Disease Models, Animal; Gene Expression Regulation; Glomerular Filtration Rate; Glucagon-Like Peptide 1; Heart; Humans; Kidney Failure, Chronic; Linagliptin; Myocardium; Natriuretic Peptide, Brain; Nephrectomy; Piperidines; Purines; Pyrazines; Quinazolines; Rats; Reverse Transcriptase Polymerase Chain Reaction; Sitagliptin Phosphate; Triazoles; Uracil; Uremia

2011