anagliptin has been researched along with Body-Weight* in 3 studies
3 other study(ies) available for anagliptin and Body-Weight
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Anagliptin suppresses diet-induced obesity through enhancing leptin sensitivity and ameliorating hyperphagia in high-fat high-sucrose diet fed mice.
Obesity is a major risk factors for type 2 diabetes, and weight loss is beneficial to diabetic patients who are obese or overweight. Dipeptidyl peptidase-4 (DPP-4) inhibitors are anti-diabetic drugs. Although it has been known that the effect of most of the DPP-4 inhibitors on body weight is neutral, several studies suggested that some DPP-4 inhibitors suppressed body weight. Nonetheless, the mechanisms underlying DPP-4 inhibitor-induced weight loss are not fully understood. In this study, the mice fed high-fat high sucrose diet (HFHSD) containing a DPP4 inhibitor, anagliptin, showed reduced food intake and body weight compared to the mice fed non-treated HFHSD, but oxygen consumption and respiratory exchange ratio (RER) were not altered. Sequential administration of leptin suppressed food intake and body weight more apparently in anagliptin treated HFHSD fed mice than non-treated HFHSD fed mice. Oxygen consumption and RER were comparable between anagliptin treated and non-treated mice after leptin administration. The number of phospho STAT3 expressed cells in the arcuate nucleus after leptin administration was increased in anagliptin treated mice compared to non-treated mice. These data suggested that anagliptin ameliorated leptin resistance induced by HFHSD and thereby decreased food intake and body weight. These effects of anagliptin could be beneficial to the treatment of obese diabetic patients. Topics: Animals; Body Weight; Diet, High-Fat; Dipeptidyl-Peptidase IV Inhibitors; Eating; Hyperphagia; Leptin; Mice; Motor Activity; Obesity; Oxygen Consumption; Pyrimidines | 2020 |
The effect of anagliptin on intimal hyperplasia of rat carotid artery after balloon injury.
The present study evaluated the effect of anagliptin on intimal hyperplasia following carotid artery injury in Sprague‑Dawley rats. Sprague‑Dawley rats weighing 280‑300 g were injured using a 2F Fogarty balloon embolectomy catheter. The rats were divided into injury‑(saline) and anagliptin‑(10 mg/kg/day) treated groups. vascular injuries were induced in the left carotid artery, followed by evaluation of neointima formation at 28 days. The right and left carotid arteries were harvested and evaluated with histological evaluation, and the plasma activity of glucagon‑like peptide 1 receptor (GLP‑1), stromal cell‑derived factor (SDF)‑1α, interleukin (IL)‑6, IL‑1β and tumor necrosis factor (TNF)‑α were detected by ELISA analysis. Treatment with anagliptin decreased balloon injury‑induced neointima formation, compared with the injury group (P<0.01). Body weight and food consumption did not alter following treatment with anagliptin. Anagliptin caused an increase in the serum active GLP‑1 concentration, compared with the injury group. In addition, serum SDF‑1α was significantly decreased by treatment with anagliptin (P<0.001). Anagliptin altered the serum activity of IL‑6, IL‑1β and TNF‑α (P<0.01). The results of the present study demonstrated that anagliptin appeared to attenuate neointimal formation by inhibiting inflammatory cytokines and chemokines following balloon injury, and that treatment with a dipeptidyl peptidase 4 inhibitor may be useful for future preclinical studies and potentially for the inhibition of thrombosis formation following percutaneous coronary intervention. Topics: Angioplasty, Balloon; Animal Feed; Animals; Body Weight; Carotid Arteries; Carotid Artery Injuries; Chemokine CXCL12; Cytokines; Disease Models, Animal; Glucagon-Like Peptide 1; Inflammation Mediators; Male; Pyrimidines; Rats; Risk Factors; Tunica Intima | 2017 |
Mechanism of lipid-lowering action of the dipeptidyl peptidase-4 inhibitor, anagliptin, in low-density lipoprotein receptor-deficient mice.
Dipeptidyl peptidase-4 inhibitors are used for treatment of patients with type 2 diabetes. In addition to glycemic control, these agents showed beneficial effects on lipid metabolism in clinical trials. However, the mechanism underlying the lipid-lowering effect of dipeptidyl peptidase-4 inhibitors remains unclear. Here, we investigated the lipid-lowering efficacy of anagliptin in a hyperlipidemic animal model, and examined the mechanism of action.. Male low-density lipoprotein receptor-deficient mice were administered 0.3% anagliptin in their diet. Plasma lipid levels were assayed and lipoprotein profile was analyzed using high-performance liquid chromatography. Hepatic gene expression was examined by deoxyribonucleic acid microarray and quantitative polymerase chain reaction analyses. Sterol regulatory element-binding protein transactivation assay was carried out in vitro.. Anagliptin treatment significantly decreased the plasma total cholesterol (14% reduction, P < 0.01) and triglyceride levels (27% reduction, P < 0.01). Both low-density lipoprotein cholesterol and very low-density lipoprotein cholesterol were also decreased significantly by anagliptin treatment. Sterol regulatory element-binding protein-2 messenger ribonucleic acid expression level was significantly decreased at night in anagliptin-treated mice (15% reduction, P < 0.05). Anagliptin significantly suppressed sterol regulatory element-binding protein activity in HepG2 cells (21% decrease, P < 0.001).. The results presented here showed that the dipeptidyl peptidase-4 inhibitor, anagliptin, exhibited a lipid-lowering effect in a hyperlipidemic animal model, and suggested that the downregulation of hepatic lipid synthesis was involved in the effect. Anagliptin might have beneficial effects on lipid metabolism in addition to a glucose-lowering effect. Topics: Animals; Body Weight; Cholesterol; Dipeptidyl-Peptidase IV Inhibitors; Disease Models, Animal; Hep G2 Cells; Humans; Hyperlipidemias; Lipoproteins; Liver; Male; Mice; Pyrimidines; Receptors, LDL; RNA, Messenger; Sterol Regulatory Element Binding Protein 1; Sterol Regulatory Element Binding Protein 2; Triglycerides | 2017 |