Tobiasenroach9355

3 was found to have a good sensitivity and reasonable specificity in predicting elevated VAT in this population.

This is the first study to validate the utility of METS-VF as a surrogate measure of visceral adiposity in south Indian individuals with morbid obesity. Given the simplicity, easy availability, reliability and inexpensive nature of this obesity indicator, it may find its widespread use in lower middle-income countries.

This is the first study to validate the utility of METS-VF as a surrogate measure of visceral adiposity in south Indian individuals with morbid obesity. Given the simplicity, easy availability, reliability and inexpensive nature of this obesity indicator, it may find its widespread use in lower middle-income countries.

An increased risk of cardiovascular mortality and morbidity has been linked with metabolic syndrome (MetS), described as the secondary risk reduction target. These patients are predisposed to high complication levels such as unstable angina-pectoris (USAP) by MetS. BBI608 As with the role of renalase in the regulation of blood pressure (BP), the study was carried out to determine the levels of renalase circulation in patients with USAP and MetS (USAP+MetS), as well as the association of renalase gene (

) rs10887800 polymorphism and USAP and MetS susceptibility.

A total of 134 patients with USAP+MetS and 134 control subjects were recruited in this case-control study.

Renalase was found to have a significantly higher level in USAP+MetS patients (23.28 ± 4.09 µg/dL) than in healthy ones (20.81 ± 2.73 µg/dL) (P < 0.001). Also, it was shown that renalase sensitivity and specificity values for the early diagnosis of USAP and MetS seemed to be 53.7% and 76.9, respectively. Moreover, the value for renalase area under curve (AUC) was 0.654 (95% CI 0.58-0.72). The frequency of rs10887800 AG and GG genotypes of RNLS gene was significantly higher in USAP+MetS patients than in control subjects, suggesting that this genotype might be a risk factor against USAP+MetS (OR = 2.114 [95% CI 1.113-4.016]; P = 0.022) and (OR = 2.057 [95% CI 1.011-4.186]; P = 0.047), respectively.

The present results showed that renalase serum levels increased in USAP and MetS patients. Moreover, the RNLS rs10887800 was reported to be associated with a higher risk of USAP+MetS.

The present results showed that renalase serum levels increased in USAP and MetS patients. Moreover, the RNLS rs10887800 was reported to be associated with a higher risk of USAP+MetS.

There are two signal transduction pathways related to glucose metabolism in C2C12 mouse myoblast cells; one through AMP-activated protein kinase (AMPK), and the other through phosphoinositide 3-kinase (PI3K). Ginger is reported to have hypoglycemic effects. The aim of this study was to determine the exact mechanism of action of ginger in those pathways.

C2C12 cells were seeded to four separate experimental groups; Control treated with 50 μg/mL DMSO in the absence of any inhibitor; Treatment 1 treated with 50 μg/mL ethyl acetate ginger extract without any inhibitor; Treatment 2 treated with 50 μg/mL extract in the presence of 20 μM AMPK inhibitor; Treatment 3 treated with 50 μg/mL extract in the presence of 25 μM PI3K inhibitor. The amount of GLUT-4 protein (an important glucose transporter) was determined in cytosolic and membrane fractions using sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blotting.

GLUT-4 concentration was significantly higher in the membrane fraction of cells treated with ethyl acetate ginger extract in the absence of any inhibitor in comparison with cells treated with this extract in the presence of each of the inhibitors (P-value < 0.05). GLUT-4 quantity in the membrane fractions in all groups was more than cytosolic fractions. The amount of GLUT-4 in membrane fraction of treated cells in the presence of PI3K inhibitor was higher than in the cells treated with this extract in the presence of AMPK inhibitor (P-value < 0.05).

Ethyl acetate ginger extract affects the amount of GLUT-4 protein in membrane and cytosolic fractions of C2C12 myoblast cells mostly through AMPK pathway but less via PI3K.

Ethyl acetate ginger extract affects the amount of GLUT-4 protein in membrane and cytosolic fractions of C2C12 myoblast cells mostly through AMPK pathway but less via PI3K.

Glucose variability (GV) is considered an important factor for cardiovascular disease (CVD) in patients with type 2 diabetes mellitus (T2DM). High GV causes endothelial dysfunction and increased oxidative stress. Dipeptidyl peptidase-4 (DPP-4) inhibitors may improve endothelial function and decrease GV. The aim of this study was to investigate the effects of vildagliptin, a DPP-4 inhibitor, compared with glibenclamide in GV and endothelial function in patients with T2DM and arterial hypertension.

This is a prospective, randomized, open and drug-controlled study. Fifty patients older than 35 years with T2DM and hypertension without CVD were randomized to receive vildagliptin (n=25) or glibenclamide (n=25), both in added-on metformin. Laboratory tests and analysis of endothelial function were performed before and 12 weeks after treatment. Endothelial function, defined by reactive hyperemia index (RHI), was analyzed by peripheral artery tonometry (endo-PAT2000). GV was evaluated by capillary glucose with intermittent monitoring device, six measurements per day, for three days, before and after treatment. The median of standard deviation (SD) of mean blood glucose (MBG) was used to evaluate GV.

GV decreased in the vildagliptin group (35.2 to 30.7,

=0.037) but did not change with glibenclamide (37.6 to 37.5,

=0.765). Glycated hemoglobin was similar in both groups. MBG decreased only in glibenclamide group, without difference with vildagliptin group (

=0.374). There were no changes in the RHI in both groups and there was no correlation between GV and RHI (

=0.658).

Vildagliptin reduces GV; however, the action on endothelial function was not demonstrated. In addition, there was no correlation between GV and endothelial function.

Vildagliptin reduces GV; however, the action on endothelial function was not demonstrated. In addition, there was no correlation between GV and endothelial function.