[1] In this paper, we study for the first time the daytime vertical E Â B drift velocities from Gadanki and Kototabang using the Doppler shifts of the 150-km echoes observed during 2008-2010, a period of low solar activity. Drift velocities are mostly positive and confined to 35 m s À1 at both the locations, except for Gadanki where on a few occasions negative drift velocities have been observed in the afternoon hours. Drift velocities generally show a decreasing trend with local time and the largest drift is generally observed in the forenoon hours consistent with extensively reported observations and models of E Â B drift. Drift velocities from Gadanki and Kototabang compared exceeding well on some days and differed remarkably on many days despite the fact that they are longitudinally separated by only 20 . The day-to-day variation in the drift velocity could be as high as 15 m s À1 at Gadanki and 7 m s À1 at Kototabang. Seasonal mean drifts over Gadanki are found to be generally larger than those of Kototabang. The observations have been compared in detail with those reported earlier based on ground-and satellite-based observations and also with the Scherliess-Fejer model. The observed differences in the drifts at the two locations, including the downward drifts, have been discussed in the light of current understanding of the longitudinal variability of E Â B drift.

Aims/Introduction:  Excessive intake of sucrose can cause severe health issues, such as diabetes mellitus. In animal studies, consumption of a high‐sucrose diet (SUC) has been shown to cause obesity, insulin resistance and glucose intolerance. However, several in vivo experiments have been carried out using diets with much higher sucrose contents (50–70% of the total calories) than are typically ingested by humans. In the present study, we examined the effects of a moderate SUC on glucose metabolism and the underlying mechanism.Materials and Methods:  C57BL/6J mice received a SUC (38.5% sucrose), a high‐starch diet (ST) or a control diet for 5 weeks. We assessed glucose tolerance, incretin secretion and liver glucose metabolism.Results:  An oral glucose tolerance test (OGTT) showed that plasma glucose levels in the early phase were significantly higher in SUC‐fed mice than in ST‐fed or control mice, with no change in plasma insulin levels at any stage. SUC‐fed mice showed a significant improvement in insulin sensitivity. Glucagon‐like peptide‐1 (GLP‐1) secretion 15 min after oral glucose administration was significantly lower in SUC‐fed mice than in ST‐fed or control mice. Hepatic glucokinase (GCK) activity was significantly reduced in SUC‐fed mice. During the OGTT, the accumulation of glycogen in the liver was suppressed in SUC‐fed mice in a time‐dependent manner.Conclusions:  These results indicate that mice that consume a moderate SUC show glucose intolerance with a reduction in hepatic GCK activity and impairment in GLP‐1 secretion. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2012.00208.x, 2012)

These observations demonstrated that Angptl4 mRNA expression was increased through the elevated free FAs in diabetic mice.

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Tranilast, N-(3,4-demethoxycinnamoyl)-anthranilic acid, is an anti-allergic agent identified as an inhibitor of mast cell degranulation. Recently, tranilast was shown to decrease albuminuria in a rat model of diabetic nephropathy and to ameliorate vascular hypertrophy in diabetic rats, suggesting that it may be clinically useful in the treatment of diabetic complications. However, the effects of tranilast on glucose tolerance have not been elucidated. Thus, the aim of this study is to investigate the effect of tranilast on insulin secretion in pancreatic beta-cells. Treatment with tranilast significantly suppressed insulin secretion in INS-1E cells and rat islets induced by 16.7 mmol/l glucose. Furthermore, tranilast inhibited tolbutamide-induced insulin secretion. Treatment with tranilast increased (86)Rb (+) efflux from COS-1 cells in which pancreatic beta-cell-type ATP-sensitive K (+) (K (ATP)) channels were reconstructed and suppressed the cytosolic ATP/ADP ratio in INS-1E cells. Interestingly, treatment with tranilast enhanced glucose uptake in INS-1E cells. In the present study, we demonstrated that tranilast inhibited glucose- and tolbutamide-induced insulin secretion through the activation of K (ATP) channels in pancreatic beta-cells.