This study aimed to assess the effect of luseogliflozin on liver fat deposition and compare luseogliflozin to metformin in type 2 diabetes (T2D) patients with non-alcoholic fatty liver disease (NAFLD). Thirty-two T2D patients with NAFLD diagnosed by computed tomography or abdominal sonography were recruited. Participants were randomly assigned to receive either luseogliflozin (2.5 mg, newly administered) or metformin (1500 mg, newly or additionally administrated). Data on the liver-to-spleen attenuation ratio (L/S), visceral fat area, body mass index, glycated hemoglobin (HbA1c), alanine aminotransferase (ALT), fasting plasma glucose, C-peptide immunoreactivity (CPR), and CPR index were collected at baseline and after 6 months. The change in L/S was significantly greater in the luseogliflozin group than in the metformin group. Similarly, the changes in the visceral fat area, HbA1c, and body mass index were significantly greater in the luseogliflozin group than in the metformin group. The changes in ALT, fasting glucose, CPR, and CPR index were not significant in both groups. In conclusion, luseogliflozin significantly reduced liver fat deposition as compared to metformin, which may indicate clinical relevant benefits for NAFLD.
Aims/IntroductionWe aimed to identify factors – glycemic control, reactive inflammatory biomarkers or vital signs – associated with mortality in diabetic patients admitted to hospital for various infections (non‐intensive care unit).Materials and MethodsWe retrospectively analyzed the cases of 620 diabetic patients admitted to hospital for various infections (non‐intensive care unit) who underwent glucose monitoring >3 times per day. We extracted data regarding reactive inflammatory biomarkers and vital signs recorded on day 1 of hospital stay, and data on bacteremia and hypoglycemia status, glycemic variability (GV; coefficient of variation and standard deviation) and mean glucose concentrations during the entire hospital stay. Univariate and stepwise multivariate logistic regression analyses were carried out to determine the association between these factors and mortality.ResultsThe mortality rate was 10.1%. Reactive inflammatory biomarkers, vital signs and bacteremia were not associated with mortality. According to the results of the adjusted analysis, hypoglycemia showed a significant positive association with mortality, increasing death risk by 266% (odds ratio [OR] 2.66, 95% confidence interval [95% CI] 1.22–5.83; P = 0.0006). High coefficient of variation and standard deviation values were significantly associated with increased mortality, increasing death risk by 18% (OR 1.18, 95% CI 1.01–1.38; P = 0.03) and 9% (OR 1.09, 95% CI 1.01–1.18; P = 0.03), respectively. Mean glucose concentrations were also significantly associated with mortality, increasing death risk by 5% (OR 1.05, 95% CI 1.02–1.08; P = 0.0008).ConclusionsGlycemic indices (especially hypoglycemia and GV), rather than reactive inflammatory biomarkers or vital signs, were associated with mortality in non‐intensive care unit diabetes mellitus patients with infections.
Aims/IntroductionWe investigated whether dulaglutide (DU)‐combined conventional insulin therapy is beneficial for glycemic control in non‐critically ill hospitalized patients with type 2 diabetes.Materials and MethodsThis study was a prospective, randomized controlled pilot study. Participants were randomized to either basal‐plus (BP) therapy, where basal insulin and corrective doses of regular insulin were administered before meals, or BP + DU therapy, where BP therapy was combined with DU. Blood glucose (BG) levels before and after every meal were measured for 7 days after assignment to groups. Because we consider the ideal BG during hospitalization to be within 100–180 mg/dL, we defined this range as the hospitalized ideal glucose range (hIGR). We compared the percentage of BG measurements within the hIGR among all BG measurements (%hIGR), mean BG, glucose variability and insulin dose between the two groups.ResultsOf 54 patients, 27 were assigned to the BP group and 27 to the BP + DU group. The %hIGR was significantly higher (44% vs 56%, P < 0.001), and the frequency of BG >240 mg/dL and BG <70 mg/dL was significantly lower in the BP + DU group than in the BP group (both P < 0.001). The mean BG (183 ± 29 vs 162 ± 30 mg/dL, P < 0.05), standard deviation (P < 0.01), coefficient of variation (P < 0.01) and total regular insulin dose (P < 0.05) in the BP + DU group were significantly lower than those in the BP group. No significant side‐effects were observed in either group.ConclusionsBP + DU therapy reduced the frequency of hyperglycemia and hypoglycemia, and resulted in a lower glucose variability.
Objective The aim of this study was to determine whether nocturnal hypoglycemia may be predicted according to morning glucose levels. Methods We retrospectively evaluated 106 patients with type 2 diabetes who underwent continuous glucose monitoring during admission. The pre-breakfast glucose level (Pre-breakfast level), highest postprandial glucose level within 3 hours after breakfast (Highest level), time from the start of breakfast to the highest postprandial glucose level (Highest time), difference between the pre-breakfast and highest postprandial breakfast glucose levels (Increase), area under the glucose curve (≥180 mg/dL) within 3 hours after breakfast (Morning AUC), post-breakfast glucose gradient (Gradient), and the increase-to-pre-breakfast ratio (Increase/Pre-breakfast) were calculated. The subjects were divided into hypoglycemic and non-hypoglycemic patients and compared for the above parameters using the t-test. A receiver operating characteristic analysis was used to determine the optimal cut-off values to predict nocturnal hypoglycemia (Hypoglycemia). Results Twenty-eight patients (26.4%) had hypoglycemia. The Pre-breakfast levels were significantly lower in patients with hypoglycemia than those without (p=0.03). The Increases were significantly higher in patients with hypoglycemia than those without (p=0.047). The Increase/Pre-breakfast ratio were significantly larger in patients with hypoglycemia than those without (p=0.0002). Their cut-off values were as follows (level, sensitivity, specificity, and area under the curve): 123 mg/dL, 0.89, 0.55, and 0.78 (p<0.0001); 90.5 mg/dL, 0.75, 0.64, and 0.76 (p<0.0001); and 90.2%, 0.75, 0.76, and 0.78 (p<0.0001), respectively. Conclusion Major increases between the pre- and post-breakfast glucose levels may predict nocturnal hypoglycemia in patients with type 2 diabetes.
Background and study aims: l-Menthol (LM), sprayed on the distal gastric mucosa, is a safe antispasmodic agent used during esophagogastroduodenoscopy (EGD). However, it seems to affect gastric mucosal endoscopic findings. Therefore, we evaluated whether LM causes specific changes and impacts the endoscopic morphology of gastric lesions. Patients and methods: A total of 98 patients scheduled to undergo EGD were randomly assigned to receive LM solution (160 mg of 0.8 % LM added to 2.5 mL of indigo carmine [IC]; n = 49; LM group) or decuple-diluted IC solution without LM (n = 49; placebo group). We compared the incidence of specific mucosal changes and the difference in the endoscopic findings of several gastric lesions between these groups. Results: Annular-reticular – like mucosal changes appeared immediately after the administration of LM solution. This change was observed in 71.4 % of the LM group compared with 12.2 % of the placebo group (P < 0.01). In the placebo group, this change was observed in 14.7 % of subjects with atrophic gastritis compared with 6.7 % of those without atrophic gastritis (P = 0.39), whereas in the LM group, this change was observed in 84.8 % of subjects with atrophic gastritis compared with 43.8 % of those without atrophic gastritis (P < 0.01). Most early gastric cancers, erosions, and ulcers observed in this study became well demarcated after LM administration, although the incidence of gastric lesions did not differ significantly between the two groups. Conclusion: LM changes the gastric mucosa into edematous mucosa, and this occurs more frequently in atrophic gastric mucosa than in pathologic lesions. LM may facilitate the demarcation of pathologic gastric lesions without intestinal metaplasia.
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