Background/AimsNon-alcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases in recent years. The aim of this study was to evaluate the effects of sitagliptin with and without a synbiotic supplement in the treatment of patients with NAFLD.MethodsIn total, 138 NAFLD patients aged 18-60 years were enrolled in the study. Patients were randomized to one of the following treatments for 16 weeks: Group I (n=68), sitagliptin 50 mg daily plus placebo (one capsule per day) or group II (n=70) sitagliptin 50 mg daily plus synbiotic (one capsule per day). Changes in fasting blood glucose (FBS), liver enzymes, lipid profile, and body mass index were compared between the groups.ResultsThe mean change in FBS with sitagliptin-placebo from baseline was -10.47±5.77 mg/dL, and that with sitagliptin-synbiotic was -13.52±4.16 mg/dL. There was a significant difference between the groups (P<0.001). The mean change in cholesterol (Chol) was -8.34±28.83 mg/dL with sitagliptin-placebo and -21.25±15.50 mg/dL with sitagliptinsynbiotic. There was a significant difference between the two groups (P=0.029). The administration of sitagliptin-placebo induced an increase of 6.13±27.04 mg/dL in low density lipoprotein (LDL), whereas sitagliptin-synbiotic induced a decrease of 14.92±15.85 mg/dL in LDL. A significant difference was observed between the two groups (P<0.001). On the other hand, in the sitagliptin-synbiotic group, there was significant improvement in aspartate aminotransferase (AST) level compared to the sitagliptin-placebo group (P=0.018).ConclusionsSitagliptin-synbiotic produced greater improvement in FBS, AST, Chol, and LDL compared to sitagliptin alone in patients with NAFLD.

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BACKGROUND Pancreatic cancer (PC) is a deadly, globally increasing cancer. The causes of PC are still insufficiently known, however smoking, diabetes mellitus (DM), and obesity have been identified as risk factors of PC, mostly in the developed countries. We evaluated these risk factors and their contribution to PC among an Iranian population. METHODS Cases and controls were selected from patients who were registered to a tertiary gastrointestinal diseases referral hospital in Tehran, Iran, from Jan 2012 to Jan 2018. Information on risk factors was collected by personal interview using a structured questionnaire. Logistic regression models were used to calculate adjusted odds ratios (AORs) and 95% confidence intervals (CIs). RESULTS We recruited 470 new patients with histopathological PC diagnosis and 526 sex and age-matched controls. Cigarette-smoking [AOR: 1.65 (1.15-2.38)], opium use [AOR: 1.58 (1.06-2.35)], DM [AOR: 1.99 (1.31-3.02)], and having a history of any cancer in a first-degree family member [AOR: 1.53 (1.14-2.05)] were associated with an increased risk of PC. We did not find an association between obesity [AOR: 0.99 (0.71-1.38)] and PC. Approximately 4.6%, 5.9%, 8.2%, and 10.9% risk of PC were related to cigarettesmoking, opium use, DM, and family history of any cancer, respectively. CONCLUSION This study supports that DM is associated with PC risk; however, similar to many studies in Asia, obesity is not associated with PC in Iranians. DM has the highest impact on PC development in Iranian women.

Background: Contrary to the reports about the useful effects of atorvastatin on blood lipids and insulin sensitivity by up-regulation of peroxisome proliferative-activated receptor gamma (PPAR-γ) expression, to our knowledge, there is inconclusive results about vitamin E. Also, there is no study to assess co-administration of vitamin E and atorvastatin on PPAR-γ mRNA expression, insulin sensitivity and lipid profile in diabetic patients. We compared this effect in hyperlipidemic subjects with type 2 diabetes mellitus (T2DM). Methods: At the present randomized clinical trial (RCT), 30 T2DM women with hyperlipidemia were categorized into the treated group with 20 mg atorvastatin plus 400 IU vitamin E supplement (n = 15) or atorvastatin plus placebo (n = 15) per day for 12 weeks. Anthropometric and biochemical measures were done at the baseline and after the 12-week intervention. PPAR-γ mRNA expression was measured in the peripheral blood mononuclear cells (PBMCs) of all patients. Results: After adjusting for the baseline measures, vitamin E resulted in significant improvements in insulin sensitivity in terms of HOMA-IR (-1.01±0.52 vs. -2.56 ± 0.54, P = 0.04) and serum insulin (-0.55±0.35 vs. -6.5 ± 1.3, P < 0.001), compared with the atorvastatin plus placebo. Adjusted for the baseline variables, compared with the atorvastatin plus placebo, vitamin E supplementation could up-regulate PPAR-γ mRNA expression (OR=5.4, 95% CI=0.8-36.9, P=0.04) in PBMC of T2DM women. Conclusions: Vitamin E supplementation along with atorvastatin may improve insulin sensitivity through up-regulation of PPAR-γ gene. More RCTs are needed to reach conclusive results. Trial registration: The present study is registered under ClinicalTrials.gov Identifier no. IRCT20170918036256N1.

BACKGROUND:Diabetes mellitus is a progressive disorder that often requires combination therapy.AIM:This study aimed to compare and study of add-on sitagliptin versus pioglitazone in patients with type 2 diabetes inadequately controlled with metformin.METHODS:This 12-week, randomised, open-label and single centre study compared sitagliptin (100 mg daily, n = 80) and pioglitazone (30 mg daily, n = 80) in type 2 diabetic patients whose disease was not adequately controlled with metformin.RESULTS:The mean change in HbA1c from baseline was -1.001 ± 0.83 with sitagliptin and -0.75 ± 1.20 with pioglitazone, and there were no significant difference between groups (P = 0.132). The mean change in fasting blood sugar (FBS) was -18.48 ± 33.32 mg/dl with sitagliptin and -20.53 ± 53.97 mg/dl with pioglitazone, and there were no significant difference between groups (P = 0.773). Sitagliptin caused 1.08 ± 2.39 kg decrease in weight, whereas pioglitazone caused 0.27 ± 2.42 kg increase in weight, with a between-group difference of 0.81 kg (P < 0.001). On the other hand, in sitagliptin group, there was greater improvement in lipid profile than pioglitazone group.CONCLUSION:Sitagliptin and Pioglitazone demonstrated similar improvements in glycemic control in type 2 diabetes mellitus patients whose diabetes had been inadequately controlled with metformin. Nevertheless, sitagliptin was more effective than pioglitazone regarding lipid and body weight change.