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Vishal Patel Amit Joharapurkar Tejal Gandhi Kirti Patel Nirav Dhanesha Samadhan Kshirsagar Vipin Dhote Jaysukh Detroja Rajesh Bahekar Mukul Jain 《Journal of Diabetes》2013,5(2):163-171
Background: In addition to its glucoregulatory actions, exendin‐4, a stable glucagon‐like peptide‐1 receptor agonist, exhibits protective effects in the pancreas and anti‐obesity effects. Suitable combination treatment with other anti‐obesity or pancreas protective agents would be an effective approach to optimize these additional effects. In the present study, we investigated the effects of the addition of omeprazole, a proton pump inhibitor, to exendin‐4 in db/db mice, an experimental model of obesity and type 2 diabetes. Methods: The effects repeated dose treatment for 14 days with exendin‐4 (8 μg/kg, s.c.) and omeprazole (30 mg/kg, s.c.) on glycemic control, food intake, and body weight were determined in obese and hyperglycemic db/db mice. The effects of these treatments on plasma gastrin, ghrelin, and leptin levels were determined, along with effects on nausea‐like symptoms. The pancreatic effects of the repeated dose treatment were assessed by measuring %HbA1c in the circulation as well as pancreatic insulin and glucagon content and glucokinase activity. Results: Combination treatment resulted in significant decreases in plasma leptin and ghrelin levels after repeated dosing. Omeprazole improved the anorectic and body weight‐lowering effects and reversed the inhibitory effect of exendin‐4 on gastrin levels after repeated dose treatment. The 14‐day combination treatment significantly reduced glucose excursion and improved insulin levels, with a concomitant decrease in %HbA1c levels. It also improved glucokinase activity and pancreatic insulin content, with a significant decrease in glucagon content. Conclusions: Combined treatment with omeprazole with exendin‐4 reduces food intake and body weight gain, most likely through changes in plasma ghrelin and leptin levels, and improves pancreatic insulin and glucagon content by improving glucokinase activity. 相似文献
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Adolfo Daniel Rodríguez‐Carrizalez José Alberto Castellanos‐González Esaú César Martínez‐Romero Guillermo Miller‐Arrevillaga David Villa‐Hernández Pedro Pablo Hernández‐Godínez Genaro Gabriel Ortiz Fermín Paul Pacheco‐Moisés Ernesto Germán Cardona‐Muñoz Alejandra Guillermina Miranda‐Díaz 《Journal of Diabetes》2014,6(2):167-175
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Efficacy of metformin‐based oral antidiabetic drugs is not inferior to insulin glargine in newly diagnosed type 2 diabetic patients with severe hyperglycemia after short‐term intensive insulin therapy
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Qingfeng Cheng Shumin Yang Changhong Zhao Zhihong Wang Zhengping Feng Rong Li Peng Ye Suhua Zhang Huacong Deng Bo Zhou Jian Long Lilin Gong Hua Qing Cheng Luo Qifu Li 《Journal of Diabetes》2015,7(2):182-191
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Epidemiology of diabetes mellitus,pre‐diabetes,undiagnosed and uncontrolled diabetes and its predictors in general population aged 15 to 75 years: A community‐based study (KERCADRS) in southeastern Iran;
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Hamid Najafipour Mojgan Sanjari Mostafa Shokoohi Ali‐Akbar Haghdoost Mehdi Afshari Mitra Shadkam Koorosh Etemad Ali Mirzazade 《Journal of Diabetes》2015,7(5):613-621
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Enumeration and functional investigation of endothelial progenitor cells in neovascularization of diabetic foot ulcer rats with a Chinese 2‐herb formula
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Jacqueline Chor Wing Tam Chun Hay Ko Kit Man Lau Ming Ho To Hin Fai Kwok Wing Sum Siu Ching Po Lau Wai Yee Chan Ping Chung Leung Kwok Pui Fung Clara Bik San Lau 《Journal of Diabetes》2015,7(5):718-728
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Glucagon‐like peptide 1 receptor agonist therapy is more efficacious than insulin glargine for poorly controlled type 2 diabetes: A systematic review and meta‐analysis
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Fu‐peng Liu Jian‐jun Dong Qing Yang Xian‐zhong Xue Zhong‐fa Ren Yi‐zhang Gan Lin Liao 《Journal of Diabetes》2015,7(3):322-328
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Pharmacological characterization of ZYDPLA1, a novel long‐acting dipeptidyl peptidase‐4 inhibitor
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Mukul R. Jain Amit A. Joharapurkar Rajesh H. Bahekar Harilal Patel Pradip Jadav Samadhan G. Kshirsagar Vishal J. Patel Kartikkumar N. Patel Vikram K. Ramanathan Pankaj R. Patel Ranjit C. Desai 《Journal of Diabetes》2015,7(5):708-717
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Prevalence of and risk factors for diabetic ketosis in Chinese diabetic patients with random blood glucose levels >13.9 mmol/L: Results from the CHina study in prEvalence of diabetiC Ketosis (CHECK) study
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Leili Gao Yufeng Li Dadong Fei Li Ma Shuchun Chen Bo Feng Qing Su Linong Ji 《Journal of Diabetes》2018,10(3):249-255
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Cardiovascular disease incidence,mortality and case fatality related to diabetes and metabolic syndrome: A community‐based prospective study (Ansung‐Ansan cohort 2001–12)
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Ji Cheol Bae Nam H. Cho Sunghwan Suh Jae Hyeon Kim Kyu Yeon Hur Sang‐Man Jin Moon‐Kyu Lee 《Journal of Diabetes》2015,7(6):791-799
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Type 2 diabetes mellitus (T2DM) is a progressive disease characterized by worsening insulin resistance and a decline in β‐cell function. Achieving good glycemic control becomes more challenging as β‐cell function continues to deteriorate throughout the disease process. The traditional management paradigm emphasizes a stepwise approach, and insulin has generally been reserved as a final armament. However, mounting evidence indicates that short‐term intensive insulin therapy used in the early stages of type 2 diabetes could improve β‐cell function, resulting in better glucose control and more extended glycemic remission than oral antidiabetic agents. Improvements in insulin sensitivity and lipid profile were also seen after the early initiation of short‐term intensive insulin therapy. Thus, administering short‐term intensive insulin therapy to patients with newly diagnosed T2DM has the potential to delay the natural process of this disease, and should be considered when clinicians initiate treatment. Although the early use of insulin is advocated by some guidelines, the optimal time to initiate insulin therapy is not clearly defined or easily recognized, and a pragmatic approach is lacking. Herein we summarize the current understanding of early intensive insulin therapy in patients with newly diagnosed T2DM, focusing on its clinical benefit and problems, as well as possible biological mechanisms of action, and discuss our perspective. 相似文献
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The forkhead box O (FoxO) subfamily has four members, namely FoxO1, FoxO3, FoxO4, and FoxO6. Unlike the other three members of the FoxO family, FoxO6 has garnered considerably less attention because of earlier reports that FoxO6 expression was limited to the brain. Recent data indicate that FoxO6 is produced in the liver of both rodents and humans. Hepatic FoxO6 activity, which remains at low basal levels in fed states, is markedly induced in fasted mice. FoxO6 activity becomes abnormally higher in the liver of mice with dietary obesity or type 2 diabetes (T2D). Genetically engineered mice with elevated FoxO6 activity in the liver exhibit prediabetes, culminating in the development of glucose intolerance, fasting hyperglycemia, and hyperinsulinemia. Conversely, inhibition of FoxO6 activity in the insulin‐resistant liver results in a reduction in fasting hyperglycemia, contributing to the amelioration of hyperinsulinemia in T2D mice. These new data suggest that FoxO6 is an important regulator of hepatic glucose metabolism in response to insulin or physiological cues. Insulin inhibits FoxO6 activity by promoting its phosphorylation and disabling its activity in the nucleus without altering its subcellular distribution via a mechanism that is distinct from other members of the FoxO subfamily. In this article, we comprehensively review the role of FoxO6 in glucose metabolism in health and disease. We also address whether FoxO6 dysregulation is a contributing factor for the pathogenesis of fasting hyperglycemia and discuss whether FoxO6 is a potential therapeutic target for improving fasting hyperglycemia in T2D. 相似文献