共查询到20条相似文献,搜索用时 46 毫秒
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Glucagon‐like peptide‐1 (GLP‐1) is the primary incretin hormone secreted from the intestine upon uptake of food to stimulate insulin secretion from pancreatic β‐cells. GLP‐1 exerts its effects by binding to its G‐protein coupled receptors and subsequently activating adenylate cyclase, leading to generation of cyclic adenosine monophosphate (cAMP). cAMP stimulates insulin secretion via activation of its effectors PKA and Epac2 in pancreatic β‐cells. In addition to its insulinotropic effects, GLP‐1 also preserves pancreatic β‐cell mass by stimulating β‐cell proliferation. Unlike the action of sulphonylureas in lowering blood glucose levels, action of GLP‐1 is affected by and interplays with glucose levels. Due to such advantages, GLP‐1‐based therapeutics have been rapidly developed and used clinically for treatment of type 2 diabetes. However, molecular mechanisms underlying how GLP‐1 potentiates diminished glucose‐stimulated insulin secretion and β‐cell proliferation under diabetic conditions are not well understood. Here, we review the actions of GLP‐1 in regulation of insulin secretion and pancreatic β‐cell proliferation. 相似文献
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Revisiting multiple models of progression of β‐cell loss of function in type 1 diabetes: Significance for prevention and cure 下载免费PDF全文
Type 1 diabetes (T1D) results from a chronic autoimmune process that leads to β‐cell destruction and exogenous insulin dependence. The natural history of T1D proposed by Eisenbarth suggested six relatively independent stages over the course of the entire disease process, which was considered to be linear and chronic. Based on this classical theory, immunotherapies aim to prevent or reverse all these periods of β‐cell loss. Over the past 30 years, much novel information about the pathogenesis of T1D proved that there are complex metabolic changes occurring throughout the entire disease process. Therefore, new possible models for the natural history of the disease have been proposed; these models, in turn, may help facilitate fresh avenues for the prevention and cure of T1D. Herein, we briefly review recent findings in this field of research, with the aim of providing a better theoretical basis for clinical practice. 相似文献
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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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Adenosine triphosphate (ATP) synthesis and release in mitochondria play critical roles in regulating insulin secretion in pancreatic β cells. Mitochondrial dysfunction is mainly characterized by a decrease in ATP production, which is a central event in the progression of pancreatic β cell dysfunction and diabetes. ATP has been demonstrated to regulate insulin secretion via several pathways: (i) Intracellular ATP directly closes ATP‐sensitive potassium channel to open L‐type calcium channel, leading to an increase in free cytosolic calcium levels and exocytosis of insulin granules; (ii) A decrease in ATP production is always associated with an increase in production of reactive oxygen species, which exerts deleterious effects on pancreatic β cell survival and insulin secretion; and (iii) ATP can be co‐secreted with insulin from pancreatic β cells, and the released ATP functions as an autocrine signal to modulate insulin secretory process via P2 receptors on the cell membrane. In this review, the recent findings regarding the role and mechanism of ATP synthesis and release in regulation of insulin secretion from pancreatic β cells will be summarized and discussed. 相似文献
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Increased T cell immunoglobulin and mucin domain containing 4 (TIM‐4) is negatively correlated with serum concentrations of interleukin‐1β in type 2 diabetes 下载免费PDF全文
Peiqing Zhao Hongxing Wang Tao Li Chengbin Lei Xiaoyan Xu Wei Wang Xiaohong Liang Chunhong Ma Lifen Gao 《Journal of Diabetes》2016,8(2):199-205
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Aini Haddouche Christine Bellanne‐Chantelot Anne Rod Luc Fournier Laurence Chiche Jean‐Francois Gautier Jose Timsit Sandrine Laboureau Lucy Chaillous Rene Valero Etienne Larger Nathalie Jeandidier Jean‐Marie Wilhelm Marc Popelier Pierre‐Jean Guillausseau Charles Thivolet Pierre Lecomte Pierre‐Yves Benhamou Yves Reznik 《Journal of Diabetes》2020,12(1):48-57
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Human herpesvirus 8 infection DNA positivity is associated with low insulin secretion: A case‐control study in a sub‐Saharan African population with diabetes 下载免费PDF全文
Eric Lontchi‐Yimagou Jérôme Legoff Jean‐Louis Nguewa Philippe Boudou Eric V. Balti Jean J. Noubiap Vicky Kamwa Barbara Atogho‐Tiedeu Marcel Azabji‐Kenfack Eric N. Djahmeni Martine Etoa Gaelle Lemdjo Vanessa Balla Mesmin Y. Dehayem Fabienne Foufelle Jean‐Claude Mbanya Jean‐Francois Gautier Eugene Sobngwi 《Journal of Diabetes》2018,10(11):866-873
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Herein we review and discuss epidemiological, clinical, and experimental studies on diabetic cystopathy, a common chronic complication of diabetes mellitus with a variety of lower urinary tract symptoms, providing directions for future research. A search of published epidemiological, clinical, or preclinical trial literature was performed using the key words “diabetes”, “diabetic cystopathy”, “diabetic bladder dysfunction”, “diabetic lower urinary tract dysfunction”, “diabetic detrusor instability”. The classic symptoms of diabetic cystopathy are decreased bladder sensation, increased bladder capacity, and impaired bladder emptying with resultant increased post‐void residual volume. However, recent clinical evidence indicates a presence of storage symptoms, such as overactive bladder symptoms. The pathophysiology of diabetic cystopathy is multifactorial, including disturbances of the detrusor, neuron, urothelium, and urethra. Hyperglycemia, oxidative stress, and polyuria play important roles in inducing voiding dysfunction in diabetic individuals. Treatment choice depends on clinical symptoms and urodynamic abnormalities. Urodynamic evaluation is the cornerstone of diagnosis and determines management strategies. Diabetes mellitus could cause a variety of lower urinary tract symptoms, leading to diabetic cystopathy with broadly varied estimates of the prevalence rates. The exact prevalence and pathogenesis of diabetic cystopathy remains to be further investigated and studied in multicenter, large‐scaled, or randomized basic and clinical trials, and a validated and standardized workup needs to be made, improving diabetic cystopathy management in clinical practice. Further studies involving only female diabetics are recommended. 相似文献