Response to comments on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:25

Response to comments on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:25

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The Role of Common Pharmaceutical Agents on the Prevention and Treatment of Pancreatic Cancer Pharmacology and therapeutic implications of current drugs for type 2 diabetes mellitus.Past and future corollaries of theories on causes of metabolic syndrome and obesity related co-morbidities part 2: a composite unifying theory review of human-specific co-adaptations to brain energy consumption.A novel humanized GLP-1 receptor model enables both affinity purification and Cre-LoxP deletion of the receptor.Short commentary on empagliflozin and its potential clinical impact Dipeptidyl peptidase-4 inhibitors in type 2 diabetes therapy--focus on alogliptin.PSCs and GLP-1R: occurrence in normal pancreas, acute/chronic pancreatitis and effect of their activation by a GLP-1R agonist.Effects of Linagliptin on Pancreatic α Cells of Type 1 Diabetic Mice.

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P2860

Response to comments on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:25

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2013 nî lūn-bûn

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2013 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2013 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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Response to comments on: Butle ...... ne tumors. Diabetes 2013;62:25

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Response to comments on: Butle ...... ne tumors. Diabetes 2013;62:25

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Response to comments on: Butle ...... ne tumors. Diabetes 2013;62:25

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Response to comments on: Butle ...... rs. Diabetes 2013;62:2595-2604

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Alexandra E Butler

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David W Dawson

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Mark Atkinson

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Tatyana Gurlo

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P2860

Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors

Current treatment options for type 2 diabetes mellitus in youth: today's realities and lessons from the TODAY study

Exendin-4 stimulates both beta-cell replication and neogenesis, resulting in increased beta-cell mass and improved glucose tolerance in diabetic rats

Chronic GLP-1 receptor activation by exendin-4 induces expansion of pancreatic duct glands in rats and accelerates formation of dysplastic lesions and chronic pancreatitis in the Kras(G12D) mouse model.

The presence of GAD and IA-2 antibodies in youth with a type 2 diabetes phenotype: results from the TODAY study.

Hepatic and glucagon-like peptide-1-mediated reversal of diabetes by glucagon receptor antisense oligonucleotide inhibitors.

Diabetic ketoacidosis in type 2 diabetes mellitus--pathophysiology and clinical presentation.

A critical analysis of the clinical use of incretin-based therapies: Are the GLP-1 therapies safe?

Pancreas volumes in humans from birth to age one hundred taking into account sex, obesity, and presence of type-2 diabetes

Comment on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:2595-2604

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10.2337/DB13-0996

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Martha Campbell-Thompson

Peter C Butler

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Response to comments on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:25

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P2860

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Response to comments on: Butler et al. Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors. Diabetes 2013;62:25

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