2015
DOI: 10.1186/s40200-016-0256-4
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Retraction Note: therapeutic stimulation of GLP-1 and GIP protein with DPP-4 inhibitors for type-2 diabetes treatment

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Cited by 3 publications
(4 citation statements)
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“…For several decades, hyperglycaemia was considered to arise from the poorly defined phenomenon of insulin resistance coupled with the immunological or biochemical toxicity to insulin‐secreting beta cells in the pancreas, manifesting as beta cell failure. More recently these have been joined by abnormalities of the incretin system, evident as the reduced effect of glucagon‐like peptide‐1 (GLP‐1), glucose‐dependent insulinotropic peptide (GIP) and related proteins . These factors are encompassed in the diseases of diabetes, most prominently the autoimmune disease of type 1 diabetes, the obesity and metabolic disease of type 2 diabetes and the hyperglycaemia of pregnancy, including gestational diabetes mellitus (GDM)…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…For several decades, hyperglycaemia was considered to arise from the poorly defined phenomenon of insulin resistance coupled with the immunological or biochemical toxicity to insulin‐secreting beta cells in the pancreas, manifesting as beta cell failure. More recently these have been joined by abnormalities of the incretin system, evident as the reduced effect of glucagon‐like peptide‐1 (GLP‐1), glucose‐dependent insulinotropic peptide (GIP) and related proteins . These factors are encompassed in the diseases of diabetes, most prominently the autoimmune disease of type 1 diabetes, the obesity and metabolic disease of type 2 diabetes and the hyperglycaemia of pregnancy, including gestational diabetes mellitus (GDM)…”
Section: Introductionmentioning
confidence: 99%
“…Over the last few decades, the efficacy of treating hyperglycaemia with available agents to prevent macrovascular diseases has been variable and remains a subject of considerable controversy. An improved understanding of the unique mechanisms of action of sodium‐glucose co‐transporter‐2 (SGLT2) inhibitors and GLP‐1 agonists is encouraging research into their cardiovascular benefits and igniting hopes for a revolution in the treatment of diabetes …”
Section: Introductionmentioning
confidence: 99%
“…Another physiological substrate of DPP4 is glucose-dependent insulin polypeptide (GIP), also known as incretin, and the level of GIP increases with inhibition of DPP4 activity [ 35 , 36 ]. Similar to GLP-1, GIP enhances insulin secretion in pancreatic beta cells in a glucose-dependent manner but appears to act in a different way on glucagon secretion [ 37 , 38 ].…”
Section: Dpp4 and Dpp4 Inhibitions In Diabetesmentioning
confidence: 99%
“…Patients with type 2 diabetes express higher levels of the DPP‐4 protein and increased enzymatic activity in the blood and tissues than healthy controls . Moreover, DPP‐4 cleaves incretins, a group of metabolic hormones that includes glucose‐dependent insulinotropic polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1) . Additionally, DPP‐4 is widely expressed in T and B cells, natural killer cells, subsets of macrophages and hematopoietic progenitor cells, as well as in the epithelial cells, endothelial cells and keratinocytes of a variety of tissues .…”
Section: Introductionmentioning
confidence: 99%