کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2838360 1165004 2016 18 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Reappraisal of GIP Pharmacology for Metabolic Diseases
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی پزشکی مولکولی
پیش نمایش صفحه اول مقاله
Reappraisal of GIP Pharmacology for Metabolic Diseases
چکیده انگلیسی

Glucagon-like peptide-1 (GLP-1) analogs are considered the best current medicines for type 2 diabetes (T2D) and obesity due to their actions in lowering blood glucose and body weight. Despite similarities to GLP-1, glucose-dependent insulinotropic polypeptide (GIP) has not been extensively pursued as a medical treatment for T2D. This is largely based on observations of diminished responses of GIP to lower blood glucose in select patients, as well as evidence from rodent knockout models implying that GIP promotes obesity. These findings have prompted the belief in some, that inhibiting GIP action might be beneficial for metabolic diseases. However, a growing body of new evidence – including data based on refined genetically modified models and improved pharmacological agents – suggests a paradigm shift on how the GIP system should be manipulated for metabolic benefits.

TrendsGIP, like GLP-1, is one of the predominant incretin hormones produced in the alimentary tract in response to food intake that function to lessen postprandial glucose excursions.Unlike GLP-1, promoting GIP action has been discredited as a viable therapeutic strategy for T2D, primarily because of its reported resistance in certain human subjects and its presumed obesogenic propensity, as deduced from rodent loss-of-function phenotypic analyses.The use of refined GIPR agonists, transgenic rodent models, and observations from conditional GIPR knockout models suggest that promoting GIP action is beneficial for T2D.Combining GIP and GLP-1 pharmacology provides enhanced potency and efficacy for treating T2D, including improvements in glycemia, body weight, and tolerability.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 22, Issue 5, May 2016, Pages 359–376
نویسندگان
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