Dual elimination of the glucagon and GLP-1 receptors in mice reveals plasticity in the incretin axis.
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Glucagon-like peptide-1 and cholecystokinin production and signaling in the pancreatic islet as an adaptive response to obesityPhysiology of proglucagon peptides: role of glucagon and GLP-1 in health and diseaseGlucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeoverFertility and pregnancy-associated ß-cell proliferation in mice deficient in proglucagon-derived peptidesAristaless-related homeobox plays a key role in hyperplasia of the pancreas islet α-like cells in mice deficient in proglucagon-derived peptidesVertical sleeve gastrectomy restores glucose homeostasis in apolipoprotein A-IV KO mice.Pancreatic GLP-1 receptor activation is sufficient for incretin control of glucose metabolism in mice.Pancreatic Neuroendocrine Tumors in Mice Deficient in Proglucagon-Derived Peptides.Contribution of brown adipose tissue activity to the control of energy balance by GLP-1 receptor signalling in miceRegulation of mouse intestinal L cell progenitors proliferation by the glucagon family of peptides.Glucagon receptor antagonism induces increased cholesterol absorption.Activation of enteroendocrine membrane progesterone receptors promotes incretin secretion and improves glucose tolerance in miceEctopic expression of GIP in pancreatic β-cells maintains enhanced insulin secretion in mice with complete absence of proglucagon-derived peptides.Liver-specific disruption of the murine glucagon receptor produces α-cell hyperplasia: evidence for a circulating α-cell growth factor.Blockade of glucagon signaling prevents or reverses diabetes onset only if residual β-cells persist.Endogenous GIP ameliorates impairment of insulin secretion in proglucagon-deficient mice under moderate beta cell damage induced by streptozotocinIncretin action in the pancreas: potential promise, possible perils, and pathological pitfalls.Update on incretin hormones.Ghrelin, the proglucagon-derived peptides and peptide YY in nutrient homeostasis.Physiology of incretins and loss of incretin effect in type 2 diabetes and obesity.The regulation of pre- and post-maturational plasticity of mammalian islet cell mass.Effects of Roux-en-Y gastric bypass on energy and glucose homeostasis are preserved in two mouse models of functional glucagon-like peptide-1 deficiency.Islet α cells and glucagon--critical regulators of energy homeostasis.Evolving function and potential of pancreatic alpha cells.Oral 2-oleyl glyceryl ether improves glucose tolerance in mice through the GPR119 receptor.A synopsis of factors regulating beta cell development and beta cell mass.The New Biology and Pharmacology of Glucagon.Immunohistochemical assessment of glucagon-like peptide 1 receptor (GLP-1R) expression in the pancreas of patients with type 2 diabetes.The glucagon-like peptide-1 receptor agonist Exendin 4 has a protective role in ischemic injury of lean and steatotic liver by inhibiting cell death and stimulating lipolysis.Cardiomyocyte glucagon receptor signaling modulates outcomes in mice with experimental myocardial infarction.The glucagon receptor is involved in mediating the body weight-lowering effects of oxyntomodulin.Regulation of glucose kinetics during exercise by the glucagon-like peptide-1 receptor.Regulation of amino acid metabolism and alpha cell proliferation by glucagon.Investigational glucagon receptor antagonists in Phase I and II clinical trials for diabetes.Glucagon receptor as a drug target: A witches' brew of eye of newt (peptides) and toe of frog (receptors).Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells.The Role of Pancreatic Preproglucagon in Glucose Homeostasis in Mice.Partial small bowel resection with sleeve gastrectomy increases adiponectin levels and improves glucose homeostasis in obese rodents with type 2 diabetes.Clinical Trials, Triumphs, and Tribulations of Glucagon Receptor Antagonists.Acute disruption of glucagon secretion or action does not improve glucose tolerance in an insulin-deficient mouse model of diabetes.
P2860
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P2860
Dual elimination of the glucagon and GLP-1 receptors in mice reveals plasticity in the incretin axis.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Dual elimination of the glucag ...... asticity in the incretin axis.
@en
Dual elimination of the glucag ...... asticity in the incretin axis.
@nl
type
label
Dual elimination of the glucag ...... asticity in the incretin axis.
@en
Dual elimination of the glucag ...... asticity in the incretin axis.
@nl
prefLabel
Dual elimination of the glucag ...... asticity in the incretin axis.
@en
Dual elimination of the glucag ...... asticity in the incretin axis.
@nl
P2093
P2860
P356
P1476
Dual elimination of the glucag ...... asticity in the incretin axis.
@en
P2093
Benjamin J Lamont
Maureen J Charron
Safina Ali
P2860
P304
P356
10.1172/JCI43615
P407
P577
2011-04-11T00:00:00Z