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Chicken Polyclonal GCG Primary Antibody for IEM, ICC - ABIN617889
Pak, Cha, Rajotte, McArthur, Yoon: Human pancreatic islet cell specific 38 kilodalton autoantigen identified by cytomegalovirus-induced monoclonal islet cell autoantibody. in Diabetologia 1991
Show all 48 Pubmed References
Human Monoclonal GCG Primary Antibody for IHC (p) - ABIN3043073
Jiang, Deng, Duan, Chen, Xiang, Lu, Ma: Somatostatin receptors SSTR2 and SSTR5 are expressed in the human thoracic duct. in Lymphology 2011
Show all 9 Pubmed References
Human Polyclonal GCG Primary Antibody for IHC (p) - ABIN3042419
Chen, Yang, Zheng, Hu, Kong, Zhang: Effect of catch-up growth after food restriction on the entero-insular axis in rats. in Nutrition & metabolism 2010
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Human Monoclonal GCG Primary Antibody for CyTOF, FACS - ABIN4900763
Kornete, Beauchemin, Polychronakos, Piccirillo: Pancreatic islet cell phenotype and endocrine function throughout diabetes development in non-obese diabetic mice. in Autoimmunity 2013
Show all 3 Pubmed References
Human Monoclonal GCG Primary Antibody for ELISA, WB - ABIN537126
De León, Crutchlow, Ham, Stoffers: Role of glucagon-like peptide-1 in the pathogenesis and treatment of diabetes mellitus. in The international journal of biochemistry & cell biology 2006
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Human Monoclonal GCG Primary Antibody for ELISA, WB - ABIN966191
Geliebter, Hashim, Gluck: Appetite-related gut peptides, ghrelin, PYY, and GLP-1 in obese women with and without binge eating disorder (BED). in Physiology & behavior 2008
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Human Polyclonal GCG Primary Antibody for ELISA - ABIN2473805
Woods, Lutz, Geary, Langhans: Pancreatic signals controlling food intake; insulin, glucagon and amylin. in Philosophical transactions of the Royal Society of London. Series B, Biological sciences 2006
Human Polyclonal GCG Primary Antibody for RIA - ABIN2473807
Figueroa, Hess, Ky, Brown, Sandig, Hermanowski-Vosatka, Twells, Todd, Austin: Expression of the type I diabetes-associated gene LRP5 in macrophages, vitamin A system cells, and the Islets of Langerhans suggests multiple potential roles in diabetes. in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2000
Human Polyclonal GCG Primary Antibody for IF (p), IHC (p) - ABIN704246
Sun, Nie, Wang, Yang, Meng, Xiao, Xiang, Li, Fu, Wang: Factors that Affect Pancreatic Islet Cell Autophagy in Adult Rats: Evaluation of a Calorie-Restricted Diet and a High-Fat Diet. in PLoS ONE 2016
Human Monoclonal GCG Primary Antibody for ELISA, WB - ABIN969171
Arnés, González, Tornero-Esteban, Sancho, Acitores, Valverde, Delgado, Villanueva-Peñacarrillo: Characteristics of GLP-1 and exendins action upon glucose transport and metabolism in type 2 diabetic rat skeletal muscle. in International journal of molecular medicine 2008
GPR119 is the oleoyl-lysophosphatidylinositol receptor that is required for GLP-1 secretion in enteroendocrine cells.
RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice.
Glucagon role in the pathophysiology of type 2 diabetes.[review]
This review summarizes the current knowledge regarding the role of GLP-1 in the protection against oxidative damage and the activation of the Nrf2 signaling pathway. [review]
Study concludes that in healthy subjects, glucagon-like peptide-1 (GLP-1) increases cardiac output acutely due to a GLP-1-induced vasodilation in adipose tissue and skeletal muscle together with an increase in cardiac work.
Chenodeoxycholic acid stimulates glucagon-like peptide-1 secretion in patients after Roux-en-Y gastric bypass.
The results demonstrate that glucagon-like peptide-1 and insulin synergistically and additively activate vagal afferent neurons.
DPP-4 activity and GLP-1total levels were higher in patients with microvascular complications associated with T2DM. Contrary to expectations, no negative correlation was seen between GLP-1 and DDP-4 levels. This result suggests the possible inefficacy of DDP-4 activity as a marker to predict in vivo degradation of endogenous GLP-1.
Data suggest that cAMP acts as amplifier of insulin secretion triggered by Ca2+ elevation in beta-cells; both messengers are also positive modulators of glucagon release from alpha-cells, but in this case cAMP signaling may be the important regulator and Ca2+ signaling has a more permissive role. [REVIEW]
This study provides evidence that, in HepG2 cells, GLP-1 may affect cholesterol homeostasis by regulating the expression of miR-758 and ABCA1.
This study reports the transition dipole strengths and frequencies of the amyloid beta-sheet amide I mode for the aggregated proteins amyloid-beta1-40, calcitonin, alpha-synuclein, and glucagon.
genetic association studies in population in China: Data confirm that an SNP in an intron of SLC47A1 (rs2289669) is associated with hypoglycemic response to metformin in patients with newly diagnosed type 2 diabetes; differential increases in basal GLP1 plasma levels are also related to this SNP. (SLC47A1 = solute carrier family 47 member 1; GLP1 = glucagon-like peptide-1)
GLP-2 augmented BRIN BD11 beta-cell proliferation, but was less efficacious in 1.1B4 cells. These data highlight the involvement of GLP-2 receptor signalling in the adaptations to pancreatic islet cell stress.
Everolimus down-regulates the systemic levels of gastrin and glucagon in patients with pancreatic neuroendocrine tumors.
Glucagon-like peptide (GLP-2) stimulates cancer myofibroblast proliferation, migration and invasion; GLP-2 acts indirectly on epithelial cells partly via increased Insulin-like growth factor (IGF) expression in myofibroblasts.
Describe model, in which the release of GIP/GLP-1 is stimulated by glucose in the proximal small intestine, and no differences in the secretion dynamics between healthy individuals and patients with T2D are identified after taking differences in glucose profiles into account.
the solvent exposure of the two Phe sites along the glucagon sequence was determined, showing that 4F-Phe6 was fully solvent exposed and 4F-Phe22 was only partially exposed
Data suggest that dose/intensity-response relationships exist between exercise intensity and total plasma PYY levels, though the effects on total plasma GLP1 levels and hunger perceptions seem unclear. (PYY = peptide YY ; GLP1 = glucagon-like peptide 1)
GLP-2 could be considered an hormone causing positive energy balance, which, however has the role to mitigate the metabolic dysfunctions associated with hyper-adiposity. [review]
Studies indicate that nutrient-induced glucagonlike peptide-1 (GLP-1) response was one of the best predictors of type 2 diabetes mellitus (T2DM) remission after Roux-en-Y-gastric-bypass (RYGB).
Data suggest that Tas1r2 and Tas1r3 are involved in regulation of Glp1 secretion in enteroendocrine cells; 3DG (3-deoxyglucosone) attenuates high glucose-stimulated Glp1 secretion by antagonizing Tas1r2/Tas1r3 subunits and downstream cAMP signaling. (Tas1r2 = sweet taste receptor subunit Tas1r2; Tas1r3 = sweet taste receptor subunit Tas1r3; Glp1 = glucagon-like peptide-1)
data show that the CREB/CRTC2-dependent transcriptional pathway is critical for regulating glucose homeostasis by controlling production of GLP-1 from the L cells at the level of transcription, maturation, and exocytosis.
the results of the present study indicated that GLP1 may be a promising target for the development of novel therapeutic strategies for HGinduced nephropathy, and may function through the activation of SIRT1
this study, we investigated whether glucagon and glucagon-like peptide-1 (GLP-1), hormones produced by alpha cells, contribute to insulin secretion in INS-1 cells, a beta cell line. Co-treatment with glucagon and exendin-4 (Ex-4), a GLP-1 receptor agonist, additively increased glucose-stimulated insulin secretion in INS-1 cells
FXR exerts its function in L cells through interacting with CREB, a crucial transcriptional regulator of cAMP-CREB signaling pathway, to inhibit its transcriptional activity. Targeting FXR to rescue GLP-1 secretion may be a promising strategy for type II diabetes.
results show that glucagon controls gene expression and metabolic zonation in the liver through a counterplay with the Wnt/beta-catenin signaling pathway.
Data (including data from studies using transgenic and knockout mice) suggest that Glp1/Glp1r signaling in insulin-secreting cells plays important role in development of glucose intolerance in obesity; however, Glp1r is not required in insulin-secreting cells for improvement in glucose intolerance after weight loss due to bariatric surgery (here, vertical sleeve gastrectomy).
Chronic stress accelerates DPP4-mediated GLP-1 degradation and alters plasma adiponectin, accelerating vascular senescence and impairing ischemia-induced neovascularization.
Data suggest that metabolism of glutamine and related analogs by Gdh in intestinal L-cells explains why Glp1 secretion, but not that of insulin by pancreatic beta-cells, is activated by these secretagogues. (Gdh = glutamate dehydrogenase; Glp1 = glucagon-like peptide 1)
Glucokinase governs an alpha-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
in colonic crypt cultures, the GLP-1 secretion induced by such Gq + Gs GPR40 agonists is indeed inhibited by blockers of both Gq and Gs and is eliminated by combining these.
Enteric GLP-1 activates NO production by enteric neurons that is impaired in type 2 diabetes. Gut microbiota dysbiosis induces enteric neuropathy. Gut microbiota dysbiosis is responsible for the GLP-1 resistance.
of glucagon-like peptide-1 in vagotomized mice may prevent VLDL overproduction and insulin resistance induced by high-fat diet.
beta-cell function, plasma active GLP-1 levels, the GLP-1R pathway in beta cells and L cell differentiation, were investigated.
CCK/GLP-1 play contributory roles in anorexia induction by trichothecenes T-2 toxin, HT-2 toxin, diacetoxyscirpenol and neosolaniol.
The role of syntaxin 1A in GLP1 release from intestinal cells as a response to external stimuli is reported.
GCG neurons likely stimulate separate populations of downstream cells to produce a change in food intake and glucose homeostasis and that these effects depend on the metabolic state of the animal.
Together, our data indicate effects of AgoPAMs that go beyond glucose lowering previously observed with GPR40 partial agonist treatment with additional potential for weight loss.
pancreatic reactivation of Gcg fully restored the effect of exendin-[9-39] to impair both oral and intraperitoneal glucose tolerance.
data demonstrate that cattle express proglucagon and glucagon-like peptide 2 receptor mRNA primarily in small intestinal and colon tissues and increased nutrient intake increases ileal proglucagon mRNA and plasma glucagon-like peptide 2
Data suggest that casein, safflower oil, sucrose, and sweetening agent rebaudioside A stimulate GLP1 release/secretion from enteroendocrine cells. (GLP1 = glucagon-like peptide 1, a peptide fragment derived from proglucagon)
The patterns of colocalization of the K cell marker, glucagon-like insulinotropic peptide, and L cell markers, glucagon like peptide-1 and peptide YY, in enteroendocrine cells of the small intestine and colon of mouse and pig, were investigated.
The findings indicate that the brainstem preproglucagon neuronal system is highly conserved between rat and non-human primate
The protein encoded by this gene is actually a preproprotein that is cleaved into four distinct mature peptides. One of these, glucagon, is a pancreatic hormone that counteracts the glucose-lowering action of insulin by stimulating glycogenolysis and gluconeogenesis. Glucagon is a ligand for a specific G-protein linked receptor whose signalling pathway controls cell proliferation. Two of the other peptides are secreted from gut endocrine cells and promote nutrient absorption through distinct mechanisms. Finally, the fourth peptide is similar to glicentin, an active enteroglucagon.
, glucagon-like peptide 1
, glucagon-like peptide 2
, glucagon-like peptide I
, glucagon-like peptide-1
, preproglucagon B
, glucagon preproprotein
, preproglucagon A
, glucagon I
, proglucagon I