2022
DOI: 10.3389/fendo.2022.984198
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Abstract: Owing to the increasing prevalence of type 2 diabetes, the development of novel hypoglycemic drugs has become a research hotspot, with the ultimate goal of developing therapeutic drugs that stimulate glucose-induced insulin secretion without inducing hypoglycemia. Vasoactive intestinal peptide (VIP), a 28-amino-acid peptide, can stimulate glucose-dependent insulin secretion, particularly by binding to VPAC2 receptors. VIP also promotes islet β-cell proliferation through the forkhead box M1 pathway, but the spe… Show more

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Cited by 6 publications
(8 citation statements)
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“…To determine if the metabolic profiles in Vipr2 VPAC2R contributes to physiological responses to metabolic and psychogenic challenges in several ways. Our results support previous studies emphasizing that VPAC2R agonists may be leveraged as attractive drug candidates for the treatment of diabetes 21,23,28,30,82 and stress-related psychopathologies. [83][84][85] 4.1 | Strengths and limitations to the study…”
Section: Wild-typesupporting
confidence: 91%
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“…To determine if the metabolic profiles in Vipr2 VPAC2R contributes to physiological responses to metabolic and psychogenic challenges in several ways. Our results support previous studies emphasizing that VPAC2R agonists may be leveraged as attractive drug candidates for the treatment of diabetes 21,23,28,30,82 and stress-related psychopathologies. [83][84][85] 4.1 | Strengths and limitations to the study…”
Section: Wild-typesupporting
confidence: 91%
“…It is unlikely that impaired hypoglycemia during insulin challenge was a direct result of loss of VPAC2R function, since activation of VPAC2 receptors does not inhibit hepatic glycogenolysis and secretion of the glycogenolytic hormone glucagon 28 . In fact, because of their inability in this process, in conjunction with their insulinotropic action, VPAC2 receptors are studied for their potential as a novel target for the treatment of T2D 28,30 . More likely is the possibility that, in the absence of VPAC2R in our mutant mice, PACAP‐ or VIP‐mediated activation of the preserved and unchallenged VPAC1 and/or PAC1 receptors, respectively, can promote glucose output via direct hepatic glycogenolytic effects and/or indirectly by stimulating pancreatic secretion of glucagon to counter insulin action 26,27,75 .…”
Section: Discussionmentioning
confidence: 99%
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