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Yi Zhang

Researcher at Shanxi Medical University

Publications -  27
Citations -  234

Yi Zhang is an academic researcher from Shanxi Medical University. The author has contributed to research in topics: Insulin & Adenylyl cyclase. The author has an hindex of 7, co-authored 27 publications receiving 125 citations.

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Journal ArticleDOI

GLP-1 Receptor Agonists: Beyond Their Pancreatic Effects

TL;DR: In this paper, the authors reviewed the therapeutic effects and possible mechanisms of action of GLP-1RAs in the nervous, cardiovascular, and endocrine systems and their correlation with metabolism, tumours and other diseases.
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Geniposide acutely stimulates insulin secretion in pancreatic β-cells by regulating GLP-1 receptor/cAMP signaling and ion channels.

TL;DR: The results collectively imply that inhibition of Kv channels is linked to geniposide-potentiated insulin secretion by acting downstream of the GLP-1R/cAMP/PKA signaling pathway.
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The adenylyl cyclase inhibitor MDL-12,330A potentiates insulin secretion via blockade of voltage-dependent K(+) channels in pancreatic beta cells.

TL;DR: The putative AC inhibitor MDL-12,330A enhances [Ca2+]i and insulin secretion via inhibition of KV channels rather than AC antagonism in beta cells, suggesting that the non-specific effects is needed to be considered for the right interpretation of the experimental results using this agent in the analyses of the role of AC in cell function.
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Inhibition of voltage-gated potassium channels mediates uncarboxylated osteocalcin-regulated insulin secretion in rat pancreatic β cells.

TL;DR: KV channels are involved in uncarboxylated osteocalcin-regulated insulin secretion in rat pancreatic β cells, and this finding provides new insight into the mechanisms of osteomiccin-modulated insulin secretion.
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The PLC/PKC/Ras/MEK/Kv channel pathway is involved in uncarboxylated osteocalcin-regulated insulin secretion in rats.

TL;DR: The results showed that uncarboxylated osteocalcin potentiated insulin secretion, inhibited Kv channels and increased [Ca2+]i compared to control, and showed that adenylyl cyclase (AC) did not influence the effect of uncar boxylated bone matrix protein on insulin secretion and KV channels, suggesting that AC is not involved in uncarBoxylated fractures-stimulated insulin secretion.