Work

Author response: The MODY-associated KCNK16 L114P mutation increases islet glucagon secretion and limits insulin secretion resulting in transient neonatal diabetes and glucose dyshomeostasis in adults

Year: 2024

Type: peer-review

Abstract: A mouse model of maturity-onset diabetes of the young illuminates that overactive TALK-1 channels limit β-cell calcium influx through membrane potential hyperpolarization, which blunts insulin secretion and causes glucose intolerance.

DOI: 10.7554/elife.89967.3.sa4

Authors: Arya Y Nakhe, Prasanna K Dadi, Jinsun Kim, Matthew T Dickerson, Soma Behera, Jordyn R Dobson, Shristi Shrestha, Jean-Philippe Cartailler, Leesa Sampson, Mark A Magnuson, David A Jacobson

Institution: Vanderbilt University

Language: English

Topic: Pancreatic function and diabetes

Subfield: Surgery

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: gold

Funders: Vanderbilt University, Vanderbilt University Medical Center, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases

Awards: G1805704937, G3143440274, G3416501184, G3865556588, Two-Pore-Domain Potassium Channels as Novel Targets for Modulating Islet Hormone Secretion, G5853943267, G6297262231, G9000052735, G9000081609, G9000106052, G9000129362, Designing selective TALK-1 inhibitors to reduce beta-cell dysfunction in diabetes

OpenAlex ID: W4396610482

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