التفاصيل البيبلوغرافية
العنوان: |
The NERP-4–SNAT2 axis regulates pancreatic β-cell maintenance and function |
المؤلفون: |
Weidong Zhang, Ayako Miura, Md Moin Abu Saleh, Koichiro Shimizu, Yuichiro Mita, Ryota Tanida, Satoshi Hirako, Seiji Shioda, Valery Gmyr, Julie Kerr-Conte, Francois Pattou, Chunhuan Jin, Yoshikatsu Kanai, Kazuki Sasaki, Naoto Minamino, Hideyuki Sakoda, Masamitsu Nakazato |
المصدر: |
Nature Communications, Vol 14, Iss 1, Pp 1-21 (2023) |
بيانات النشر: |
Nature Portfolio, 2023. |
سنة النشر: |
2023 |
المجموعة: |
LCC:Science |
مصطلحات موضوعية: |
Science |
الوصف: |
Abstract Insulin secretion from pancreatic β cells is regulated by multiple stimuli, including nutrients, hormones, neuronal inputs, and local signalling. Amino acids modulate insulin secretion via amino acid transporters expressed on β cells. The granin protein VGF has dual roles in β cells: regulating secretory granule formation and functioning as a multiple peptide precursor. A VGF-derived peptide, neuroendocrine regulatory peptide-4 (NERP-4), increases Ca2+ influx in the pancreata of transgenic mice expressing apoaequorin, a Ca2+-induced bioluminescent protein complex. NERP-4 enhances glucose-stimulated insulin secretion from isolated human and mouse islets and β-cell–derived MIN6-K8 cells. NERP-4 administration reverses the impairment of β-cell maintenance and function in db/db mice by enhancing mitochondrial function and reducing metabolic stress. NERP-4 acts on sodium-coupled neutral amino acid transporter 2 (SNAT2), thereby increasing glutamine, alanine, and proline uptake into β cells and stimulating insulin secretion. SNAT2 deletion and inhibition abolish the protective effects of NERP-4 on β-cell maintenance. These findings demonstrate a novel autocrine mechanism of β-cell maintenance and function that is mediated by the peptide–amino acid transporter axis. |
نوع الوثيقة: |
article |
وصف الملف: |
electronic resource |
اللغة: |
English |
تدمد: |
2041-1723 |
Relation: |
https://doaj.org/toc/2041-1723 |
DOI: |
10.1038/s41467-023-43976-8 |
URL الوصول: |
https://doaj.org/article/13b28fe0aa5b471fb9ba3b62af44728f |
رقم الانضمام: |
edsdoj.13b28fe0aa5b471fb9ba3b62af44728f |
قاعدة البيانات: |
Directory of Open Access Journals |