蛋白FABP4 和核苷激酶的激素复合物调节胰岛功能。 脂肪细胞在脂肪分解过程中会分泌一种名为脂肪酸结合蛋白4（FABP4）的分子 、参于组成蛋白复合物fabkin1、异常或慢性脂肪分解会损伤胰岛B细胞、导致1型糖尿病。可抗体治。本文为糖尿病、肥胖症，心血管内分泌代谢疾病等关联基础医学研究论文。
(Google Translate: )
"Nature" discovered a new hormone, which has an important relationship with diabetes and obesity!
A hormone complex of the protein FABP4 and nucleoside kinases regulates islet function. Fat cells secrete a molecule called fatty acid binding protein 4 (FABP4) during lipolysis, which is involved in the composition of the protein complex fabkin1. Abnormal or chronic lipolysis can damage islet B cells and lead to type 1 diabetes. Can be cured. This article is a paper on basic medical research related to diabetes, obesity, cardiovascular endocrine and metabolic diseases, etc.
（グーグル翻訳： ）
「ネイチャー」が糖尿病や肥満と重要な関係を持つ新ホルモンを発見！
タンパク質 FABP4 とヌクレオシド キナーゼのホルモン複合体は、島の機能を調節します。 脂肪細胞は、脂肪分解中に脂肪酸結合タンパク質 4 (FABP4) と呼ばれる分子を分泌します。これは、タンパク質複合体 fabkin1 の組成に関与しています。異常または慢性的な脂肪分解は、膵島 B 細胞を損傷し、1 型糖尿病につながる可能性があります。 治せる。 この記事は、糖尿病、肥満、循環器・内分泌・代謝疾患などに関する基礎医学研究に関する論文です。
学术经纬
2021/12/20
论文
论文标题：A hormone complex of FABP4 and nucleoside kinases regulates islet function
作者：Prentice, Kacey J., Saksi, Jani, Robertson, Lauren T., Lee, Grace Y., Inouye, Karen E., Eguchi, Kosei, Lee, Alexandra, Cakici, Ozgur, Otterbeck, Emily, Cedillo, Paulina, Achenbach, Peter, Ziegler, Anette-Gabriele, Calay, Ediz S., Engin, Feyza, Hotamisligil, Gökhan S.
期刊：Nature
发表时间：2021/12/08
数字识别码：10.1038/s41586-021-04137-3
摘要：The liberation of energy stores from adipocytes is critical to support survival in times of energy deficit; however, uncontrolled or chronic lipolysis associated with insulin resistance and/or insulin insufficiency disrupts metabolic homeostasis1,2. Coupled to lipolysis is the release of a recently identified hormone, fatty-acid-binding protein 4 (FABP4)3. Although circulating FABP4 levels have been strongly associated with cardiometabolic diseases in both preclinical models and humans4,5,6,7, no mechanism of action has yet been described8,9,10. Here we show that hormonal FABP4 forms a functional hormone complex with adenosine kinase (ADK) and nucleoside diphosphate kinase (NDPK) to regulate extracellular ATP and ADP levels. We identify a substantial effect of this hormone on beta cells and given the central role of beta-cell function in both the control of lipolysis and development of diabetes, postulate that hormonal FABP4 is a key regulator of an adipose–beta-cell endocrine axis. Antibody-mediated targeting of this hormone complex improves metabolic outcomes, enhances beta-cell function and preserves beta-cell integrity to prevent both type 1 and type 2 diabetes. Thus, the FABP4–ADK–NDPK complex, Fabkin, represents a previously unknown hormone and mechanism of action that integrates energy status with the function of metabolic organs, and represents a promising target against metabolic disease.
