日本科學(xué)家在11月21日出版的美國《科學(xué)》雜志上報告說，肝臟中一種蛋白質(zhì)活躍可使胰腺中分泌胰島素的貝塔細胞增殖。
胰島素是一種具備降血糖功能的激素,，由胰腺中的貝塔細胞分泌,。日本東北大學(xué)教授片桐秀樹領(lǐng)導(dǎo)的研究小組注意到,，動物一旦肥胖,，它們肝臟中的蛋白質(zhì)“ERK”就會變得活躍,，胰腺中貝塔細胞的數(shù)量也會相應(yīng)增加。
研究人員推測“ERK”蛋白質(zhì)的活躍引發(fā)貝塔細胞增殖,，并通過實驗證實了這一點,。他們通過基因改造技術(shù)使實驗鼠肝臟中的“ERK”蛋白質(zhì)更容易變得活躍，結(jié)果,，其胰腺中貝塔細胞的數(shù)量增加到正常值的兩倍,，血糖值也相應(yīng)下降。
研究人員切斷實驗鼠肝臟和胰腺間的神經(jīng)回路,，然后再進行同樣的實驗,，胰腺中的貝塔細胞便不再增殖。這證明了“ERK”蛋白質(zhì)的作用通過神經(jīng)傳遞到胰腺,，最終使胰腺中的貝塔細胞增殖,。
這項研究成果有望為治療糖尿病帶來新思路，但“ERK”蛋白質(zhì)的活躍有引發(fā)癌癥的可能,，研究小組計劃進一步研究能否通過刺激肝臟和胰腺間神經(jīng)回路的某一部位,，達到與激活“ERK”蛋白質(zhì)相同的效果。（生物谷Bioon.com）
生物谷推薦原始出處：
Science 21 November 2008: DOI: 10.1126/science.1163971
Regulation of Pancreatic β Cell Mass by Neuronal Signals from the Liver
Junta Imai,1 Hideki Katagiri,2* Tetsuya Yamada,1 Yasushi Ishigaki,1 Toshinobu Suzuki,1,2 Hirohito Kudo,1,2 Kenji Uno,2 Yutaka Hasegawa,1 Junhong Gao,2 Keizo Kaneko,1,2 Hisamitsu Ishihara,1 Akira Niijima,3 Masamitsu Nakazato,4 Tomoichiro Asano,5 Yasuhiko Minokoshi,6 Yoshitomo Oka1
Metabolic regulation in mammals requires communication between multiple organs and tissues. The rise in the incidence of obesity and associated metabolic disorders, including type 2 diabetes, has renewed interest in interorgan communication. We used mouse models to explore the mechanism whereby obesity enhances pancreatic β cell mass, pathophysiological compensation for insulin resistance. We found that hepatic activation of extracellular regulated kinase (ERK) signaling induced pancreatic β cell proliferation through a neuronal-mediated relay of metabolic signals. This metabolic relay from the liver to the pancreas is involved in obesity-induced islet expansion. In mouse models of insulin-deficient diabetes, liver-selective activation of ERK signaling increased β cell mass and normalized serum glucose levels. Thus, interorgan metabolic relay systems may serve as valuable targets in regenerative treatments for diabetes.
1 Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
2 Division of Advanced Therapeutics for Metabolic Diseases, Center for Translational and Advanced Animal Research, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
3 Niigata University School of Medicine, Niigata 951-8150, Japan.
4 Third Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan.
5 Department of Medical Science, Graduate School of Medicine, University of Hiroshima, Hiroshima, Japan.
6 Division of Endocrinology and Metabolism, Department of Developmental Physiology, National Institute for Physiological Sciences, Okazaki, Japan.
