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Identification of a novel mechanism regulating β-cell mass: Neuronal relay from the liver to pancreatic β-cells

Junta Imai, Yoshitomo Oka and Hideki Katagiri

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Recent studies have demonstrated that β-cell replication plays a central role in maintaining adult β-cell mass. β-cell proliferative activity changes dynamically to meet systemic needs throughout life. One condition in which β-cell proliferation is enhanced is obesity-related insulin resistance. However, the mechanism underlying this compensatory β-cell response is not well understood. We have identified a neuronal relay, originating in the liver, which enhances both insulin secretion and pancreatic β-cell proliferation. Blockade of this neural relay in murine obesity models inhibited pancreatic islet expansion during obesity development, showing this inter-organ communication system to be physiologically involved in compensatory β-cell proliferation. While there is controversy about which mechanism, proliferation of pre-existing β-cells or production of new β cells from progenitor cells, plays the dominant role in maintaining or regulating β-cell mass, we herein provide an example that proliferation of pre-existing β-cells contributes to a β-cell increment in obesity-related insulin resistance. Furthermore, we have shown the potential for clinical application of this inter-organ system as a therapeutic target for insulin-deficient diabetes.

Imai J, Katagiri H, Yamada T, Ishigaki Y, Suzuki T, Kudo H, Uno K, Hasegawa Y, Gao J, Kaneko K, Ishihara H, Niijima A, Nakazato M, Asano T, Minokoshi Y, Oka Y. Regulation of pancreatic β cell mass by neuronal signals from the liver. Science 2008; 322:1250-4.

Authors

Junta Imai

Divisions of Molecular Metabolism and Diabetes Center for Translational and Advanced Animal Research Tohoku University Graduate School of Medicine, Japan

Yoshitomo Oka

Divisions of Molecular Metabolism and Diabetes Center for Translational and Advanced Animal Research Tohoku University Graduate School of Medicine, Japan

Hideki Katagiri Corresponding author: katagiri@mail.tains.tohoku.ac.jp

Divisions of 2Advanced Therapeutics for Metabolic Diseases, for Translational and Advanced Animal Research Tohoku University Graduate School of Medicine, Japan

This is an open-access article

 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.