Transgenic insulin released from G cells preferentially signals in the liver |
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Authors: | Lu Yu-Chun Rozengurt Enrique Zhukova Elena |
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Institution: | Department of Medicine, Division of Digestive Diseases, David Geffen School of Medicine at UCLA and CURE: Digestive Diseases Research Center, Los Angeles, CA 90095, USA. |
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Abstract: | We have previously produced transgenic G-InsKi mice, a model allowing regulated portal insulin delivery from gastric G cells without using beta cells. Here, we report that in G-InsKi mice portal levels of transgenic human insulin are 6-fold higher than in peripheral circulation. Peptone-induced release of transgenic human insulin from G cells preferentially stimulated signaling cascades in the liver rather than in peripheral insulin-sensitive tissues, as judged by tyrosine phosphorylation of insulin receptor beta subunit and phosphorylation of protein kinase Akt/PKB at Thr-308. G-InsKi mice provide a novel animal model for elucidating direct effects of insulin on liver functions. |
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Keywords: | Transgenic G-InsKi mice Insulin G cell Diabetes Liver Hepatic insulin receptor phosphorylation Hepatic Akt phosphorylation Hepatic glucose production Senescence Akita mice |
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