کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2022597 | 1542415 | 2011 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Abnormally decreased NO and augmented CO production in islets of the leptin-deficient ob/ob mouse might contribute to explain hyperinsulinemia and islet survival in leptin-resistant type 2 obese diabetes
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Abnormally decreased NO and augmented CO production in islets of the leptin-deficient ob/ob mouse might contribute to explain hyperinsulinemia and islet survival in leptin-resistant type 2 obese diabetes Abnormally decreased NO and augmented CO production in islets of the leptin-deficient ob/ob mouse might contribute to explain hyperinsulinemia and islet survival in leptin-resistant type 2 obese diabetes](/preview/png/2022597.png)
چکیده انگلیسی
⺠Our recent data showed that CO has a signaling messenger function in rodent pancreatic islets. ⺠Present results show that islets from young and adult ob/ob mice displayed very low NO production. ⺠In contrast, production of CO, a NOS inhibitor, was impressively raised in ob/ob mice. ⺠While GLP-1 and GIP suppressed NOS activities from ob/ob mice leptin had opposite effects. ⺠This beneficial effect might have its clinical counterpart in human type 2 obese diabetes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Regulatory Peptides - Volume 170, Issues 1â3, 10 October 2011, Pages 43-51
Journal: Regulatory Peptides - Volume 170, Issues 1â3, 10 October 2011, Pages 43-51
نویسندگان
Javier Jimenez-Feltstrom, Albert Salehi, Sandra Meidute Abaraviciene, Ragnar Henningsson, Ingmar Lundquist,