کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2195632 1550854 2016 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
A long-term high-fat, high-sucrose diet in Bama minipigs promotes lipid deposition and amyotrophy by up-regulating the myostatin pathway
ترجمه فارسی عنوان
یک رژیم غذایی با طول عمر بالا و چربی بالا در شیرینی های باما باعث بالا رفتن میزان رسوب چربی و آمیوتروفی می شود با تنظیم مسیر مایواستاتین
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
چکیده انگلیسی


• Long-term high-fat high-sucrose diet promotes lipid deposition.
• Long-term high-fat high-sucrose diet promotes amyotrophy.
• The amyotrophy is induced by upregulating the MSTN pathway.

Skeletal muscle is as an important regulator of blood glucose and glycolipid metabolism and is closely related to motor ability. The underlying mechanisms by which dietary ectopic lipids in skeletal muscle prevents muscle growth remain elusive. We utilized miniature Bama swine as a model to mimic human obesity using prolonged dietary induction. After 23 months on a high-fat, high-sucrose diet, metabolic disorders were induced in the animals, which exhibited increased body weight, extensive lipid deposition in the skeletal muscle and amyotrophy. Microarray profiles demonstrated the up-regulation of genes related to fat deposition and muscle growth inhibition. We outline a clear potential pathway that in combination with increased 11β-hydroxysteroid dehydrogenase type 1, promotes expression of a major inhibitor, myostatin, by converting corticosterone to cortisol, which leads to the growth inhibition of skeletal muscle. This research provides new insights into the treatment of muscle diseases induced by obesity.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 425, 15 April 2016, Pages 123–132
نویسندگان
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