کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10756403 | 1050383 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Macrophage migration inhibitory factor diminishes muscle glucose transport induced by insulin and AICAR in a muscle type-dependent manner
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
AMPKAICAREDL5′AMP-activated protein kinase - 5'AMP پروتئین کیناز فعال شده استTibialis Anterior - Tibialis قدامیextensor digitorum longus - اکستانسور بلند شست انگشتانinterleukin - اینترلوکینtumor necrosis factor-α - تومور نکروز عامل αMIF - شهرMacrophage migration inhibitory factor - عامل مهارکننده مهاجرت ماکروفاژSkeletal muscle - عضله اسکلتیTNF-α - فاکتور نکروز توموری آلفاlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Myokine - میوکینglucose transport - گلوکز حمل و نقل
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Skeletal muscle is a primary organ that uses blood glucose. Insulin- and 5â²AMP-activated protein kinase (AMPK)-regulated intracellular signaling pathways are known as major mechanisms that regulate muscle glucose transport. It has been reported that macrophage migration inhibitory factor (MIF) is secreted from adipose tissue and heart, and affects these two pathways. In this study, we examined whether MIF is a myokine that is secreted from skeletal muscles and affects muscle glucose transport induced by these two pathways. We found that MIF is expressed in several different types of skeletal muscle. Its secretion was also confirmed in C2C12 myotubes, a skeletal muscle cell line. Next, the extensor digitorum longus (EDL) and soleus muscles were isolated from mice and treated with recombinant MIF in an in vitro muscle incubation system. MIF itself did not have any effect on glucose transport in both types of muscles. However, glucose transport induced by a submaximal dose of insulin was diminished by co-incubation with MIF in the soleus muscle. MIF also diminished glucose transport induced by a maximal dose of 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), an AMPK activator, in the EDL muscle. These results suggest that MIF is a negative regulator of insulin- and AICAR-induced glucose transport in skeletal muscle. Since MIF secretion from C2C12 myotubes to the culture medium decreased during contraction evoked by electrical stimulations, MIF may be involved in the mechanisms underlying exercise-induced sensitization of glucose transport in skeletal muscle.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 444, Issue 4, 21 February 2014, Pages 496-501
Journal: Biochemical and Biophysical Research Communications - Volume 444, Issue 4, 21 February 2014, Pages 496-501
نویسندگان
Shouta Miyatake, Yasuko Manabe, Akiko Inagaki, Yasuro Furuichi, Mayumi Takagi, Masato Taoka, Toshiaki Isobe, Kiichi Hirota, Nobuharu L. Fujii,