کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2195616 1550852 2016 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Circulating and visceral adipose miR-100 is down-regulated in patients with obesity and Type 2 diabetes
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Circulating and visceral adipose miR-100 is down-regulated in patients with obesity and Type 2 diabetes
چکیده انگلیسی


• Blood miR-100 is lower in obese normoglycemic, lean and obese patients with T2D compared to lean normoglycemic individuals.
• Visceral adipose miR-100 is lower in obese patients with T2D compared to those without T2D.
• miR-100 inhibition resulted in increased adipocyte differentiation.
• IGFR and mTOR are direct targets of miR-100 in pre-adipocytes.

Obesity is a major public health problem conferring substantial excess risk for Type 2 diabetes (T2D). The role of microRNAs (miRNAs) in obesity and adipose tissue is not clearly defined. We hypothesize that circulating miRNA expression profiles vary according to differences in body mass index (BMI) and T2D and circulating miRNAs may reflect adipose tissue expression. Compared to healthy, lean individuals, circulating miR-100 was significantly lower in obese normoglycemic subjects and subjects with T2D. In visceral adipose tissue, expression of miR-100 was lower from obese subjects with T2D compared to obese subjects without T2D. miR-100 expression was significantly lower after adipogenic induction in human visceral, subcutaneous adipocytes and 3T3-L1 adipocytes. miR-100 reduced expression of mammalian target of rapamycin (mTOR) and Insulin Growth Factor Receptor (IGFR) directly. Differentiation of 3T3-L1 was accelerated by inhibition of miR-100 and reduced by miR-100 mimic transfection. Our data provide the first evidence of an association of circulating miR-100 with obesity and diabetes. Additionally, our in-vitro findings, and the miR-100 expression patterns in site-specific adipose tissue suggest miR-100 to modulate IGFR, mTOR and mediate adipogenesis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 427, 15 May 2016, Pages 112–123
نویسندگان
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