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Non‐coding RNA Editing Involved in Adipose Dysfunction during Aging
Author(s) -
Seidler Abbagael,
Marcelo Aileen,
Page Jamika,
Santanam Nalini
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.757.4
Subject(s) - adipogenesis , adipose tissue , endocrinology , medicine , biology , dicer , drosha , insulin resistance , microrna , insulin , genetics , gene , rna , rna interference
Adipose tissue is one of the key endocrine organs that maintain lipid and glucose homeostasis. Adipose dysfunction increases upon aging, and results in dramatic alterations in fat mass, distribution and function. This leads to age associated metabolic dysfunction and increased risk to cardiometabolic diseases. Continuous replenishment of mature adipocytes by differentiation of pre‐adipocytes is a must for normal adipose function. We recently showed decrease in adipogenesis during aging was due to dysfunction in microRNA's (miRNA) involved in adipogenesis (miR‐143). This dysfunction may be attributed to changes in enzymes involved in biogenesis of miRNA (DROSHA, DICER) or enzymes involved in modifying its function (ADAR). We determined the differences in the expression levels of these enzymes in Fisher 344 x Brown Norway hybrid rats (FBN) at ages 8 mo and 25 mo old (n=3). There were sex specific differences in the levels of both biogenesis and editing genes in peri‐gonadal adipose tissue from FBN rats with aging. The DROSHA and DICER levels were higher but editing enzymes (ADARs) lower in female rats and the reverse in male rats with aging. Sanger sequencing of miR‐143 (a key miRNA in adipogenesis) showed edited sequence in old rats compared to younger rats. Sex‐specific post‐transcriptional regulation of miRNA(s) involved in adipogenesis during aging in whole adipose tissue will also be explored in pre‐adipocytes and mature adipocytes from aging rats and correlated to metabolic changes leading to insulin resistance. Support or Funding Information Supported by NIH‐NIA‐R15 AG051062 (NS); Marshall University Biomedical Sciences Graduate Program, the Marshall University Foundation Summer Research Internship for Minority Students Fund, and by NIH Grant P20GM103434 to the West Virginia IDeA Network for Biomedical Research Excellence