期刊
JOURNAL OF LIPID RESEARCH
卷 49, 期 2, 页码 308-323出版社
ELSEVIER
DOI: 10.1194/jlr.M700199-JLR200
关键词
differentiation; glucose; proliferation; protein synthesis; insulin-sensitive obese; insulin-resistant obese
Obesity and insulin resistance are independent risk factors for metabolic syndrome, diabetes, and cardiovascular disease. Adipose tissue samples from nonobese (NO), insulin-sensitive obese (ISO), and insulin-resistant obese (IRO) subjects from subcutaneous (SC) and omental (OM) adipose tissue (n = 28) were analyzed by microarray and confirmed by real-time PCR. Insulin signaling gene expression changes were greater in OM than in SC tissue and were related to insulin resistance rather than to obesity; few genes correlated with body mass index. Insulin receptor and insulin receptor substrate 1 (IRS-1) increased in the IRO versus pooled insulin-sensitive (NO+ISO) subjects. In glucose transport, PI3K alpha and PDK2 decreased in IRO subjects, whereas PI3K gamma, Akt2, GLUT4, and GLUT1 increased. IRS-1 regulators Jnk and IKK increased in IRO (P< 0.01 and P < 0.001 respectively). In protein synthesis, most genes examined were downregulated in IRO subjects, including mTor, Rheb, and 4EBP and eIF members (all P< 0.05). In proliferation, SHC, SOS, and Raf1 (P< 0.05) were increased, whereas Ras and MEK1/2 kinase 1 (P, 0.05) were decreased, in IRO subjects. Finally, in differentiation, PPAR gamma, CEBP alpha, and CEBP beta decreased, whereas PPAR delta, CEBP gamma, and CEBP epsilon increased, in IRO subjects (P< 0.05). Together, microarray and real-time PCR data demonstrate that insulin resistance rather than obesity is associated with altered gene expression of insulin signaling genes, especially in OM adipose tissue.
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