IGF‐I attenuates FFA‐induced activation of JNK1 phosphorylation and TNFα expression in human subcutaneous preadipocytes

• Published in: Obesity (Silver Spring, Md.) Vol. 21; no. 9; pp. 1843 - 1849
• Main Authors: Neacsu, Otilia, Cleveland, Kelly, Xu, Haiyan, Tchkonia, Tamara T., Kirkland, James L., Boney, Charlotte M.
• Format: Journal Article
• Language: English
• Published: United States 01.09.2013
• Subjects: Adipocytes - drug effects; Adipocytes - metabolism; Adult; Anthracenes - pharmacology; Body Fat Distribution; Fatty Acids, Nonesterified - metabolism; Fatty Acids, Nonesterified - pharmacology; Female; Humans; Inflammation Mediators - metabolism; Insulin Resistance; Insulin-Like Growth Factor I - metabolism; Insulin-Like Growth Factor I - pharmacology; Intra-Abdominal Fat - drug effects; Intra-Abdominal Fat - metabolism; JNK Mitogen-Activated Protein Kinases - metabolism; Lipopeptides - metabolism; Male; Obesity - metabolism; Omentum; Phosphorylation; Proto-Oncogene Proteins c-akt - metabolism; Subcutaneous Fat, Abdominal - drug effects; Subcutaneous Fat, Abdominal - metabolism; Toll-Like Receptors - metabolism; Tumor Necrosis Factor-alpha - metabolism

Objective Free fatty acids (FFAs) are increased in visceral fat and contribute to insulin resistance through multiple mechanisms, including c‐Jun N‐terminal kinase (JNK) activation and expression of TNFα. Given that insulin‐like growth factor‐1 (IGF‐1)‐mediated proliferation is impaired in omental c...