Induction of adiponectin, a fat-derived antidiabetic and antiatherogenic factor, by nuclear receptors.

By M. Iwaki, M. Matsuda, N. Maeda, T. Funahashi, Yuji Matsuzawa, M. Makishima, I. Shimomura. Diabetes, 2003

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Increased oxidative stress in obesity and its impact on metabolic syndrome. (2004, background): “were determined by Western blotting (40).”
Adipose Tissue Hypoxia in Obesity and Its Impact on Adipocytokine Dysregulation (2007, neutral): “differentiate into adipocytes, as described previously (25).”
Adipocytokines: mediators linking adipose tissue, inflammation and immunity (2006, background): “, as is activation of peroxisome-proliferator-activated receptor-γ ( PPARγ ) by its ligands thiazolidinediones, which are important for the treatment of type 2 diabetes mellitu”
Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice. (2007, background): “SREBP may not be involved in the inhibition, since it is not directly regulated by hypoxia (14).”
Regulation of energy metabolism by long-chain fatty acids. (2014, neutral): “by TZDs [194].”
Adiponectin mediates the metabolic effects of FGF21 on glucose homeostasis and insulin sensitivity in mice. (2013, background): “Our present study demonstrated that both the acute and chronic effects of FGF21 on adiponectin production are mediated in part by PPARg, a nuclear receptor that controls the gene transcription as well as the protein secretion of adiponectin (Wang et al., 2007; Iwaki et al., 2003).”