Hindsight: Regulation of Nitric Oxide in Adipose TissueSaturday, July 7, 2012
Nitric oxide (NO) is an important cellular signaling molecule involved in many physiological and pathological processes. In adipose tissue, it has been shown to influence adipogenesis, insulin-stimulated glucose uptake, and lipolysis.
In 2004, we published a paper in the Journal of Lipid Research, in which we described the regulation of genes involved in the generation of nitric oxide in human adipose tissue.
The enzymes responsible for NO formation in adipose cells are endothelial NO synthase (eNOS) and inducible NO synthase (iNOS), whereas neuronal NO synthase (bNOS) is not expressed in adipocytes.
We characterized the expression pattern and the influence of adipogenesis, obesity, and weight loss on genes belonging to the NO system in human subcutaneous adipose cells by combining in vivo and in vitro studies.
We detected the expression of most of the genes known to belong to the NO system (eNOS, iNOS, subunits of the soluble guanylate cyclase, and both genes encoding cGMP-dependent protein kinases) in human adipose tissue and isolated human adipocytes.
In vitro adipogenic differentiation increased the expression level of iNOS significantly, whereas eNOS expression levels were not influenced.
The genes encoding eNOS, iNOS, and cGMP-dependent protein kinase 1 were expressed at higher levels in obese women, however, their expression was not influenced by 5% weight loss.
We also showed that insulin and angiotensin II (Ang II) increased NO production by human preadipocytes in vitro.
Based on these results, we suggested that increased eNOS and iNOS expression in adipocytes, perhaps secondary to local effects of insulin and Ang II may increase adipose tissue production of NO in obesity, which in turn, may affect adipogenesis, lipolysis or other aspects of adipocyte function.
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