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Interleukin-6 derived from cutaneous deficiency of stearoyl-CoA desaturase- 1 may mediate metabolic organ crosstalk among skin, adipose tissue and liver
- Dumas, Sabrina N., Guo, Chang-an, Kim, Jason K., Friedline, Randall H., Ntambi, James M.
- Biochemical and biophysical research communications 2019 v.508 no.1 pp. 87-91
- adiposity, chemical bonding, energy expenditure, fatty liver, glucose, hair follicles, high fat diet, insulin resistance, interleukin-6, keratinocytes, lipolysis, liver, messenger RNA, mice, obesity, palmitic acid, phenotype, protein synthesis, pyruvate carboxylase, stearic acid, stearoyl-CoA desaturase, white adipose tissue
- Stearoyl-CoA desaturase 1 (SCD1), a lipogenic enzyme that adds a double bond at the delta 9 position of stearate (C18: 0) and palmitate (C16: 0), has been proven to be important in the development of obesity. Mice with skin-specific deficiency of SCD1 (SKO) display increased whole-body energy expenditure, which is protective against adiposity from a high-fat diet because it improves glucose clearance, insulin sensitivity, and hepatic steatosis. Of note, these mice also display elevated levels of the “pro-inflammatory” plasma interleukin-6 (IL-6). In whole skin of SKO mice, IL-6 mRNA levels are increased, and protein expression is evident in hair follicle cells and in keratinocytes. Recently, the well-known role of IL-6 in causing white adipose tissue lipolysis has been linked to indirectly activating the gluconeogenic enzyme pyruvate carboxylase 1 in the liver, thereby increasing hepatic glucose production. In this study, we suggest that skin-derived IL-6 leads to white adipose tissue lipolysis, which contributes to the lean phenotype of SKO mice without the incidence of meta-inflammation that is associated with IL-6 signaling.