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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.
Authors Dumas SN, Guo CA, Kim JK, Friedline RH, Ntambi JM
Submitted By Submitted Externally on 4/15/2019
Status Published
Journal Biochemical and biophysical research communications
Year 2019
Date Published 1/1/2019
Volume : Pages 508 : 87 - 91
PubMed Reference 30470572
Abstract 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.


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