Leptin suppresses stearoyl-CoA desaturase 1 by mechanisms independent of insulin and sterol regulatory element-binding protein-1c. Biddinger, S. B, Miyazaki, M., Boucher, J., Ntambi, J. M, & Kahn, C R. 55(7):2032–41, 7, 2006.
Leptin suppresses stearoyl-CoA desaturase 1 by mechanisms independent of insulin and sterol regulatory element-binding protein-1c. [link]Paper  doi  abstract   bibtex   
Stearoyl-CoA desaturase (SCD)1 catalyzes the rate-limiting reaction of monounsaturated fatty acid (MUFA) synthesis and plays an important role in the development of obesity. SCD1 is suppressed by leptin but induced by insulin. We have used animal models to dissect the effects of these hormones on SCD1. In the first model, leptin-deficient ob/ob mice were treated with either leptin alone or with both leptin and insulin to prevent the leptin-mediated fall in insulin. In the second model, mice with a liver-specific knockout of the insulin receptor (LIRKO) and their littermate controls (LOXs) were treated with leptin. As expected, leptin decreased SCD1 transcript, protein, and activity by >60% in ob/ob and LOX mice. However, the effects of leptin were not diminished by the continued presence of hyperinsulinemia in ob/ob mice treated with both leptin and insulin or the absence of insulin signaling in LIRKO mice. Furthermore, genetic knockout of sterol regulatory element-binding protein (SREBP)-1c, the lipogenic transcription factor that mediates the effects of insulin on SCD1, also had no effect on the ability of leptin to decrease either SCD1 transcript or activity. Thus, the effect of leptin on SCD1 in liver is independent of insulin and SREBP-1c, and leptin, rather than insulin, is the major regulator of hepatic MUFA synthesis in obesity-linked diabetes.
@article{Biddinger-2006-ID14,
  title     = {Leptin suppresses stearoyl-CoA desaturase 1 by mechanisms independent of
               insulin and sterol regulatory element-binding protein-1c.},
  abstract  = {Stearoyl-CoA desaturase ({SCD})1 catalyzes the rate-limiting reaction of
               monounsaturated fatty acid ({MUFA}) synthesis and plays an important role
               in the development of obesity. {SCD}1 is suppressed by leptin but induced
               by insulin. We have used animal models to dissect the effects of these
               hormones on {SCD}1. In the first model, leptin-deficient ob/ob mice were
               treated with either leptin alone or with both leptin and insulin to prevent
               the leptin-mediated fall in insulin. In the second model, mice with a
               liver-specific knockout of the insulin receptor ({LIRKO}) and their
               littermate controls ({LOX}s) were treated with leptin. As expected, leptin
               decreased {SCD}1 transcript, protein, and activity by >60\% in ob/ob and
               {LOX} mice. However, the effects of leptin were not diminished by the
               continued presence of hyperinsulinemia in ob/ob mice treated with both
               leptin and insulin or the absence of insulin signaling in {LIRKO} mice.
               Furthermore, genetic knockout of sterol regulatory element-binding protein
               ({SREBP})-1c, the lipogenic transcription factor that mediates the effects
               of insulin on {SCD}1, also had no effect on the ability of leptin to
               decrease either {SCD}1 transcript or activity. Thus, the effect of leptin
               on {SCD}1 in liver is independent of insulin and {SREBP}-1c, and leptin,
               rather than insulin, is the major regulator of hepatic {MUFA} synthesis in
               obesity-linked diabetes.},
  author    = {Biddinger, Sudha B and Miyazaki, Makoto and Boucher, Jeremie and Ntambi,
               James M and Kahn, C Ronald},
  volume    = {55},
  number    = {7},
  pages     = {2032--41},
  year      = {2006},
  month     = {7},
  url       = {http://www.pubmed.org/16804073},
  pmid      = {16804073},
  doi       = {10.2337/db05-0742},
  keywords  = {Animals, Insulin, Mice, Body Weight, Leptin, Stearoyl-CoA Desaturase, Base
               Sequence, Blood Glucose, {DNA} Primers, Energy Intake, Mice, Knockout,
               Mice, Obese, Polymerase Chain Reaction, Receptor, Insulin, Receptors,
               Leptin, Sterol Regulatory Element Binding Protein 1},
  file      = {FULLTEXT:pdfs/000/000/000000014.pdf:PDF}
}
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