IRIG: Leptin in Nature Medicine and FFA receptor review in JBC

The central activity of leptin is well established for the
control of food intake. This activity was believed to control adipose
tissue mass through inhibition of appetite. It was not clear if the
central leptin signal can be passed to adipose tissue directly through
nerves. Now, this possibility is supported by a recent study in Nature
Medicine. The paper suggests that leptin activates PI3K signaling
pathway in the brain, and generates a nerve signal, which is delivered
to the adipose tissue by the sympathetic nerves. In this mechanism,
leptin inhibits white adipose tissue mass through suppression of
lipogenesis. Interestingly, leptin finishes the job without activation
of the classical STAT3 signaling pathway in the brain, which is required
for inhibition of appetite by leptin.
See details in attached PDF file.
This paper is recommended by Dr. Hans‑Rudolf Berthoud at PBRC.

Receptors for free fatty acids (FFA) have drawn a lot of
attention in research for the FFA signaling pathways. Many cell membrane
receptors have been proposed to mediate FFA signal into the cells. These
included TLR4, CD36, FATP, and G‑protein related receptors. Recently,
the G‑protein related receptors have gained more territory in the fields
of metabolism, obesity and diabetes. For example, GPR40 is a G‑protein
receptor for FFA. It specifically mediates FFA signal in pancreatic
B‑cells. Knockout of GPR40 was shown to prevent insulin resistance
without influencing adiposity. If you like to know more about this group
of receptors,
see attached review article from JBC.



Have a nice weekend,



Jianping at PBRC/LSU

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Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center (PBRC)
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225)763‑3163
E‑mail: yej@pbrc.edu
Webpage: http://labs.pbrc.edu/generegulation/index.htm
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IRIR stands for "Insulin Resistance Interest Group", an electronic and
non‑profitable activity for promotion of basic research in metabolic
syndrome. The activity was started by me in 2003 at the Pennington
Biomedical Research Center. If you prefer to stop receiving this type of
e‑mail in the future, please let me know. I will be happy to make a
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