May 2007
IRIG: Muscle insulin resistance
05/22/2007 06:58
Accumulation of
triglycerides in skeletal muscle was taken as an
indicator of muscle insulin resistance. However,
this idea was challenged by a reverse
association of TG and insulin resistance in the
trained athlete muscle. Increasing evidence suggests
that not TG, but intermediates of FFAs (DAG and
ceramide), are the problem in muscle for insulin
resistance. This concept is re-enforced by two new
studies in JCI as following.
In last e-mail, I provided a PDF file of my review that is not printable. Now, the printable file is attached. Thanks a lot for your interest in the printable file.
Acute exercise increases triglyceride synthesis in skeletal muscle and prevents fatty acid–induced insulin resistance
Simon Schenk and Jeffrey F. Horowitz
published 17 May 2007, 10.1172/JCI30566 [Abstract] [PDF]
Upregulation of myocellular DGAT1 augments triglyceride synthesis in skeletal muscle and protects against fat-induced insulin resistanceLi Liu, Yiying Zhang, Nancy Chen, Xiaojing Shi, Bonny Tsang, and Yi-Hao Yu published 17 May 2007, 10.1172/JCI30565 [Abstract] [PDF]
by Jianping at PBRC
-----------------------------------
Jianping Ye, MD Professor of Molecular Biology Pennington Biomedical Research Center Louisiana State University System 6400 Perkins Road Baton Rouge, LA 70808 Phone: (225) 763-3163 Fax: (225) 763-2525 E-mail: yej@pbrc.edu
In last e-mail, I provided a PDF file of my review that is not printable. Now, the printable file is attached. Thanks a lot for your interest in the printable file.
Acute exercise increases triglyceride synthesis in skeletal muscle and prevents fatty acid–induced insulin resistance
Simon Schenk and Jeffrey F. Horowitz
published 17 May 2007, 10.1172/JCI30566 [Abstract] [PDF]
Upregulation of myocellular DGAT1 augments triglyceride synthesis in skeletal muscle and protects against fat-induced insulin resistanceLi Liu, Yiying Zhang, Nancy Chen, Xiaojing Shi, Bonny Tsang, and Yi-Hao Yu published 17 May 2007, 10.1172/JCI30565 [Abstract] [PDF]
by Jianping at PBRC
-----------------------------------
Jianping Ye, MD Professor of Molecular Biology Pennington Biomedical Research Center Louisiana State University System 6400 Perkins Road Baton Rouge, LA 70808 Phone: (225) 763-3163 Fax: (225) 763-2525 E-mail: yej@pbrc.edu
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IRIG: Obesity in "Cell" and "Science"
05/20/2007 21:18
In the current issue of
Cell, a
very nice review article summarizes recent
advance in hormone control of food intake,
a central topic in the study of obesity.
Hormones or peptides produced by fat cells, the
gastrointestinal tract, and the pancreas are
discussed in the regulation of appetite. The
molecular pathway is proposed for each
hormones.
In the current issue of Science, a new gene by the name of FTO (fat mass and obesity associated gene) is reported as a genetic factor predisposing to obesity. This gene is identified through a genowise screening of human genes. Mutation of this gene is associated with an increase in body weight or BMI.
In obesity, hyperinsulinemia and insulin resistance stays together. Their relationship represents a question of chicken and egg. Although most people believe that insulin resistance happens before hyperinsulinemia in obesity, the concept remains to be tested. With an interest into this question, I reviewed literature and wrote an article to support hyperinsulinemia for insulin resistance. I have received many requests for it through e-mail. Here, I wish to share it with you. Comments are welcome.
Attached are the PDF files of three papers mentioned above.
By Jianping at PBRC
—-----------------------------------------------------
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
In the current issue of Science, a new gene by the name of FTO (fat mass and obesity associated gene) is reported as a genetic factor predisposing to obesity. This gene is identified through a genowise screening of human genes. Mutation of this gene is associated with an increase in body weight or BMI.
In obesity, hyperinsulinemia and insulin resistance stays together. Their relationship represents a question of chicken and egg. Although most people believe that insulin resistance happens before hyperinsulinemia in obesity, the concept remains to be tested. With an interest into this question, I reviewed literature and wrote an article to support hyperinsulinemia for insulin resistance. I have received many requests for it through e-mail. Here, I wish to share it with you. Comments are welcome.
Attached are the PDF files of three papers mentioned above.
By Jianping at PBRC
—-----------------------------------------------------
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
IRIG: PGC-1a in Nature and Metformin in JCI
05/09/2007 21:30
PGC-1a (PPARg
coactivator 1a) is a transcription coactivator for
many transcription factors that are involved in the
regulation of glucose and fat metabolism. PGC-1a has
been a model to demonstrate the role of
nuclear cofactor in the control of metabolism.
PGC-1a stimulates gluconeogenesis
through induction of key enzymes PEPCK and
G6Pase, promotes fatty acid oxidation and heat
production through mitochondrial biosynthysis and
UCP1 expression. In a recent issue of "Nature",
PGC-1a is reported to link biological clock to
energy metabolism in mice (See attached PDF
file).
The study further supports the role of PGC-1a in
the regulation of energy (glucose and fat)
metabolism.
Metformin is a popular medicine in the control of blood glucose in patients with metabolic syndrom. The action mechanism of metformin is related to stimulation of glycolysis for glucose consumption. This activity is dependent on uptake of metformin by cells. In a recent issue of JCI, it is reported that cellular uptake of metformin is determined by a transmembrane protein by the name of organic cation transporter 1 (OCT1). In the absence of OCT1, metformin failed to exhibit its therapeutic activity in the OCT1 knockout mice. Given the high degree polymorphism of OCT1 gene in human, this study provides molecular basis for personalized medicine. Attached is the PDF file of the paper and the editorial.
By Jianping at PBRC
—----------------------------------
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
Metformin is a popular medicine in the control of blood glucose in patients with metabolic syndrom. The action mechanism of metformin is related to stimulation of glycolysis for glucose consumption. This activity is dependent on uptake of metformin by cells. In a recent issue of JCI, it is reported that cellular uptake of metformin is determined by a transmembrane protein by the name of organic cation transporter 1 (OCT1). In the absence of OCT1, metformin failed to exhibit its therapeutic activity in the OCT1 knockout mice. Given the high degree polymorphism of OCT1 gene in human, this study provides molecular basis for personalized medicine. Attached is the PDF file of the paper and the editorial.
By Jianping at PBRC
—----------------------------------
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
IRIG: Regulation of fat inflammation by STAMP (Cell paper)
05/09/2007 21:28
Inflammation
contributes to insulin resistance in obesity.
However, it is not clear what molecular pathway is
involved in initiation of the chronic inflammation
(such as TNFa, IL-6 expression and macrophage
infiltration) in adipose tissue under obesity.
Although FFA and ER stress have been shown to
contribute to the inflammatory response, the whole
story seems far from completed. The search
for new molecule or mechanism is undergoing in
adipose tissue. In this respect, a new study
published in the current issue of "Cell" demonstrates
that a transmembrane protein "STAMP2" is a new
molecule for the story. STAMP2 belongs to the
STAMP or STEAP family of six transmembrane domain
proteins. Members of this family are
metalloreductases that are important for the
cellular import of iron and copper. Loss of STAMP2 in
mice leads to increased inflammatory response in
adipose tissue. See full text of the paper in
attached PDF file.
By Jianping at PBRC
—-----------------------------
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu
By Jianping at PBRC
—-----------------------------
Jianping Ye, MD
Professor of Molecular Biology
Pennington Biomedical Research Center
Louisiana State University System
6400 Perkins Road
Baton Rouge, LA 70808
Phone: (225) 763-3163
Fax: (225) 763-2525
E-mail: yej@pbrc.edu