Dec 2008
IRIG: Chronic inflammation in adipose tissue: How and Why?
12/15/2008 09:50
Chronic inflammation
occurs in adipose tissue in obesity. This
is observed in many excellent studies with an increase in inflammation
cytokines and macrophage infiltration. It has been a question, why does
the inflammation occurs, and how does it mean? For your reference, here
are some results from our studies. The inflammation is likely a result
of hypoxia response in adipose tissue (1), and inflammation may serves
as a signal to stimulate angiogenesis in adipose tissue (2). The hypoxia
response may promote macrophage infiltration through induction of
chemokines (MIF) (1) as well as adipocyte death (3). The hypoxia may
contribute to systemic insulin resistance by increasing FFA and
decreasing adiponectin in circulation since it inhibits storage (TAG)
and secretion functions in adipocytes (1; 3). Adipose tissue hypoxia may
explain many other malfunction in adipose tissue and insulin resistance
in obstructive sleep apnea in obesity (4). Possible cause of the adipose
tissue hypoxia is discussed in a review (4). To keep the post short, I
am sorry that related studies by other labs are not cited here. They are
in the review article (Attached PDF file).
1. Ye J, Gao Z, Yin J, He H: Hypoxia is a potential risk factor for
chronic inflammation and adiponectin reduction in adipose tissue of
ob/ob and dietary obese mice. Am J Physiol Endocrinol Metab
293:E1118‑E1128, 2007
2. Pang C, Gao Z, Yin J, Zhang J, Jia W, Ye J: Macrophage Infiltration
into Adipose Tissue May Promote Angiogenesis for Adipose Tissue
Remodeling in Obesity. Am J Physiol Endocrinol Metab 295:E313‑E322, 2008
3. Yin J, Gao Z, He Q, Ye J: Role of hypoxia in obesity‑induced
disorders of glucose and lipid metabolism in adipose tissue. Am J
Physiol Endocrinol Metab doi:10.1152/ajpendo.90760.2008
4. Ye J: Emerging Role of Adipose Tissue Hypoxia in Obesity and Insulin
Resistance. Int J Obes DOI: Dec. 9th 2007, 2008
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
E‑mail: yej@pbrc.edu
Webpage: http://labs.pbrc.edu/generegulation/index.htm
IRIR stands for "Insulin Resistance Interest Group", an electronic and
non‑profitable academic 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 change in the e‑mail list. The previous posts can be found at:
http://c-ada.org/journalclub/journalclub.html. Your comments on the
post are welcome.
is observed in many excellent studies with an increase in inflammation
cytokines and macrophage infiltration. It has been a question, why does
the inflammation occurs, and how does it mean? For your reference, here
are some results from our studies. The inflammation is likely a result
of hypoxia response in adipose tissue (1), and inflammation may serves
as a signal to stimulate angiogenesis in adipose tissue (2). The hypoxia
response may promote macrophage infiltration through induction of
chemokines (MIF) (1) as well as adipocyte death (3). The hypoxia may
contribute to systemic insulin resistance by increasing FFA and
decreasing adiponectin in circulation since it inhibits storage (TAG)
and secretion functions in adipocytes (1; 3). Adipose tissue hypoxia may
explain many other malfunction in adipose tissue and insulin resistance
in obstructive sleep apnea in obesity (4). Possible cause of the adipose
tissue hypoxia is discussed in a review (4). To keep the post short, I
am sorry that related studies by other labs are not cited here. They are
in the review article (Attached PDF file).
1. Ye J, Gao Z, Yin J, He H: Hypoxia is a potential risk factor for
chronic inflammation and adiponectin reduction in adipose tissue of
ob/ob and dietary obese mice. Am J Physiol Endocrinol Metab
293:E1118‑E1128, 2007
2. Pang C, Gao Z, Yin J, Zhang J, Jia W, Ye J: Macrophage Infiltration
into Adipose Tissue May Promote Angiogenesis for Adipose Tissue
Remodeling in Obesity. Am J Physiol Endocrinol Metab 295:E313‑E322, 2008
3. Yin J, Gao Z, He Q, Ye J: Role of hypoxia in obesity‑induced
disorders of glucose and lipid metabolism in adipose tissue. Am J
Physiol Endocrinol Metab doi:10.1152/ajpendo.90760.2008
4. Ye J: Emerging Role of Adipose Tissue Hypoxia in Obesity and Insulin
Resistance. Int J Obes DOI: Dec. 9th 2007, 2008
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
E‑mail: yej@pbrc.edu
Webpage: http://labs.pbrc.edu/generegulation/index.htm
IRIR stands for "Insulin Resistance Interest Group", an electronic and
non‑profitable academic 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 change in the e‑mail list. The previous posts can be found at:
http://c-ada.org/journalclub/journalclub.html. Your comments on the
post are welcome.
|
IRIG: Tissue crosstalk in "Cell" and "Science"
12/01/2008 16:22
The pathogenesis of
systemic insulin resistance involves in
crosstalk among multiple organs/tissues including fat, muscle, liver,
pancreas, gut and brain. It is well accepted that the languages in such
crosstalk are hormones and nerve signals among these organs/tissues.
However, words that are used in these languages (signal mediators)
remains to be fully identified or interpreted. This issue is addressed
by several recent reports in Cell and Science. Below is the brief
introduction.
Fat control of muscle and liver: In Cell, a new product of
adipose tissue named "lipokine" was reported to mediate fat tissue
signal in the control of metabolism in muscle and liver. This new
molecule (real name: C16:1n7‑palmitoleate) is identified with lipidomics
approach. It strongly stimulates muscle insulin action and suppresses
hepatosteatosis. The data reveal a lipid‑mediated endocrine network and
supports a new concept "lipokine" in the crosstalk. This is recommended
by Dr. Steven Smith at PBRC. See PDF file in attachment 1.
Liver control of pancreas: In Science, liver is reported to
regulate B‑cell growth in pancreas through a nerve signal. In the study,
activation of extracellular regulated kinase (ERK) in liver was found to
promote pancreatic B‑cell proliferation. This signaling pathway is
involved in obesity‑induced islet expansion in obesity. It even can
increase B‑cell mass and normalized serum glucose levels in type 1
diabetes model. The study enriches our understanding of nerve in
liver‑pancreas crosstalk. See PDF file in attachment 2.
Gut control of brain: In Cell, a new "Gut‑ Derived
Circulating Factor" is reported to inhibit food intake through the
hypothalamus in the brain. This new factor is
N‑acylphosphatidylethanolamine (NAPE). It is a relatively abundant
plasma lipid and secreted in the small intestine in response to ingested
fat. Systemic administration of NAPE, at physiologic doses, decreases
food intake in rats without causing conditioned taste aversion. The
study highlights the role of lipid in the crosstalk. See PDF file in
attachment 3.
Have a nice Thanksgiving holiday!
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
E‑mail: yej@pbrc.edu
IRIR stands for "Insulin Resistance Interest Group", an electronic and
non‑profitable academic 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 change in the e‑mail list. The previous posts can be found at:
http://c-ada.org/journalclub/journalclub.html
crosstalk among multiple organs/tissues including fat, muscle, liver,
pancreas, gut and brain. It is well accepted that the languages in such
crosstalk are hormones and nerve signals among these organs/tissues.
However, words that are used in these languages (signal mediators)
remains to be fully identified or interpreted. This issue is addressed
by several recent reports in Cell and Science. Below is the brief
introduction.
Fat control of muscle and liver: In Cell, a new product of
adipose tissue named "lipokine" was reported to mediate fat tissue
signal in the control of metabolism in muscle and liver. This new
molecule (real name: C16:1n7‑palmitoleate) is identified with lipidomics
approach. It strongly stimulates muscle insulin action and suppresses
hepatosteatosis. The data reveal a lipid‑mediated endocrine network and
supports a new concept "lipokine" in the crosstalk. This is recommended
by Dr. Steven Smith at PBRC. See PDF file in attachment 1.
Liver control of pancreas: In Science, liver is reported to
regulate B‑cell growth in pancreas through a nerve signal. In the study,
activation of extracellular regulated kinase (ERK) in liver was found to
promote pancreatic B‑cell proliferation. This signaling pathway is
involved in obesity‑induced islet expansion in obesity. It even can
increase B‑cell mass and normalized serum glucose levels in type 1
diabetes model. The study enriches our understanding of nerve in
liver‑pancreas crosstalk. See PDF file in attachment 2.
Gut control of brain: In Cell, a new "Gut‑ Derived
Circulating Factor" is reported to inhibit food intake through the
hypothalamus in the brain. This new factor is
N‑acylphosphatidylethanolamine (NAPE). It is a relatively abundant
plasma lipid and secreted in the small intestine in response to ingested
fat. Systemic administration of NAPE, at physiologic doses, decreases
food intake in rats without causing conditioned taste aversion. The
study highlights the role of lipid in the crosstalk. See PDF file in
attachment 3.
Have a nice Thanksgiving holiday!
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
E‑mail: yej@pbrc.edu
IRIR stands for "Insulin Resistance Interest Group", an electronic and
non‑profitable academic 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 change in the e‑mail list. The previous posts can be found at:
http://c-ada.org/journalclub/journalclub.html