Soy May Treat Cardiovascular Disease

[Ironjustic]

"Soy-derived phospholipids offer a novel therapeutic
opportunity."

Pandey NR, Sparks DL Phospholipids as cardiovascular
therapeutics. [Journal Article] Curr Opin Investig Drugs 2008
Mar; 9(3):281-5.

A uniquely formulated soy phospholipid is being developed as
a potential therapeutic for the treatment and prevention of
heart disease. Three phase I and one phase I/II clinical
trials have been completed with soy phosphatidylinositol
(PI). The compound was shown to be safe in all trials and at
doses over 5
g.Clinical studies have also shown early-stage efficacy to
suggest that PI is able to raise plasma HDL-cholesterol and
apolipoprotein A-I levels, and reduce triglyceride levels in
humans. PI directly impacts plasma HDL levels through a MAPK
stimulation of HDL production by the liver. Research has
shown that the linoleic acid content of soy PI is critical
to a peroxisome proliferator-activated receptor alpha
dependent stimulation of HDL secretion. Soy-derived
phospholipids uniquely affect cellular signaling and
transcriptional processes. These lipids are safe and
efficacious in humans and may therefore offer a novel
therapeutic opportunity to treat cardiovascular disease.
--------------------------------------------------------------
-------------------

Current opinion in investigational drugs (London, England :
2000) [Curr Opin Investig Drugs]

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

[Andrew B.]

Smarter to lose the black fat...

http://HeartMDPhD.com/BlackFat

http://HeartMDPhD.com/OffalFat

... by eating less, down to the right amount:

http://HeartMDPhD.com/BeSmart

Be hungry... be healthy... be hungrier... be euglycemic:

http://TheWellnessFoundation.com/BeHealthy

Prayerfully in the infinite power and might of the Holy
Spirit,

Andrew <><
--
Andrew B. Chung, MD/PhD Lawful steward of
http://EmoryCardiology.com Brethren of the KING of kings and
LORD of lords. http://HeartMDPhD.com/ChristianBrethren

ironjustice wrote:
> "Soy-derived phospholipids offer a novel therapeutic
> opportunity."
>
> Pandey NR, Sparks DL Phospholipids as cardiovascular
> therapeutics. [Journal Article] Curr Opin Investig Drugs
> 2008 Mar; 9(3):281-5.
>
> A uniquely formulated soy phospholipid is being developed as
> a potential therapeutic for the treatment and prevention of
> heart disease. Three phase I and one phase I/II clinical
> trials have been completed with soy phosphatidylinositol
> (PI). The compound was shown to be safe in all trials and at
> doses over 5
> g.Clinical studies have also shown early-stage efficacy to
> suggest that PI is able to raise plasma HDL-cholesterol
> and apolipoprotein A-I levels, and reduce triglyceride
> levels in humans. PI directly impacts plasma HDL levels
> through a MAPK stimulation of HDL production by the liver.
> Research has shown that the linoleic acid content of soy
> PI is critical to a peroxisome proliferator-activated
> receptor alpha dependent stimulation of HDL secretion.
> Soy-derived phospholipids uniquely affect cellular
> signaling and transcriptional processes. These lipids are
> safe and efficacious in humans and may therefore offer a
> novel therapeutic opportunity to treat cardiovascular
> disease.
> ------------------------------------------------------------
> ---------------------
>
> Current opinion in investigational drugs (London, England :
> 2000) [Curr Opin Investig Drugs]
>
>
> Who loves ya. Tom
>
>
> Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
>
>
> Man Is A Herbivore! http://tinyurl.com/a3cc3
>
>
> DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

[Ironjustic]

On Mar 8, 5:05 am, "Andrew B. Chung, MD/PhD"
<heartdo...@emorycardiology.com> wrote:Smarter to lose the
black fat... <<

Now with the problem with visceral adipose fat being found to
be related to iron .. IE: loosely bound iron .. I would say by
removing this loosely bound iron would ALSO remove the
visceral adipose fat (VAT).

Therefore .. I think we agree .. visceral adipose fat has to
go .. YOU because of the inflammation and ME because it will
go as an effect OF .. iron .. **removal**.
IE: remove the iron and the VAT (visceral adipose tissue) will
disappear.

"Thiazolidinediones might be a useful strategy"

Molecular Cardiology

Visceral Adipose Tissue Inflammation Accelerates
Atherosclerosis in Apolipoprotein E-Deficient Mice Miina K.
=D6hman, MD, PhD; Yuechun Shen, MD; Chinyere I. Obimba, BS;
Andrew P. Wright, BS; Mark Warnock, BS; Daniel A. Lawrence,
PhD; Daniel T. Eitzman, MD
=46rom the University of Michigan, Department of Internal
=Medicine,
Division of Cardiology, Ann Arbor (M.K.=D6., Y.S., C.I.O.,
A.P.W., M.W.,
I.E.A., D.T.E.), and Ann Arbor Veterans Adminstration
Hospital, Ann Arbor (D.T.E.), Mich.

Correspondence to Daniel T. Eitzman, MD, University of
Michigan, Cardiology, 7301A MSRB III, 1150 W Medical Center
Dr, Ann Arbor, MI 48109-0644. E-mail deitzman@umich.edu

Received May 24, 2007; accepted December 5, 2007.

Background-- Fat inflammation may play an important role in
comorbidities associated with obesity such as atherosclerosis.

Methods and Results-- To first establish feasibility of fat
transplantation, epididymal fat pads were harvested from
wild-type C57BL/6J mice and transplanted into leptin-deficient
(Lepob/ob) mice. Fat transplantation produced physiological
leptin levels and prevented obesity and infertility in
Lepob/ob mice. However, the transplanted fat depots were
associated with chronically increased macrophage infiltration
with characteristics identical to those observed in fat
harvested from obese animals. The inflammation in transplanted
adipose depots was regulated by the same factors that have
been implicated in endogenous fat inflammation such as
monocyte chemoattractant protein-1. To determine whether this
inflamed adipose depot could affect vascular disease in mice,
epididymal fat depots were transplanted into
atherosclerosis-prone apolipoprotein E-deficient ApoE-/- mice.
Plasma from ApoE-/- mice receiving fat transplants contained
increased leptin, resistin, and monocyte chemoattractant
protein-1 compared with plasma from sham-operated ApoE-/-
mice. Furthermore, mice transplanted with visceral fat
developed significantly more atherosclerosis compared with
sham-operated animals, whereas transplants with subcutaneous
fat did not affect atherosclerosis despite a similar degree of
fat inflammation. Treatment of transplanted ApoE-/- mice with
pioglitazone decreased macrophage content of the transplanted
visceral fat pad and reduced plasma monocyte chemoattractant
protein-1. Importantly, pioglitazone also reduced
atherosclerosis triggered by inflammatory visceral fat but had
no protective effect on atherosclerosis in the absence of the
visceral fat transplantation.

Conclusions-- Our results indicate that visceral
adipose-related inflammation accelerates atherosclerosis in
mice. Drugs such as thiazolidinediones might be a useful
strategy to specifically attenuate the vascular disease
induced by visceral inflammatory fat.

--------------------------------------------------------------
---------------=
----

--------------------------------------------------------------
---------------=
---------------------------------------

<<snip>> the thiazolidinediones may protect cells from the
damaging effects of free iron by keeping the iron-sulfur
cluster attached to mitoNEET. <<snip>>

Source: University of California - San Diego Date:
September 6, 2007

Discovery May Pave The Way For A New Class Of Diabetes Drugs
Science Daily - A multidisciplinary team led by researchers at
the University of California, San Diego has determined the
structure of a protein found in cells that shows potential as
a target for the development of new drugs to treat diabetes.

The study, published September 4 in the journal Proceedings of
the National Academy of Sciences, described the structure of a
protein- MitoNEET-that was previously identified as a site
where diabetes drugs could operate. The discovery of the
protein's three-dimensional structure makes it possible to
design small molecules that interact with it and modify its
function. The researchers say that MitoNEET has a novel
three-dimensional structure that makes it a particularly
interesting candidate for the design of innovative compounds
that can bind to it.

"This is the first time that a protein like this has ever been
found," said Patricia Jennings, a professor in UCSD's
department of Chemistry and Biochemistry who led the study
along with Mark Paddock, a project scientist in UCSD's Physics
department. "It is a brand new structure, a unique beast,
which makes it an exciting target for structure-based drug
design. We are grateful about the highly collaborative spirit
of the UCSD community that brought such diverse expertise and
helped us tackle such a complex project."

"Our work may provide a basis for the design of newer diabetes
drugs that have potentially greater specificity and fewer side
effects than existing ones," added Paddock.

Following the initial work of co-authors Sandra Wiley, Anne
Murphy and Jack Dixon at UCSD's School of Medicine, and in
collaboration with Herbert Axelrod and Aina Cohen at the
Stanford Synchrotron Radiation Laboratory and Rachel
Nechushtai at the Hebrew University of Jerusalem, also
co-authors on the paper, the team determined that mitoNEET is
an iron-sulfur protein. Iron-sulfur proteins have a variety of
functions, including electron transfer, which is critical to
cell metabolism, and the storage and transport of iron. In its
free state, iron is highly toxic to cells and can lead to
oxidative stress-the accumulation of reactive compounds that
can damage the cell.

MitoNEET's iron-sulfur cluster is loosely bound, a property
that may be linked to one of its functions. When mitoNEET
binds the type 2 diabetes drug Actos(R), the iron-sulfur
cluster becomes more stable. This drug was thought to work
through an entirely different mechanism involving a different
protein. However, the finding by Jerry Colca, presently at
Metabolic Solutions Development Company in Kalamazoo,
Michigan, that the thiazolidinediones-the class of diabetes
drugs of which Actos(R) is a member-bind to mitoNEET
indicated a possible mechanism involving mitoNEET. Colca's
finding inspired the UCSD-led study, which suggests that
Actos(R) and similar drugs may protect cells from the
damaging effects of free iron by keeping the iron-sulfur
cluster attached to mitoNEET.

>From mitoNEET's structure, location and properties, it could
>also play

a role as a sensor of oxidative stress in the cell. Oxidative
stress is a problem in many diseases including diabetes.
MitoNEET is confined to the mitochondria-structures within
cells that convert nutrients into energy-where reactive
compounds accumulate as nutrients are metabolized. MitoNEET's
structure would allow it to transfer electrons to and from,
and therefore detect, these compounds.

"MitoNEET may be an example of an ever increasing group of
proteins found to have more than one function. I think we are
at the beginning of what is sure to be an interesting and
biologically important puzzle." said Paddock.

"It is intriguing to see these different pieces coming
together," explained Jennings. "There is growing evidence that
mitochondrial dysfunction and compromised oxidative capacity
is a problem in diabetes. MitoNEET has iron-sulfur clusters
that can transfer electrons, and it binds insulin-sensitizing
drugs. Now that we know the structure and physical properties
of the protein we can use this knowledge for drug studies and
studies of biological function."

The team plans to use the new structural information for
designing more sophisticated experiments to test function and
structure-based drug design to create drugs that interact
better with mitoNEET. Collaborative experiments are currently
underway with Colca's group at Metabolic Solutions
Development Company.

"This work is a great example of the possible synergies of a
multidisciplinary and multinational effort," said Paddock.
"Instrumental in these results were the combined efforts of
the US and Israeli teams."

Other UCSD co-authors of the paper were Edward Abresch in
Physics and Melinda Roy and Dominique Capraro in Chemistry and
Biochemistry.

The study was supported by the National Institutes of Health,
the Department of Energy and the Zevi Hermann Shapira
Foundation.

Note: This story has been adapted from a news release issued
by University of California - San Diego.

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

CLINICAL PERSPECTIVE

Related Article:

Clinical Summaries Circulation 2008 117: 711-713. [Full Text]
(Circulation. 2008;117:798-805.)
(c) 2008 American Heart Association, Inc.

--------------------------------------------------------------
---------------=
----

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

> Smarter to lose the black fat...
>
> http://HeartMDPhD.com/BlackFat
>
> http://HeartMDPhD.com/OffalFat
>
> ... by eating less, down to the right amount:
>
> http://HeartMDPhD.com/BeSmart
>
> Be hungry... be healthy... be hungrier... be euglycemic:
>
> http://TheWellnessFoundation.com/BeHealthy
>
> Prayerfully in the infinite power and might of the
> Holy Spirit,
>
> Andrew <><
> --
> Andrew B. Chung, MD/PhD Lawful steward
> ofhttp://EmoryCardiology.com Brethren of the KING of kings
> and LORD of lords.http://HeartMDPhD.com/Chri=
stianBrethren
>
>
>
> ironjustice wrote:
> > "Soy-derived phospholipids offer a novel therapeutic
> > opportunity."
>
> > Pandey NR, Sparks DL Phospholipids as cardiovascular
> > therapeutics. [Journal Article] Curr Opin Investig Drugs
> > 2008 Mar; 9(3):281-5.
>
> > A uniquely formulated soy phospholipid is being developed
> > as a potential therapeutic for the treatment and
> > prevention of heart disease. Three phase I and one phase
> > I/II clinical trials have been completed with soy
> > phosphatidylinositol (PI). The compound was shown to be
> > safe in all trials and at doses over 5
> > g.Clinical studies have also shown early-stage efficacy to
> > suggest that PI is able to raise plasma HDL-cholesterol
> > and apolipoprotein A-I levels, and reduce triglyceride
> > levels in humans. PI directly impacts plasma HDL levels
> > through a MAPK stimulation of HDL production by the
> > liver. Research has shown that the linoleic acid content
> > of soy PI is critical to a peroxisome
> > proliferator-activated receptor alpha dependent
> > stimulation of HDL secretion. Soy-derived phospholipids
> > uniquely affect cellular signaling and transcriptional
> > processes. These lipids are safe and efficacious in
> > humans and may therefore offer a novel therapeutic
> > opportunity to treat cardiovascular disease. -----------
> > --------------------------------------------------------
> > -------=
---------
>
> > Current opinion in investigational drugs (London, England
> > : 2000) [Curr Opin Investig Drugs]
>
> > Who loves ya. Tom
>
> > Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
>
> > Man Is A Herbivore!
> > http://tinyurl.com/a3cc3
>
> > DEAD PEOPLE WALKING http://tinyurl.com/zk9fk- Hide quoted
> > text -
>
> - Show quoted text -

[Ironjustic]

On Mar 8, 8:01 am, ironjustice <teamtan...@hotmail.com> wrote:
visceral adipose fat being found to be related to iron .. IE:
loosely bound iron <<

"Accumulation of visceral adipose tissue is also associated
with iron metabolism"

Diabetes Care 30:616-621, 2007 DOI: 10.2337/dc06-1581
(c) 2007 by the American Diabetes Association

Pathophysiology/Complications Original Article

Circulating Visfatin Is Associated With Parameters of Iron
Metabolism in Subjects With Altered Glucose Tolerance Jos=E9
Manuel Fern=E1ndez-Real, MD, PHD, Jos=E9 Mar=EDa Moreno,
Berta Chico,=

Abel L=F3pez-Bermejo, MD, PHD and Wifredo Ricart, MD
=46rom the Department of Diabetes, Endocrinology and
=Nutrition,
University Hospital of Girona Dr. Josep Trueta, Girona, Spain

Address correspondence and reprint requests to J.M.
Fern=E1ndez-Real, MD, PhD, Department of Diabetes,
Endocrinology and Nutrition, Hospital de Girona "Dr. Josep
Trueta," Ctra. Fran=E7a s/n, 17007 Girona, Spain. E- mail:
uden.jmfernandezreal@htrueta.scs.es

OBJECTIVE--Visfatin is a novel adipokine that is predominantly
secreted by visceral adipose tissue. Accumulation of visceral
adipose tissue is also associated with iron metabolism.
Despite the coincidence of visfatin expression in iron-rich
tissues, no study has investigated the possible interaction of
visfatin with parameters of iron metabolism.

RESEARCH DESIGN AND METHODS--We evaluated insulin sensitivity
and parameters of iron metabolism in 95 men with normal
glucose tolerance (NGT) and 43 men with altered glucose
tolerance.

RESULTS--Men with newly diagnosed type 2 diabetes had
significantly increased serum visfatin in parallel with
increased serum prohepcidin and serum ferritin compared with
the other groups. In all subjects as a whole, circulating
visfatin was not found to be significantly linked to insulin
sensitivity (r =3D 0.07, P =3D 0.4) but was significantly
associated with serum prohepcidin concentration (r =3D 0.40, P
< .0001). Obesity status and glucose tolerance status
influenced the relationships among visfatin, insulin
sensitivity, and parameters of iron metabolism. Among men with
altered glucose tolerance, serum visfatin was strongly
associated with serum prohepcidin (r =3D 0.61, P < .0001) and
serum soluble transferrin receptor (sTfR) (r =3D -0.51, P <
.0001). In nonobese subjects, sTfR (P =3D 0.02) and
prohepcidin (P =3D .04) contributed independently to visfatin
variance after controlling for age and BMI. When insulin
sensitivity was added to the model, only the latter (P =3D
0.006) contributed to 17% of visfatin variance. In obese men,
however, only sTfR (P =3D 0.04) contributed independently to
visfatin variance in this latter model.

CONCLUSIONS--Serum visfatin concentration is significantly
associated with parameters of iron metabolism, especially in
subjects with altered glucose tolerance.

Abbreviations: NGT, normal glucose tolerance * sTfR, soluble
transferrin receptor

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

> On Mar 8, 5:05 am, "Andrew B. Chung,
> MD/PhD"<heartdo...@emorycardiology.co=
m> wrote:Smarter to lose the black
>
> fat... <<
>
> Now with the problem with visceral adipose fat being found
> to be related to iron .. IE: loosely bound iron .. I would
> say by removing this loosely bound iron would ALSO remove
> the visceral adipose fat (VAT).
>
> Therefore .. I think we agree .. visceral adipose fat has to
> go .. YOU because of the inflammation and ME because it will
> go as an effect OF .. iron .. **removal**.
> IE: remove the iron and the VAT (visceral adipose tissue)
> will disappear.
>
> "Thiazolidinediones might be a useful strategy"
>
> Molecular Cardiology
>
> Visceral Adipose Tissue Inflammation Accelerates
> Atherosclerosis in Apolipoprotein E-Deficient Mice Miina K.
> =D6hman, MD, PhD; Yuechun Shen, MD; Chinyere I. Obimba, BS;
> Andrew P. Wright, BS; Mark Warnock, BS; Daniel A. Lawrence,
> PhD; Daniel T. Eitzman, MD From the University of Michigan,
> Department of Internal Medicine, Division of Cardiology, Ann
> Arbor (M.K.=D6., Y.S., C.I.O., A.P.W., M.W.,
> D.A.L., D.T.E.), and Ann Arbor Veterans Adminstration
> Hospital, Ann Arbor (D.T.E.), Mich.
>
> Correspondence to Daniel T. Eitzman, MD, University of
> Michigan, Cardiology, 7301A MSRB III, 1150 W Medical Center
> Dr, Ann Arbor, MI 48109-0644. E-mail deitz...@umich.edu
>
> Received May 24, 2007; accepted December 5, 2007.
>
> Background-- Fat inflammation may play an important role in
> comorbidities associated with obesity such as
> atherosclerosis.
>
> Methods and Results-- To first establish feasibility of fat
> transplantation, epididymal fat pads were harvested from
> wild-type C57BL/6J mice and transplanted into
> leptin-deficient (Lepob/ob) mice. Fat transplantation
> produced physiological leptin levels and prevented obesity
> and infertility in Lepob/ob mice. However, the transplanted
> fat depots were associated with chronically increased
> macrophage infiltration with characteristics identical to
> those observed in fat harvested from obese animals. The
> inflammation in transplanted adipose depots was regulated by
> the same factors that have been implicated in endogenous fat
> inflammation such as monocyte chemoattractant protein-1. To
> determine whether this inflamed adipose depot could affect
> vascular disease in mice, epididymal fat depots were
> transplanted into atherosclerosis-prone apolipoprotein
> E-deficient ApoE-/- mice. Plasma from ApoE-/- mice receiving
> fat transplants contained increased leptin, resistin, and
> monocyte chemoattractant protein-1 compared with plasma from
> sham-operated ApoE-/- mice. Furthermore, mice transplanted
> with visceral fat developed significantly more
> atherosclerosis compared with sham-operated animals, whereas
> transplants with subcutaneous fat did not affect
> atherosclerosis despite a similar degree of fat
> inflammation. Treatment of transplanted ApoE-/- mice with
> pioglitazone decreased macrophage content of the
> transplanted visceral fat pad and reduced plasma monocyte
> chemoattractant protein-1. Importantly, pioglitazone also
> reduced atherosclerosis triggered by inflammatory visceral
> fat but had no protective effect on atherosclerosis in the
> absence of the visceral fat transplantation.
>
> Conclusions-- Our results indicate that visceral
> adipose-related inflammation accelerates atherosclerosis in
> mice. Drugs such as thiazolidinediones might be a useful
> strategy to specifically attenuate the vascular disease
> induced by visceral inflammatory fat.
>
> ------------------------------------------------------------
> ---------------=
-------
>
> ------------------------------------------------------------
> ---------------=
------------------------------------------
>
> <<snip>> the thiazolidinediones may protect cells from the
> damaging effects of free iron by keeping the iron-sulfur
> cluster attached to mitoNEET. <<snip>>
>
> Source: University of California - San Diego Date:
> September 6, 2007
>
> Discovery May Pave The Way For A New Class Of Diabetes Drugs
> Science Daily - A multidisciplinary team led by researchers
> at the University of California, San Diego has determined
> the structure of a protein found in cells that shows
> potential as a target for the development of new drugs to
> treat diabetes.
>
> The study, published September 4 in the journal Proceedings
> of the National Academy of Sciences, described the structure
> of a protein- MitoNEET-that was previously identified as a
> site where diabetes drugs could operate. The discovery of
> the protein's three-dimensional structure makes it possible
> to design small molecules that interact with it and modify
> its function. The researchers say that MitoNEET has a novel
> three-dimensional structure that makes it a particularly
> interesting candidate for the design of innovative compounds
> that can bind to it.
>
> "This is the first time that a protein like this has ever
> been found," said Patricia Jennings, a professor in UCSD's
> department of Chemistry and Biochemistry who led the study
> along with Mark Paddock, a project scientist in UCSD's
> Physics department. "It is a brand new structure, a unique
> beast, which makes it an exciting target for structure-based
> drug design. We are grateful about the highly collaborative
> spirit of the UCSD community that brought such diverse
> expertise and helped us tackle such a complex project."
>
> "Our work may provide a basis for the design of newer
> diabetes drugs that have potentially greater specificity and
> fewer side effects than existing ones," added Paddock.
>
> Following the initial work of co-authors Sandra Wiley, Anne
> Murphy and Jack Dixon at UCSD's School of Medicine, and in
> collaboration with Herbert Axelrod and Aina Cohen at the
> Stanford Synchrotron Radiation Laboratory and Rachel
> Nechushtai at the Hebrew University of Jerusalem, also
> co-authors on the paper, the team determined that mitoNEET
> is an iron-sulfur protein. Iron-sulfur proteins have a
> variety of functions, including electron transfer, which is
> critical to cell metabolism, and the storage and transport
> of iron. In its free state, iron is highly toxic to cells
> and can lead to oxidative stress-the accumulation of
> reactive compounds that can damage the cell.
>
> MitoNEET's iron-sulfur cluster is loosely bound, a property
> that may be linked to one of its functions. When mitoNEET
> binds the type 2 diabetes drug Actos(R), the iron-sulfur
> cluster becomes more stable. This drug was thought to work
> through an entirely different mechanism involving a
> different protein. However, the finding by Jerry Colca,
> presently at Metabolic Solutions Development Company in
> Kalamazoo, Michigan, that the thiazolidinediones-the class
> of diabetes drugs of which Actos(R) is a member-bind to
> mitoNEET indicated a possible mechanism involving mitoNEET.
> Colca's finding inspired the UCSD-led study, which suggests
> that Actos(R) and similar drugs may protect cells from the
> damaging effects of free iron by keeping the iron-sulfur
> cluster attached to mitoNEET.
>
> >From mitoNEET's structure, location and properties, it
> >could also play
>
> a role as a sensor of oxidative stress in the cell.
> Oxidative stress is a problem in many diseases including
> diabetes. MitoNEET is confined to the
> mitochondria-structures within cells that convert nutrients
> into energy-where reactive compounds accumulate as nutrients
> are metabolized. MitoNEET's structure would allow it to
> transfer electrons to and from, and therefore detect, these
> compounds.
>
> "MitoNEET may be an example of an ever increasing group of
> proteins found to have more than one function. I think we
> are at the beginning of what is sure to be an interesting
> and biologically important puzzle." said Paddock.
>
> "It is intriguing to see these different pieces coming
> together," explained Jennings. "There is growing evidence
> that mitochondrial dysfunction and compromised oxidative
> capacity is a problem in diabetes. MitoNEET has iron-sulfur
> clusters that can transfer electrons, and it binds
> insulin-sensitizing drugs. Now that we know the structure
> and physical properties of the protein we can use this
> knowledge for drug studies and studies of biological
> function."
>
> The team plans to use the new structural information for
> designing more sophisticated experiments to test function
> and structure-based drug design to create drugs that
> interact better with mitoNEET. Collaborative experiments are
> currently underway with Colca's group at Metabolic Solutions
> Development Company.
>
> "This work is a great example of the possible synergies of a
> multidisciplinary and multinational effort," said Paddock.
> "Instrumental in these results were the combined efforts of
> the US and Israeli teams."
>
> Other UCSD co-authors of the paper were Edward Abresch in
> Physics and Melinda Roy and Dominique Capraro in Chemistry
> and Biochemistry.
>
> The study was supported by the National Institutes of
> Health, the Department of Energy and the Zevi Hermann
> Shapira Foundation.
>
> Note: This story has been adapted from a news release issued
> by University of California - San Diego.
>
> Who loves ya. Tom
>
> Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
> CLINICAL PERSPECTIVE
>
> Related Article:
>
> Clinical Summaries Circulation 2008 117: 711-713. [Full
> Text] (Circulation. 2008;117:798-805.)
> (c) 2008 American Heart Association, Inc.
>
> ------------------------------------------------------------
> ---------------=
-------
>
> Who loves ya. Tom
>
> Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > Smarter to lose the black fat...
>
> >http://HeartMDPhD.com/BlackFat
>
> >http://HeartMDPhD.com/OffalFat
>
> > ... by eating less, down to the right amount:
>
> >http://HeartMDPhD.com/BeSmart
>
> > Be hungry... be healthy... be hungrier... be euglycemic:
>
> >http://TheWellnessFoundation.com/BeHealthy
>
> > Prayerfully in the infinite power and might of the Holy
> > Spirit,
>
> > Andrew <><
> > --
> > Andrew B. Chung, MD/PhD Lawful steward
> > ofhttp://EmoryCardiology.com
>
> ...
>
> read more >>- Hide quoted text -
>
> - Show quoted text -

[truth]

Our armchair endo opines:

"Smarter to lose the black fat..."

Truth:

In pursuit of which would actually mark one as quite stupid as
"black fat" does not exist.

To do so would be to follow the advice born of a distortion of
a cognitive lateral lurch not tied to reality; any of them.

Truth is simple.

God bless.