Soy May Treat Cardiovascular Disease

[ironjustice]

"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. Chung, MD/PhD]

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

[ironjustice]

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. Öhman, 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.Ö., 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 [email protected]

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/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- Hide quoted text -
>
> - Show quoted text -

[ironjustice]

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
José Manuel Fernández-Real, MD, PHD, José María Moreno, Berta Chico,
Abel López-Bermejo, MD, PHD and Wifredo Ricart, MD
From the Department of Diabetes, Endocrinology and Nutrition,
University Hospital of Girona Dr. Josep Trueta, Girona, Spain

Address correspondence and reprint requests to J.M. Fernández-Real,
MD, PhD, Department of Diabetes, Endocrinology and Nutrition, Hospital
de Girona "Dr. Josep Trueta," Ctra. França s/n, 17007 Girona, Spain. E-
mail: [email protected]

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 = 0.07, P = 0.4) but was significantly
associated with serum prohepcidin concentration (r = 0.40, P <
0.0001). 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 = 0.61, P <
0.0001) and serum soluble transferrin receptor (sTfR) (r = -0.51, P <
0.0001). In nonobese subjects, sTfR (P = 0.02) and prohepcidin (P =
0.04) contributed independently to visfatin variance after controlling
for age and BMI. When insulin sensitivity was added to the model, only
the latter (P = 0.006) contributed to 17% of visfatin variance. In
obese men, however, only sTfR (P = 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.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. Öhman, 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.Ö., 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 -