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Riboflavin alleviates cardiac failure in Type I diabetic cardiomyopathy (in animal model)
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None Given
May 5, 2012, 4:27:33 PM5/5/12
to
Apparently a whopping dose though only a super mega dose may
be need ;-) YMMV
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282438/?tool=pubmed
1. Heart Int. 2011 Sep 29;6(2):e21.
Epub 2011 Nov 22.
Riboflavin alleviates cardiac failure in Type I
diabetic cardiomyopathy.
Wang G, Li W, Lu X, Zhao X.
Department of Pathophysiology,
Wannan Medical College,
Wuhu, China.
Heart failure (HF) is a common and serious comorbidity of diabetes.
Oxidative
stress has been associated with the pathogenesis of chronic diabetic
complications including cardiomyopathy. The ability of antioxidants to
inhibit
injury has raised the possibility of new therapeutic treatment for
diabetic heart
diseases. Riboflavin constitutes an essential nutrient for humans and
animals and
it is an important food additive. Riboflavin, a precursor of flavin
mononucleotide (FMN) and flavin adenine dinucleotide (FAD), enhances
the
oxidative folding and subsequent secretion of proteins. The objective
of this
study was to investigate the cardioprotective effect of riboflavin in
diabetic
rats. Diabetes was induced in 30 rats by a single injection of
streptozotocin
(STZ) (70 mg /kg). Riboflavin (20 mg/kg) was orally administered to
animals
immediately after induction of diabetes and was continued for eight
weeks. Rats
were examined for diabetic cardiomyopathy by left ventricular (LV)
remadynamic
function. Myocardial oxidative stress was assessed by measuring the
activity of
superoxide dismutase (SOD), the level of malondialdehyde (MDA) as well
as heme
oxygenase-1 (HO-1) protein level. Myocardial connective tissue growth
factor
(CTGF) level was measured by Western blot in all rats at the end of
the study. In
the untreated diabetic rats, left ventricular systolic pressure (LVSP)
rate of
pressure rose (+dp/dt), and rate of pressure decay (-dp/dt) were
depressed while
left ventricular end-diastolic pressure (LVEDP) was increased, which
indicated
the reduced left ventricular contractility and slowing of left
ventricular
relaxation. The level of SOD decreased, CTGF and HO-1 protein
expression and MDA
content rose. Riboflavin treatment significantly improved left
ventricular
systolic and diastolic function in diabetic rats, there were
persistent increases
in significant activation of SOD and the level of HO-1 protein, and a
decrease in
the level of CTGF. These results suggest that riboflavin treatment
ameliorates
myocardial function and improves heart oxidant status, whereas raising
myocardial
HO-1 and decreasing myocardial CTGF levels have beneficial effects on
diabetic
cardiomyopathy.
PMCID: PMC3282438
PMID: 22355488 [PubMed - in process]
be need ;-) YMMV
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282438/?tool=pubmed
1. Heart Int. 2011 Sep 29;6(2):e21.
Epub 2011 Nov 22.
Riboflavin alleviates cardiac failure in Type I
diabetic cardiomyopathy.
Wang G, Li W, Lu X, Zhao X.
Department of Pathophysiology,
Wannan Medical College,
Wuhu, China.
Heart failure (HF) is a common and serious comorbidity of diabetes.
Oxidative
stress has been associated with the pathogenesis of chronic diabetic
complications including cardiomyopathy. The ability of antioxidants to
inhibit
injury has raised the possibility of new therapeutic treatment for
diabetic heart
diseases. Riboflavin constitutes an essential nutrient for humans and
animals and
it is an important food additive. Riboflavin, a precursor of flavin
mononucleotide (FMN) and flavin adenine dinucleotide (FAD), enhances
the
oxidative folding and subsequent secretion of proteins. The objective
of this
study was to investigate the cardioprotective effect of riboflavin in
diabetic
rats. Diabetes was induced in 30 rats by a single injection of
streptozotocin
(STZ) (70 mg /kg). Riboflavin (20 mg/kg) was orally administered to
animals
immediately after induction of diabetes and was continued for eight
weeks. Rats
were examined for diabetic cardiomyopathy by left ventricular (LV)
remadynamic
function. Myocardial oxidative stress was assessed by measuring the
activity of
superoxide dismutase (SOD), the level of malondialdehyde (MDA) as well
as heme
oxygenase-1 (HO-1) protein level. Myocardial connective tissue growth
factor
(CTGF) level was measured by Western blot in all rats at the end of
the study. In
the untreated diabetic rats, left ventricular systolic pressure (LVSP)
rate of
pressure rose (+dp/dt), and rate of pressure decay (-dp/dt) were
depressed while
left ventricular end-diastolic pressure (LVEDP) was increased, which
indicated
the reduced left ventricular contractility and slowing of left
ventricular
relaxation. The level of SOD decreased, CTGF and HO-1 protein
expression and MDA
content rose. Riboflavin treatment significantly improved left
ventricular
systolic and diastolic function in diabetic rats, there were
persistent increases
in significant activation of SOD and the level of HO-1 protein, and a
decrease in
the level of CTGF. These results suggest that riboflavin treatment
ameliorates
myocardial function and improves heart oxidant status, whereas raising
myocardial
HO-1 and decreasing myocardial CTGF levels have beneficial effects on
diabetic
cardiomyopathy.
PMCID: PMC3282438
PMID: 22355488 [PubMed - in process]
Colt T
May 5, 2012, 4:59:34 PM5/5/12
to
The the FDA will make it not otc and give it to a drug co to market,
even tho it should be grandfathered.
even tho it should be grandfathered.
None Given
May 6, 2012, 2:48:32 PM5/6/12
to
On May 5, 1:59 pm, Colt...@webtv.net (Colt T) wrote:
> The the FDA will make it not otc and give it to a drug co to market,
> even tho it should be grandfathered.
Yup that is about my take the subject. That which is legal is not
> The the FDA will make it not otc and give it to a drug co to market,
> even tho it should be grandfathered.
by necessity either moral or good.
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