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High-Dose Menaquinone-7 Supplementation Reduces Cardiovascular Calcification in a Murine Model of Extraosseous Calcification.

Scheiber D, Veulemans V, Horn P, Chatrou ML, Potthoff SA, Kelm M, Schurgers LJ, Westenfeld R - Nutrients (2015)

Bottom Line: Furthermore, MK-7 supplementation increased aortic MGP messenger ribonucleic acid (mRNA) expression (10-fold; p < 0.05).CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation.The protective effect of MK-7 may be related to the inhibition of secondary mineralization of damaged vascular structures.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. daniel.scheiber@med.uni-duesseldorf.de.

ABSTRACT
Cardiovascular calcification is prevalent in the aging population and in patients with chronic kidney disease (CKD) and diabetes mellitus, giving rise to substantial morbidity and mortality. Vitamin K-dependent matrix Gla-protein (MGP) is an important inhibitor of calcification. The aim of this study was to evaluate the impact of high-dose menaquinone-7 (MK-7) supplementation (100 µg/g diet) on the development of extraosseous calcification in a murine model. Calcification was induced by 5/6 nephrectomy combined with high phosphate diet in rats. Sham operated animals served as controls. Animals received high or low MK-7 diets for 12 weeks. We assessed vital parameters, serum chemistry, creatinine clearance, and cardiac function. CKD provoked increased aortic (1.3 fold; p < 0.05) and myocardial (2.4 fold; p < 0.05) calcification in line with increased alkaline phosphatase levels (2.2 fold; p < 0.01). MK-7 supplementation inhibited cardiovascular calcification and decreased aortic alkaline phosphatase tissue concentrations. Furthermore, MK-7 supplementation increased aortic MGP messenger ribonucleic acid (mRNA) expression (10-fold; p < 0.05). CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation. Our results show that high-dose MK-7 supplementation inhibits the development of cardiovascular calcification. The protective effect of MK-7 may be related to the inhibition of secondary mineralization of damaged vascular structures.

No MeSH data available.


Related in: MedlinePlus

Echocardiography of diastolic interventricular septum diameter (LVISD) in cm. Echocardiography was performed in all animals after 12 weeks of study protocol. CKD animals developed significantly increased LVISD compared to controls. Co = control group; Co-K2 = MK-7 supplemented control group; CKD = 5/6 nephrectomized group; CKD-K2 = MK-7 supplemented 5/6 nephrectomized group; cm = centimeters. Significant differences: *p < 0.05, **p < 0.01.
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nutrients-07-05318-f010: Echocardiography of diastolic interventricular septum diameter (LVISD) in cm. Echocardiography was performed in all animals after 12 weeks of study protocol. CKD animals developed significantly increased LVISD compared to controls. Co = control group; Co-K2 = MK-7 supplemented control group; CKD = 5/6 nephrectomized group; CKD-K2 = MK-7 supplemented 5/6 nephrectomized group; cm = centimeters. Significant differences: *p < 0.05, **p < 0.01.

Mentions: Echocardiography: To quantify the impact of CKD and arterial hypertension on cardiovascular function we analyzed hypertrophy, contractility, and valvular function in the various treatment groups. CKD and CKD-K2 animals exhibited significant myocardial hypertrophy, as depicted by increased diameters of the interventricular septum (by about 50%; CKD vs. Co, p < 0.01) (Figure 10). Myocardial contractility, as detected by fractional shortening, remained normal in all the animals studied. No relevant valvular disease or overt signs of valvular calcification were detected throughout the experiments (data not shown).


High-Dose Menaquinone-7 Supplementation Reduces Cardiovascular Calcification in a Murine Model of Extraosseous Calcification.

Scheiber D, Veulemans V, Horn P, Chatrou ML, Potthoff SA, Kelm M, Schurgers LJ, Westenfeld R - Nutrients (2015)

Echocardiography of diastolic interventricular septum diameter (LVISD) in cm. Echocardiography was performed in all animals after 12 weeks of study protocol. CKD animals developed significantly increased LVISD compared to controls. Co = control group; Co-K2 = MK-7 supplemented control group; CKD = 5/6 nephrectomized group; CKD-K2 = MK-7 supplemented 5/6 nephrectomized group; cm = centimeters. Significant differences: *p < 0.05, **p < 0.01.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555157&req=5

nutrients-07-05318-f010: Echocardiography of diastolic interventricular septum diameter (LVISD) in cm. Echocardiography was performed in all animals after 12 weeks of study protocol. CKD animals developed significantly increased LVISD compared to controls. Co = control group; Co-K2 = MK-7 supplemented control group; CKD = 5/6 nephrectomized group; CKD-K2 = MK-7 supplemented 5/6 nephrectomized group; cm = centimeters. Significant differences: *p < 0.05, **p < 0.01.
Mentions: Echocardiography: To quantify the impact of CKD and arterial hypertension on cardiovascular function we analyzed hypertrophy, contractility, and valvular function in the various treatment groups. CKD and CKD-K2 animals exhibited significant myocardial hypertrophy, as depicted by increased diameters of the interventricular septum (by about 50%; CKD vs. Co, p < 0.01) (Figure 10). Myocardial contractility, as detected by fractional shortening, remained normal in all the animals studied. No relevant valvular disease or overt signs of valvular calcification were detected throughout the experiments (data not shown).

Bottom Line: Furthermore, MK-7 supplementation increased aortic MGP messenger ribonucleic acid (mRNA) expression (10-fold; p < 0.05).CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation.The protective effect of MK-7 may be related to the inhibition of secondary mineralization of damaged vascular structures.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. daniel.scheiber@med.uni-duesseldorf.de.

ABSTRACT
Cardiovascular calcification is prevalent in the aging population and in patients with chronic kidney disease (CKD) and diabetes mellitus, giving rise to substantial morbidity and mortality. Vitamin K-dependent matrix Gla-protein (MGP) is an important inhibitor of calcification. The aim of this study was to evaluate the impact of high-dose menaquinone-7 (MK-7) supplementation (100 µg/g diet) on the development of extraosseous calcification in a murine model. Calcification was induced by 5/6 nephrectomy combined with high phosphate diet in rats. Sham operated animals served as controls. Animals received high or low MK-7 diets for 12 weeks. We assessed vital parameters, serum chemistry, creatinine clearance, and cardiac function. CKD provoked increased aortic (1.3 fold; p < 0.05) and myocardial (2.4 fold; p < 0.05) calcification in line with increased alkaline phosphatase levels (2.2 fold; p < 0.01). MK-7 supplementation inhibited cardiovascular calcification and decreased aortic alkaline phosphatase tissue concentrations. Furthermore, MK-7 supplementation increased aortic MGP messenger ribonucleic acid (mRNA) expression (10-fold; p < 0.05). CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation. Our results show that high-dose MK-7 supplementation inhibits the development of cardiovascular calcification. The protective effect of MK-7 may be related to the inhibition of secondary mineralization of damaged vascular structures.

No MeSH data available.


Related in: MedlinePlus