Two male study groups with adiposity and hypertriglyceridemia were at risk for hypertension and alcohol use declined renal endothelium

Abstract


Men who attended a Bavarian General Medicine Practice were confidentially invented here. Two male study groups were enrolled to characterize adiposity or hypertriglyceridemia showing that these men were at baseline risk for hypertension [1]. Adverse alcohol consumption mediated dysfunction of renal endothelium as shown here and before [1]. This study found that alcohol use aggravated dyslipidemia, fatty liver disease and critical fasting blood glucose of obese men predicting then late hepatorenal disorders. Overall, two male study groups showed a relevant proportion of men who reported alcohol consumption showing then critical morning urines indicating dysfunction of renal endothelium. The present report looked also at healthy men who reported positive lifestyle behaviour and at men with nonalcohol adiposity and nonalcohol hypertriglyceridemia who then showed normal morning urines indicating functional renal endothelium. Relatively young men at risk were motivated to replace adverse alcohol use by healthy liquids without alcohol and by higher quality of food.


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Korth, R. (2012) Two male study groups with adiposity and hypertriglyceridemia were at risk for hypertension and alcohol use declined renal endothelium. Health, 4, 1390-1395. doi: 10.4236/health.2012.412A201.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] Korth, R.M. (2006) Gender obesity, alcohol use, hyper- lipide-mia, hypertension and decline of renal endothelial barriers, Journal of Men’s Health and Gender, 3, 279-289. doi:10.1016/j.jmhg.2005.08.006
[2] Korth, R.M. (2002) AHA-syndromes, Chemistry Physics of Lipids, 118, 96-97.
[3] Korth, R., Zimmermann, K. and Richter, W. (1994) “Lipoprotein-associated paf (LA-paf) was found in washed human platelets and monocyte-macrophage-like U937 cells. Chemistry Physic of Lipids, 70, 109-119. doi:10.1016/0009-3084(94)90079-5
[4] Korth, R.M. (2000) Comparison of phosphocholines in human plasma and cere-brospinal fluid (CSF). The Faseb Journal, 14, A72.
[5] Korth, R., Bidault, J., Palmatier, R., Beneveniste J. and Ninio, E. (1993) Human platelets release a paf-acether: Acetylhydrolase similar to that in plasma, Lipids, 28, 193-199. doi:10.1007/BF02536639
[6] Korth, R.M. (1997) VLDL and PAF binding to human endothelial cells. Chemistry and Phys-ics of Lipids, 88, 134.
[7] Korth, R.M. (2005) Gender dyslip-idemia and ether phos- pholipids, The Faseb Journal, 19, 109.
[8] Korth, R.M. (2007) Obesity mediated hypertension while alcohol use declined renal endothelial barriers of women. The Faseb Journal, 21, A1361.
[9] Barzilay, J.J., Peterson, D., Cushman, M., Heckbert, S.R., Cao, J.J., Blaum, C., Tracy, R.P., Klein, R. and Herrington, D.M. (2004) The relationship of cardiovascular risk factors to microalbuminuria in older adults with or without diabetes mellitus or hypertension. The Car-diovascular Health Study, American Kidney Disease, 44, 25-34. doi:10.1053/j.ajkd.2004.03.022
[10] Vasan, R.S. (2005) Rela-tive importance of borderline and elevated levels of coronary heart disease risk factors. Annals of Internal Medicine, 142, 393-402.
[11] Berenson, G.S., Srinivasan, S.R., Bao, W., Newmann, W.P., Tracy, R.E. and Wattigney, W.A. (1998) Associa- tion between multiple cardiovascular risk factors and atherosclerosis in children and young adults, New England Journal of Medicine, 338, 1650-1656. doi:10.1056/NEJM199806043382302
[12] Sanyal, A.J., Cha-lasani, N., Kowdley, K.V., McCullough, A., Diel, A.M., Bass, N.M., Neuschwander-Tetri, B.A., Lavine, J.E., Tonascia, J., Unalp, A., Van Natta, M., Clark, J., Brunt, E.M., Kleiner, D.E., Hoofnagle, J.H. and Robuck, P.R. (2010) Pioglitazone, Vitamin E, or placebo for nonalcoholic steatohepatitis. New Engand Journal of Me- dicine, 362, 1675-1685. doi:10.1056/NEJMoa0907929
[13] Coustan, D.R., Lowe, L.P., Metzger, B.E. and Dyer, A.R. (2007) The hyperglycemia and adverse pregnany outcome (paving the way for new diagnostic criteria for gestational diabetes mellitus). American Journal Obstetic and Gyne- cology, 202, 654-657.
[14] Gupta, B.P., Murad, M.H., Clifton, M.M., Prokop, L., Nehra, A. and Ko-pecky, S.L. (2011) “The effect of life- style modification and cardiovascular risk factor reduc- tion on erectil dysfunction: a systemic review and meta-analyis. Archives Internal Medicine, 171, 1797-17803. doi:10.1001/archinternmed.2011.440
[15] Bertoiy, M.L., Waring, M.E., Gupta, P.S., Roberts, M.B. and Eaton, C.B. (2011) “Hypertension Guidelines Implications. Hypertension, 58, 361-366. doi:10.1161/HYPERTENSIONAHA.111.175463
[16] Querzfurth, H.W. (2010) Mechanism of disease Alzhei- mer’ disease. New England Journal Medicine, 362, 329- 344.
[17] Korth, R.M., Hirafuji, M., Beneveniste, J. and Russo-Marie, F. (1995) Human umbilical vein endothelial cells: Specific binding of platelet-activating factor and cytosolic calcium flux. Biochemical Pharmacology, 49, 1793-1799. doi:10.1016/0006-2952(95)00025-U
[18] Hiramoto, M., Yo-shida, H., Imaizumi, T., Yoshimizu, N. and Satoh, K. (1997) A mutation in plasma platetet activating factor acetylhydrolases (VAL279-Phe) is a genetic risk factor for stroke. Stroke, 28, 2417-2420. doi:10.1161/01.STR.28.12.2417
[19] Wen, X.Y., Hegele, R.A., Wang, J., Wang, D.Y., Cheung, J., Wilson, M., Yanyapour, M., Bai, Y., Zhuang, L., Skaug, J., Young, T.K., Conelly, P.W., Koop, B.F., Tsui, L.C. and Stewart, A.K. (2003) Identification of a novel lipase gene mutated in lpd mice wth hypertriglyceridemia and associated with dyslipidemia in humans. Human Molecular Genetics, 12, 1131-1143. doi:10.1093/hmg/ddg124
[20] Romeo, S., Kozlitina, J., Xing, C., Pertsemlidis, A., Cox, D., Pennachio, L.A., Boerwinkle, E., Cohen, J.C. and Hobbs, H. (2008) “Genetic variation in PNPLA3 confess susceptibility to nonalcoholic fatty liver disease. Nature Genetics, 40, 1461-1465. doi:10.1038/ng.257
[21] Sacks, F.M., Svetkey, L.P., Vollmer, W.M., Appel, L.J., Bray, G.A., Harsha, D., Obarzanek, E., Conlin, P.R., Miller, E.R., Simons-Morton, D.G., Karanja, N. and Lin, P.H.L.N. (2001) “DASH-Sodium Collaboration Re-search Group. Effects on blood pressure of reduced dietary so- dium and the dietary approaches to stop hypertension (DASH) diet. New England Journal Medicine, 344, 3-10. doi:10.1056/NEJM200101043440101
[22] Volek, J.S., Fer-nandez, M.L., Feinman, R.D. and Phinney, S.D. (2008) Dietary carbohydrate restriction induces a unique metablic state positively affecting atherogenic dy- slipidemia, fatty acid partioning, and metabolic syndrome. Progress in Lipid Research, 47, 307-318. doi:10.1016/j.plipres.2008.02.003
[23] Humphries, S. (2011) Task force for the management of dyslipidemias of the European Society of Cardiology and the European Atherosclerosis Society. Atherosclerosis, 21751.
[24] Kraus, A.R. (2008) Alkoholkonsum, alkoholbezogene probleme und trends. Ergeb-nisse des epidemiologischen suchtsurvey 2003. Robert Koch Institut, Gesundheitsberichterstattung des Bundes, 40.
[25] Korth, R.M. (2000) www.fidabus.com
[26] Korth, R.M. (2001) www.fidaaha.com

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