Daily News: Vitamins

New Hyperhomocysteinemia Data Have Been Reported by Researchers at Peoples Hospital

NewsRx.com

10-11-13

By a News Reporter-Staff News Editor at Cardiovascular Week -- Investigators publish new report on Diet and Nutrition Disorders. According to news reporting originating in Guangdong, People's Republic of China, by NewsRx journalists, research stated, "The present study investigated whether lowering plasma homocysteine (Hcy) with folic acid (FA) could attenuate hyperhomocysteinemia (HHcy)-associated glomerular damage and possible mechanisms. The HHcy animal model was established by intragastric administration with L-methionine in rats."

The news reporters obtained a quote from the research from Peoples Hospital, "FA was also given intragastrically. Plasma Hcy and creatinine and urinary albumin were measured. Histological and ultrastructural changes were observed by light and electron microscopes. The expression of alpha-smooth muscle actin (alpha-SMA), proliferating cell nuclear antigen (PCNA) and transforming growth factor-betal (TGF-beta 1) in the kidney was examined by immunohistochemical staining and western blot analysis. The administration of L-methionine induced HHcy in rats. The HHcy rats developed glomerulosclerosis and fibrosis. Plasma creatinine concentration and urinary albumin excretion were also significantly increased in HHcy rats. Effacement and extensively fusion of podocyte foot process was observed in HHcy rats, which was associated with decreased expression of nephrin protein in renal cortex of HHcy rats. Supplementation with FA lowered plasma Hcy significantly. Plasma creatinine concentration and urinary albumin excretion were also significantly attenuated by FA. Morphologically, HHcy-associated glomerulosclerosis, fibrosis, podocyte foot process effacement and loss of podocyte nephrin, were significantly improved by FA. The expressions of alpha-SMA, PCNA and TGF-beta 1 were increased in renal cortex of HHcy rats, and which were also partially reversed by FA. These data suggest that elevated plasma Hcy is an important pathogenic factor for glomerular damage."

According to the news reporters, the research concluded: "Lowering plasma Hcy by FA can inhibit TGF-beta 1 expression and attenuate HHcy-induced glomerular damage."

For more information on this research see: Folic acid attenuates hyperhomocysteinemia-induced glomerular damage in rats. Microvascular Research, 2013;89():146-152. Microvascular Research can be contacted at: Academic Press Inc Elsevier Science, 525 B St, Ste 1900, San Diego, CA 92101-4495, USA. (Elsevier - www.elsevier.com; Microvascular Research - www.elsevier.com/wps/product/cws_home/622916)

Our news correspondents report that additional information may be obtained by contacting L. Cao, Guangdong Prov Peoples Hosp, Guangzhou 510080, Guangdong, People's Republic of China. Additional authors for this research include X.Y. Lou, Z.X. Zou, N.N. Mou, W.K. Wu, X.Q. Huang and H.M. Tan (see also Diet and Nutrition Disorders).

Keywords for this news article include: Asia, Guangdong, Podocytes, Cardiology, Avitaminosis, Malnutrition, Cardiovascular, Epithelial Cells, Deficiency Diseases, Hyperhomocysteinemia, Vitamin B Deficiency, Malabsorption Syndromes, People's Republic of China, Diet and Nutrition Disorders, Nutritional and Metabolic Diseases, Inborn Errors Amino Acid Metabolism

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