J 2016

Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood

SAKUYAMA, Hiroe; Minami KATOH; Honoka WAKABAYASHI; Anthony ZULLI; Peter KRUŽLIAK et al.

Základní údaje

Originální název

Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood

Autoři

SAKUYAMA, Hiroe; Minami KATOH; Honoka WAKABAYASHI; Anthony ZULLI; Peter KRUŽLIAK a Yoshio UEHARA

Vydání

Journal of Biomedical Science, BioMed website, BioMed Central, London, England, 2016, 1021-7770

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10601 Cell biology

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.799

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/16:00100479

Organizační jednotka

Lékařská fakulta

EID Scopus

Klíčová slova anglicky

Salt restriction; Low birth weight; Low birth rate; Programing; Growth retardation; Hypertension; Salt sensitivity; Insulin resistance; Dyslipidemia

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 11. 5. 2018 15:13, Soňa Böhmová

Anotace

V originále

Recent studies reported the critical role of the intrauterine environment of a fetus in growth or the development of disease in adulthood. In this article we discussed the implications of salt restriction in growth of a fetus and the development of growth-related disease in adulthood. Salt restriction causes retardation of fatal growth or intrauterine death thereby leading to low birth weight or decreased birth rate. Such retardation of growth along with the upregulation of the renin angiotensin system due to salt restriction results in the underdevelopment of cardiovascular organs or decreases the number of the nephron in the kidney and is responsible for onset of hypertension in adulthood. In addition, gestational salt restriction is associated with salt craving after weaning. Moreover, salt restriction is associated with a decrease in insulin sensitivity. A series of alterations in metabolism due to salt restriction are probably mediated by the upregulation of the renin angiotensin system and an epigenetic mechanism including proinflammatory substances or histone methylation. Part of the metabolic disease in adulthood may be programmed through such epigenetic changes. The modification of gene in a fetus may be switched on through environment factors or life style after birth. The benefits of salt restriction have been assumed thus far; however, more precise investigation is required of its influence on the health of fetuses and the onset of various diseases in adulthood.