These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Altered dipsogenic responses and expression of angiotensin receptors in the offspring exposed to prenatal high sucrose.
    Author: Wu L, Mao C, Liu Y, Shi A, Xu F, Zhang L, Xu Z.
    Journal: Peptides; 2011 Jan; 32(1):104-11. PubMed ID: 20965221.
    Abstract:
    The present study determined water and salt intake as well as expression of AT(1) and AT(2) receptors in the brain and kidney in the adult offspring rats prenatally exposed to high sucrose. Following the exposure during pregnancy, water intake and salt intake at baseline levels were not changed in the adult offspring. However, after 24h water deprivation, consumption of water and salt was significantly increased compared to that of the control. Plasma sodium and osmolality levels remained the same between the offspring in the control and the exposed groups, while hematocrit was higher in the offspring exposed to prenatal high sucrose immediately following water deprivation. Density of renal AT(1) receptor protein was the same between the control and the exposed group, while AT(2) receptor protein in the kidney was significantly increased in the offspring exposed to prenatal high sucrose in association of thicker basal membrane of glomerular. In the forebrain, both AT(1) and AT(2) receptor levels were significantly increased in the offspring with history of prenatal high sucrose. In addition, water deprivation induced more c-fos expression in the central dipsogenic areas, including the paraventricular and supraoptic nuclei in the offspring exposed to prenatal high sucrose. The results suggested that prenatal high intake of sucrose may affect development of pathways in regulation of dipsogenic behavior in face of dehydration, which was associated with altered expression of AT(1) or/and AT(2) receptors in the kidney and brain.
    [Abstract] [Full Text] [Related] [New Search]