Perinatal taurine depletion followed by high sugar intake (postweaning) alters the renin-angiotensin system (RAS) and glucose regulation in adult female rats. This study tests the hypothesis that in adult female rats, RAS and estrogen contribute to insulin resistance resulting from perinatal taurine imbalance. Female Sprague-Dawley rats were fed normal rat chow with 3% β-alanine (taurine depletion, TD), 3% taurine (taurine supplementation, TS), or water alone (control, C) from conception to weaning. Their female offspring were fed normal rat chow with 5% glucose in water (TDG, TSG, CG) or water alone (TDW, TSW, CW) throughout the experiment. At 7-8 weeks of age, animals were studied with or without captopril inhibition of the RAS and with or without estrogen receptor inhibition by tamoxifen. Compared to CW and CG groups, perinatal taurine depletion but not supplementation slightly increased plasma insulin levels. High sugar intake slightly increased plasma insulin only in TSG. Captopril treatment significantly increased plasma insulin in all groups except CG (the greatest increase was in TDG). Changes in insulin resistance and insulin secretion paralleled the changes in plasma insulin levels. In contrast, tamoxifen treatment increased insulin resistance and decreased insulin secretion only in TDG and this group displayed hyperglycemia and glucose intolerance. These data indicate that perinatal taurine imbalance alters the interplay of RAS and estrogen on glucose-insulin regulation in adult female rats.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/978-1-4614-6093-0_8 | DOI Listing |
Antioxidants (Basel)
November 2023
Department of Pharmacy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan.
Taurine is a natural antioxidant with antihypertensive properties. Maternal chronic kidney disease (CKD) has an impact on renal programming and increases the risk of offspring hypertension in later life. The underlying mechanisms cover oxidative stress, a dysregulated hydrogen sulfide (HS) system, dysbiotic gut microbiota, and inappropriate activation of the renin-angiotensin-aldosterone system (RAAS).
View Article and Find Full Text PDFBackground: Cerebral palsy (CP) is a neurodevelopmental disorder characterized by motor impairment. In this study, we aimed to describe the characteristics of amino acids (AA) in the plasma of children with CP and identify AA that could play a potential role in the auxiliary diagnosis and treatment of CP.
Methods: Using high performance liquid chromatography, we performed metabolomics analysis of AA in plasma from 62 CP children and 60 healthy controls.
Aust N Z J Obstet Gynaecol
October 2022
Institute for Social Science Research, The University of Queensland, Brisbane, Queensland, Australia.
Background: Adverse childhood experiences (ACEs) are associated with many health problems in women during pregnancy, including depression/anxiety, gestational diabetes and adverse birth outcomes. However, unlike other health risk factors, screening for ACEs has not been widely implemented in antenatal care settings.
Aims: The aim of the scoping review was to explore the challenges in screening for ACEs in antenatal care settings and to provide the lessons learnt and evidence that guide the practice of ACE screening for both healthcare providers and pregnant women.
Adv Exp Med Biol
July 2022
SUNY Neuroscience Research Institute, SUNY Old Westbury, Old Westbury, NY, USA.
Lead (Pb) is a developmental neurotoxicant that disrupts the GABA-shift and subsequently causes alterations in the brain's excitation-to-inhibition (E/I) balance. This finding suggests that neurodevelopmental Pb exposures may increase the risk of brain excitability and/or seizure susceptibility. Prior studies have suggested that neurodevelopmental Pb exposures may cause excitotoxicity of cholinergic neurons, but little to no research has further investigated these potential relationships.
View Article and Find Full Text PDFAdv Exp Med Biol
July 2022
SUNY Neuroscience Research Institute, SUNY Old Westbury, Old Westbury, NY, USA.
Lead (Pb) is a developmental neurotoxicant that causes alterations in the brain's excitation-to-inhibition (E/I) balance by disrupting the development of the GABAergic systems. These GABAergic disruptions have persistent neurobiological and neurobehavioral structure-function relationships that can be examined using animal models of Pb exposure. Further, taurine, a GABA- agonist, has been shown to offer neuroprotection against neurodevelopmental Pb exposure and senescence.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!