Maternal high salt diet altered Adenosine‐mediated vasodilatation via PKA/BK channel pathway in offspring rats

Wu, Jue; Li, Na; Liu, Yanping; Li, Weisheng; He, Axin; Zhu, Di; Feng, Xueqin; Liu, Bailin; Shi, Ruixiu; Zhang, Yujuan; Lv, Jian; Xu, Zhice

doi:10.1002/mnfr.201600963

Cited by 6 publications

(4 citation statements)

References 48 publications

(63 reference statements)

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Section: Discussionmentioning

confidence: 99%

“…Prenatal malnutrition, similar to other risk factors, has been demonstrated to cause the development of various adult illnesses, including cardiovascular, metabolic, and nervous diseases. [1][2][3][4][5][6][7] However, the mechanisms underlying this effect are still relatively unclear. In the present study, the maternal FBG level was significantly increased by high sucrose feeding during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…An increasing amount of evidence indicates that adverse in utero environments can affect the growth and development of offspring later in life. Prenatal risk factors such as high salt, high sucrose, high fat, hypoxia, nicotine/smoke exposure, and malnutrition often cause short‐term and/or life‐long health problems in offspring . Thus, ascertaining whether postnatal lifestyle and nutritional intake mitigates or worsens the impacts of prenatal exposure is important and interesting research.…”

Section: Introductionmentioning

confidence: 99%

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Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring

Zhang

Zhu

Zhang

et al. 2018

Molecular Nutrition Food Res

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Both prenatal and prenatal-plus-postnatal high sucrose exposure substantially affect biological functions related to insulin homeostasis. IRS-1(S612) protein phosphorylation appears to be a part of the molecular mechanism underlying these effects. These results add to the understanding of how high sucrose intake contributes to insulin resistance and diabetes pathogenesis and how postnatal nutrition and lifestyle may mitigate detrimental prenatal exposures.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring

Zhang

Zhu

Zhang

et al. 2018

Molecular Nutrition Food Res

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“…We previously established a rat model of HSD (8% NaCl) during pregnancy and found that prenatal HSD affected their offspring's coronary artery contractility, glucose tolerance, and insulin sensitivity. [13][14][15] These recent studies aimed to identify defects in the system that the offspring exposed to maternal HSD during pregnancy. As part of this study, we sought to determine whether HSD impacts oocyte and embryo quality and examine the mechanisms involved.…”

Section: Introductionmentioning

confidence: 99%

High‐Salt Diet Causes Defective Oocyte Maturation and Embryonic Development to Impair Female Fertility in Mice

He,

Zheng,

Liu

et al. 2023

Molecular Nutrition Food Res

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Scope: High salinity has been reported to induce many human disorders in tissues and organs to interfere with their normal physiological functions. However, it is unknown how salinity affects the development of female germ cells. This study suggests that a high‐salt diet (HSD) may weaken oocyte quality to impair female fertility in mice and investigates the underlying mechanisms.Methods and results: C57BL/6 female mice are fed with a regular diet (Control) or a high‐salt diet (HSD). Oocyte maturation, fertilization rate, embryonic development, and female fertility are evaluated. In addition, the spindle organization, actin polymerization, and kinetochore‐microtubule attachment of oocytes are examined in both groups. Moreover, single‐cell transcriptome data are used to demonstrate how HSD alters the transcript levels of genes. The observations confirm that HSD leads to female subfertility due to the deterioration of oocyte and embryo quality. The mechanism underlying reveals HSD compromises the oocytes' autophagy, apoptosis level, and mitochondrial function.Conclusion: The work illustrates that a high concentration of salt diet results in oocyte meiotic arrest, fertilization failure, and early developmental defection that embryos undergo to reduce female fertility in mice by perturbing the level of autophagy and apoptosis, mitochondrial function in oocytes.

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Inhibition of Maternal c-Src Ameliorates the Male Offspring Hypertension by Suppressing Inflammation and Neurotransmitters in the Paraventricular Nucleus

Wang

et al. 2021

Cardiovasc Toxicol

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Maternal high salt diet altered Adenosine‐mediated vasodilatation via PKA/BK channel pathway in offspring rats

Abstract: Prenatal HS diets altered Adenosine-mediated coronary artery vasodilatation in the offspring, which was linked to downregulation of cAMP/PKA/BK channel pathway.

Cited by 6 publications

References 48 publications

Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring

Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring

High‐Salt Diet Causes Defective Oocyte Maturation and Embryonic Development to Impair Female Fertility in Mice

Inhibition of Maternal c-Src Ameliorates the Male Offspring Hypertension by Suppressing Inflammation and Neurotransmitters in the Paraventricular Nucleus

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