The inflammatory environment mediated by a high-fat diet inhibited the development of mammary glands and destroyed the tight junction in pregnant mice.

2020 ◽  
Vol 11 (9) ◽  
pp. 8193-8201
Author(s):  
Wenjin Guo ◽  
Juxiong Liu ◽  
Shuang Hou ◽  
Guiqiu Hu ◽  
He Ma ◽  
...  

Long-term intake of a high-fat diet seriously affects the health of pregnant women and leads to increased levels of inflammation in the mammary gland.

2009 ◽  
Vol 297 (5) ◽  
pp. E1171-E1178 ◽  
Author(s):  
Esther M. E. van Straten ◽  
Hester van Meer ◽  
Nicolette C. A. Huijkman ◽  
Theo H. van Dijk ◽  
Julius F. W. Baller ◽  
...  

There is increasing evidence that the metabolic state of the mother during pregnancy affects long-term glucose and lipid metabolism of the offspring. The liver X receptors (LXR)α and -β are key regulators of cholesterol, fatty acid, and glucose metabolism. LXRs are activated by oxysterols and expressed in fetal mouse liver from day 10 of gestation onward. In the present study, we aimed to elucidate whether in utero pharmacological activation of LXR would influence fetal fatty acid and glucose metabolism and whether this would affect lipid homeostasis at adult age. Exposure of pregnant mice to the synthetic LXR agonist T0901317 increased hepatic mRNA expression levels of Lxr target genes and hepatic and plasma triglyceride levels in fetuses and dams. T0901317 treatment increased absolute de novo synthesis and chain elongation of hepatic oleic acid in dams and fetuses. T0901317 exposure in utero influenced lipid metabolism in adulthood in a sex-specific manner; hepatic triglyceride content was increased (+45%) in male offspring and decreased in female offspring (−42%) when they were fed a regular chow diet compared with untreated sex controls. Plasma and hepatic lipid contents and hepatic gene expression patterns in adult male or female mice fed a high-fat diet were not affected by T0901317 pretreatment. We conclude that LXR treatment of pregnant mice induces immediate effects on lipid metabolism in dams and fetuses. Despite the profound changes during fetal life, long-term effects appeared to be rather mild and sex selective without modulating the lipid response to a high-fat diet.


2021 ◽  
Author(s):  
Qi Guan ◽  
Xinwen Ding ◽  
Lingyue Zhong ◽  
Chuang Zhu ◽  
Pan Nie ◽  
...  

Long term high-fat diet (HF) can cause metabolic disorders, which might induce fatty liver. Fermented whole cereal food exhibit healthy potential due to their unique phytochemical composition and probiotics. In...


2021 ◽  
Vol 22 (4) ◽  
pp. 1647
Author(s):  
Brandi Miller ◽  
Rabina Mainali ◽  
Ravinder Nagpal ◽  
Hariom Yadav

The prevalence of type 2 diabetes mellitus (T2D) is increasing worldwide, and there are no long-term preventive strategies to stop this growth. Emerging research shows that perturbations in the gut microbiome significantly contribute to the development of T2D, while microbiome modulators may be beneficial for T2D prevention. However, microbiome modulators that are effective, safe, affordable, and able to be administered daily are not yet available. Based on our previous pro- and prebiotic studies, we developed a novel synbiotic yogurt comprised of human-origin probiotics and plant-based prebiotics and investigated its impact on diet- and streptozotocin-induced T2D in mice. We compared the effects of our synbiotic yogurt to those of a commercially available yogurt (control yogurt). Interestingly, we found that the feeding of the synbiotic yogurt significantly reduced the development of hyperglycemia (diabetes) in response to high-fat diet feeding and streptozotocin compared to milk-fed controls. Surprisingly, the control yogurt exacerbated diabetes progression. Synbiotic yogurt beneficially modulated the gut microbiota composition compared to milk, while the control yogurt negatively modulated it by significantly increasing the abundance of detrimental bacteria such as Proteobacteria and Enterobacteriaceae. In addition, the synbiotic yogurt protected pancreatic islet morphology compared to the milk control, while the control yogurt demonstrated worse effects on islets. These results suggest that our newly developed synbiotic yogurt protects against diabetes in mice and can be used as a therapeutic to prevent diabetes progression.


Placenta ◽  
2021 ◽  
Author(s):  
Shanshan Zhao ◽  
Dongyu Wang ◽  
Zhuyu Li ◽  
Shuqia Xu ◽  
Haitian Chen ◽  
...  

2021 ◽  
pp. 113470
Author(s):  
Everett Altherr ◽  
Aundrea Rainwater ◽  
Darian Kaviani ◽  
Qijun Tang ◽  
Ali D. Güler

2021 ◽  
pp. 1-14
Author(s):  
Jian Bao ◽  
Zheng Liang ◽  
Xiaokang Gong ◽  
Jing Yu ◽  
Yifan Xiao ◽  
...  

Background: Alzheimer’s disease (AD) is the most common form of dementia in older adults and extracellular accumulation of amyloid-β (Aβ) is one of the two characterized pathologies of AD. Obesity is significantly associated with AD developing factors. Several studies have reported that high fat diet (HFD) influenced Aβ accumulation and cognitive performance during AD pathology. However, the underlying neurobiological mechanisms have not yet been elucidated. Objective: The objective of this study was to explore the underlying neurobiological mechanisms of HFD influenced Aβ accumulation and cognitive performance during AD pathology. Methods: 2.5-month-old male APP/PS1 mice were randomly separated into two groups: 1) the normal diet (ND) group, fed a standard diet (10 kcal%fat); and 2) the HFD group, fed a high fat diet (40 kcal%fat, D12492; Research Diets). After 4 months of HFD or ND feeding, mice in the two groups were subjected for further ethological, morphological, and biochemical analyses. Results: A long-term HFD diet significantly increased perirenal fat and impaired dendritic integrity and aggravated neurodegeneration, and augmented learning and memory deficits in APP/PS1 mice. Furthermore, the HFD increased beta amyloid cleaving enzyme 1 (BACE1) dephosphorylation and SUMOylation, resulting in enhanced enzyme activity and stability, which exacerbated the deposition of amyloid plaques. Conclusion: Our study demonstrates that long-term HFD consumption aggravates amyloid-β accumulation and cognitive impairments, and that modifiable lifestyle factors, such as obesity, can induce BACE1 post-modifications which may contribute to AD pathogenesis.


2016 ◽  
Vol 60 (1) ◽  
pp. 28536 ◽  
Author(s):  
Noemi A. V. Roza ◽  
Luiz F. Possignolo ◽  
Adrianne C. Palanch ◽  
José A. R. Gontijo

2017 ◽  
Vol 27 (1) ◽  
pp. 67-73
Author(s):  
Rosilene Rodrigues Kaizer ◽  
Eduarda Costa ◽  
Cínthia Melazzo de Andrade ◽  
Roberta Schmatz ◽  
Jessié Martins Gutierres ◽  
...  
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