Maternal green tea polyphenol intake during lactation attenuates kidney injury in high-fat-diet-fed male offspring programmed by maternal protein restriction in rats

2018 ◽  
Vol 56 ◽  
pp. 99-108 ◽  
Author(s):  
Saori Kataoka ◽  
Toshio Norikura ◽  
Shin Sato
2020 ◽  
Vol 11 (11) ◽  
pp. 9924-9935
Author(s):  
Jinbao Huang ◽  
Wenjiao Li ◽  
Wenjing Liao ◽  
Qing Hao ◽  
Dong Tang ◽  
...  

Dietary EGCG maintains the intestinal immune homeostasis, which might play a role in preventing systemic inflammation and NAFLD.


2019 ◽  
Vol 65 (1) ◽  
pp. 34-46 ◽  
Author(s):  
Chihiro Ushiroda ◽  
Yuji Naito ◽  
Tomohisa Takagi ◽  
Kazuhiko Uchiyama ◽  
Katsura Mizushima ◽  
...  

2013 ◽  
Vol 305 (12) ◽  
pp. E1444-E1451 ◽  
Author(s):  
Hyun-Ju Jang ◽  
Simone D. Ridgeway ◽  
Jeong-a Kim

Insulin resistance, a hallmark of metabolic disorders, is a risk factor for diabetes and cardiovascular disease. Impairment of insulin responsiveness in vascular endothelium contributes to insulin resistance. The reciprocal relationship between insulin resistance and endothelial dysfunction augments the pathophysiology of metabolism and cardiovascular functions. The most abundant green tea polyphenol, epigallocatechin-3-gallate (EGCG), has been shown to have vasodilator action in vessels by activation of endothelial nitric oxide synthase (eNOS). However, it is not known whether EGCG has a beneficial effect in high-fat diet (HFD)-induced endothelial dysfunction. Male C57BL/6J mice were fed either a normal chow diet (NCD) or HFD with or without EGCG supplement (50 mg·kg−1·day−1) for 10 wk. Mice fed a HFD with EGCG supplement gained less body weight and showed improved insulin sensitivity. In vehicle-treated HFD mice, endothelial function was impaired in response to insulin but not to acetylcholine, whereas the EGCG-treated HFD group showed improved insulin-stimulated vasodilation. Interestingly, EGCG intake reduced macrophage infiltration into aortic tissues in HFD mice. Treatment with EGCG restored the insulin-stimulated phosphorylation of eNOS, insulin receptor substrate-1 (IRS-1), and protein kinase B (Akt), which was inhibited by palmitate (200 μM, 5 h) in primary bovine aortic endothelial cells. From these results, we conclude that supplementation of EGCG improves glucose tolerance, insulin sensitivity, and endothelial function. The results suggest that EGCG may have beneficial health effects in glucose metabolism and endothelial function through modulating HFD-induced inflammatory response.


2019 ◽  
Vol 47 (3) ◽  
pp. 412-421
Author(s):  
Sávio dos Santos Barbosa ◽  
Ana Paula da Fonseca Arcoverde Cabr Mello ◽  
Viviane de Oliveira Nogueira ◽  
Ially Fabiane da Silva ◽  
Palloma Emanuelle Dornelas de Melo ◽  
...  

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Mousumi Bose ◽  
Joshua D Lambert ◽  
Jihyeung Ju ◽  
Kenneth R Reuhl ◽  
Sue A Shapses ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Jia Zheng ◽  
Ling Zhang ◽  
Jiayi Liu ◽  
Yanli Li ◽  
Junqing Zhang

Substantial evidence indicated that maternal malnutrition could increase the susceptibility to obesity, insulin resistance, and type 2 diabetes in adulthood. It is increasingly apparent that the brain, especially the hypothalamus, plays a critical role in glucose homeostasis. However, little information is known about the mechanisms linking maternal protein restriction combined with post-weaning high-fat (HF) feeding with altered expression of brain neurotransmitters, and investigations into the epigenetic modifications of hypothalamus in offspring have not been fully elucidated. Our objective was to explore the effects of maternal protein restriction combined with post-weaning HF feeding on glucose metabolism and hypothalamic POMC methylation in male offspring mice. C57/BL6 mice were fed on either low-protein (LP) or normal chow (NC) diet throughout gestation and lactation. Then, the male offspring were randomly weaned to either NC or high-fat (HF) diet until 32 weeks of age. Gene expressions and DNA methylation of hypothalamic proopiomelanocortin (POMC) and melanocortin receptor 4 (MC4R) were determined in male offspring. The results showed that birth weights and body weights at weaning were both significantly lower in male offspring mice of the dams fed with a LP diet. Maternal protein restriction combined with post-weaning high-fat feeding, predisposes higher body weight, persistent glucose intolerance (from weaning to 32 weeks of age), hyperinsulinemia, and hyperleptinemia in male offspring mice. POMC and MC4R expressions were significantly increased in offspring mice fed with maternal LP and postnatal high-fat diet (P < 0.05). Furthermore, maternal protein restriction combined with post-weaning high-fat feeding induced hypomethylation of POMC promoter in the hypothalamus (P < 0.05) and POMC-specific methylation (%) was negatively correlated with the glucose response to a glucose load in male offspring mice (r = −0.42, P = 0.039). In conclusion, maternal LP diet combined with post-weaning high-fat feeding predisposed the male offspring to impaired glucose metabolism and hypothalamic POMC hypomethylation. These findings can advance our thinking about hypothalamic POMC gene methylation between maternal LP diet combined with post-weaning high-fat feeding and metabolic health in offspring.


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