Maternal high fructose diet exacerbates white adipose tissue thermogenic process in offspring upon exposure to cold temperature

Life Sciences ◽  
2021 ◽  
pp. 120066
Author(s):  
A. Alzamendi ◽  
I. Miguel ◽  
M.G. Zubiría ◽  
S.E. Gambaro ◽  
E. Spinedi ◽  
...  
2017 ◽  
Vol 123 ◽  
pp. 14-24 ◽  
Author(s):  
Thereza Cristina Lonzetti Bargut ◽  
Larissa Pereira Santos ◽  
Daiana Guimarães Lopes Machado ◽  
Marcia Barbosa Aguila ◽  
Carlos Alberto Mandarim-de-Lacerda

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Zeid Khitan ◽  
Mohit Harsh ◽  
Komal Sodhi ◽  
Joseph I. Shapiro ◽  
Nader G. Abraham

Background.Fructose metabolism is an unregulated metabolic pathway and excessive fructose consumption is known to activate ROS. HO-1 is a potent antioxidant gene that plays a key role in decreasing ROS and isoprostanes. We examined whether the fructose-mediated increase in adipocyte dysfunction involves an increase in isoprostanes and that pharmacological induction of HO-1 would decrease both isoprostane levels and adipogenesis.Methods and Results.We examined the effect of fructose, on adipogenesis in human MSCs in the presence and absence of CoPP, an inducer of HO-1. Fructose increased adipogenesis and the number of large lipid droplets while decreasing the number of small lipid droplets (P<0.05). Levels of heme and isoprostane in fructose treated MSC-derived adipocytes were increased. CoPP reversed these effects and markedly increased HO-1 and the Wnt signaling pathway. The high fructose diet increased heme levels in adipose tissue and increased circulating isoprostane levels (P<0.05versus control). Fructose diets decreased HO-1 and adiponectin levels in adipose tissue. Induction of HO-1 by CoPP decreased isoprostane synthesis (P<0.05versus fructose).Conclusion.Fructose treatment resulted in increased isoprostane production and adipocyte dysfunction, which was reversed by the increased expression of HO-1.


2018 ◽  
Vol 476 ◽  
pp. 110-118 ◽  
Author(s):  
Biljana Bursać ◽  
Ana Djordjevic ◽  
Nataša Veličković ◽  
Danijela Vojnović Milutinović ◽  
Snježana Petrović ◽  
...  

2013 ◽  
Vol 110 (3) ◽  
pp. 456-465 ◽  
Author(s):  
Nataša Veličković ◽  
Ana Djordjevic ◽  
Ana Vasiljević ◽  
Biljana Bursać ◽  
Danijela Vojnović Milutinović ◽  
...  

High fructose consumption is commonly associated with insulin resistance, disturbed glucose homeostasis and low-grade inflammation. Increased glucocorticoid production within adipose tissue has been implicated in the pathogenesis of fructose-induced metabolic syndrome. Immunosuppressive actions of glucocorticoids can be counter-regulated by macrophage migration inhibitory factor (MIF), which is recognised as a key molecule in metabolic inflammation. In the present study, we hypothesised that coordinated action of glucocorticoids and MIF can mediate the effects of a high-fructose diet on adipose tissue and liver inflammation. We examined the effects of long-term consumption of a 10 % fructose solution on corticosterone (CORT) and MIF levels in rat blood plasma, liver and adipose tissue, as well as MIF and TNF-α mRNA expression and NF-κB activation in the same tissues. The high-fructose diet led to an increase in both CORT and MIF in the adipose tissue, and a highly significant positive correlation between their levels was observed. The attenuated NF-κB activation and unaltered TNF-α mRNA expression noticed in the adipose tissue could be interpreted as an outcome of the opposing actions of CORT and MIF. In contrast to adipose tissue, inflammation in the liver was characterised by NF-κB activation, an increased TNF-α mRNA level and unchanged levels of MIF protein, MIF mRNA and CORT. Overall, these findings suggest that a high-fructose diet differently affects the levels of glucocorticoids and MIF in the adipose tissue and liver, implicating that fructose over-consumption has tissue-specific effects on regulation of metabolic inflammation.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Mehmet Bilgehan Pektas ◽  
Halit Bugra Koca ◽  
Gokhan Sadi ◽  
Fatma Akar

The effects of high-fructose diet on adipose tissue insulin signaling and inflammatory process have been poorly documented. In this study, we examined the influences of long-term fructose intake and resveratrol supplementation on the expression of genes involved in insulin signaling and the levels of inflammatory cytokines and sex hormones in the white adipose tissues of male and female rats. Consumption of high-fructose diet for 24 weeks increased the expression of genes involved in insulin signaling includingIR,IRS-1,IRS-2,Akt,PI3K,eNOS,mTOR, andPPARγ, despite induction of proinflammatory markers, iNOS, TNFα, IL-1β, IL-18, MDA, and ALT, as well as anti-inflammatory factors, IL-10 and Nrf2 in adipose tissues from males and females. Total and free testosterone concentrations of adipose tissues were impaired in males but increased in females, although there were no changes in their blood levels. Resveratrol supplementation markedly restored the levels of MDA, IL6, IL-10, and IL-18, as well asiNOS,Nrf2, andPI3KmRNA, in adipose tissues of both genders. Dietary fructose activates both insulin signaling and inflammatory pathway in the adipose tissues of male and female rats proposing no correlation between the tissue insulin signaling and inflammation. Resveratrol has partly modulatory effects on fructose-induced changes.


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