Exposure to bioaccumulative organochlorine compounds alters adipogenesis, fatty acid uptake, and adipokine production in NIH3T3-L1 cells

Howell, George; Mangum, Lauren H.

doi:10.1016/j.tiv.2010.10.015

Cited by 103 publications

(107 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, three other epidemiological investigations found inverse associations (Lim and Jee 2014;Mullerova et al 2008) or trends (Kern et al 2004) of adiponectin with PCBs or related chemicals, and stronger effects in subgroups with elevated BMI (Lim and Jee 2014;Mullerova et al 2008). Experimental evidence that PCB 153 (Taxvig et al 2012) and DDE (Howell, III and Mangum 2011) stimulate release of adiponectin from mature adipocytes supports these results. Reasons for difference in the effect of PCBs on adiponectin in these investigations and in the current study are not clear, but could be related to variability in population characteristics and exposures.…”

Section: Discussionmentioning

confidence: 64%

Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers

Turyk

Fantuzzi

Persky

et al. 2015

Environmental Research

View full text Add to dashboard Cite

Background Exposure to persistent organic pollutants (POPs) is associated with increased diabetes risk, although the mechanism of action is not well delineated. Methods We investigated established diabetes biomarkers that could implicate potential mechanistic pathways, including C-reactive protein (CRP), a marker of systemic inflammation; gamma glutamyl transferase (GGT), a liver enzyme associated with oxidative stress; and adiponectin, an adipokine modulating glucose regulation and fatty acid oxidation. These biomarkers as well as hemoglobin A1c (HA1c), and POPs [polychlorinated biphenyls (PCBs), p,p-dichlorodiphenyldichloroethylene (DDE) and polybrominated diphenyl ethers (PBDEs)] were measured in a cohort of Great Lakes sport caught fish (GLSCF) consumers. We examined associations of POPs and fish consumption with HA1c and incident diabetes, and evaluated mediation and moderation by diabetes biomarkers. Results Odds of incident diabetes were elevated with exposure to DDE and PCBs. DDE and PCB 118 were positively, and fish meals were inversely, associated with HA1c. CRP was inversely associated with saltwater and total fish meals, particularly in persons with higher adiposity, but did not mediate the associations of fish meals with HA1c. There were few associations of adiponectin, CRP and GGT with POPs, with the exception of positive associations of GGT with PCB 118 and with PBDEs in older persons, and a positive association of adiponectin with PBDEs. Adiponectin, CRP and GGT did not mediate associations of DDE and PCBs with HA1c or incident diabetes. However, the association of DDE with HA1c was stronger in persons with higher CRP, GGT and BMI, and lower adiponectin, while the association of PCB 118 with HA1c was stronger in persons with higher GGT. Conclusions These findings suggest that adiponectin, CRP and GGT did not mediate effects of POPs on diabetes or HA1c. However, POPs may have stronger effects on blood glucose in persons at higher risk for diabetes.

show abstract

Section: Discussionmentioning

confidence: 64%

Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers

Turyk

Fantuzzi

Persky

et al. 2015

Environmental Research

View full text Add to dashboard Cite

show abstract

“…In 3T3-L1 adipocytes, the organochlorine pesticides DDE, oxychlordane, and dieldrin have been reported to increase basal fatty acid uptake (160) and BPA was demonstrated to increase lipid accumulation (32). Administration of PCB-77 to mice resulted in greater body weight and adipocyte hypertrophy (34).…”

Section: Effects Of Pops On At Functionmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

136

View full text Add to dashboard Cite

We examine the role of adipose tissue, typically considered an energy storage site, as a potential site of toxicant accumulation. Although the production of most persistent organic pollutants (POPs) was banned years ago, these toxicants persist in the environment due to their resistance to biodegradation and widespread distribution in various environmental forms (e.g., vapor, sediment, water). As a result, human exposure to these toxicants is inevitable. Largely due to their lipophilicity, POPs bioaccumulate in adipose tissue, resulting in greater body burdens of these environmental toxicants with obesity. POPs of major concern include polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDDs/PCDFs), and polybrominated biphenyls and diphenyl ethers (PBBs/PBDEs), among other organic compounds. In this review, we 1) highlight the physical characteristics of toxicants that enable them to partition into and remain stored in adipose tissue, 2) discuss the specific mechanisms of action by which these toxicants act to influence adipocyte function, and 3) review associations between POP exposures and the development of obesity and diabetes. An area of controversy relates to the relative potential beneficial versus hazardous health effects of toxicant sequestration in adipose tissue.

show abstract

“…Cells were cultured in 6-well plates (2×10 6 cells per well) and treated with 0, 2, 4, 8 mM of acetate, 10 µM of BML-275 or 10 µM of BML-275 + 4 mM of acetate for 6 h. Oil Red O staining was performed according to previously described methods [12]. Briefly, cells were fixed with 10% buffered formalin for at least 30 min.…”

Section: Methodsmentioning

confidence: 99%

Acetic Acid Influences BRL-3A Cell Lipid Metabolism via the AMPK Signalling Pathway

Xiao

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Acetic acid (AcOH), a short-chain fatty acid, is reported to have some beneficial effects on metabolism. Therefore, the aim of this study was to investigate the regulatory mechanism of acetic acid on hepatic lipid metabolism in BRL-3A cells. Methods: We cultured and treated BRL-3A cells with different concentrations of sodium acetate (neutralized acetic acid) and BML-275 (an AMPKα inhibitor). The total lipid droplet area was measured by oil red O staining, and the triglyceride content was determined by a triglyceride detection kit. We detected mRNA and protein levels of lipid metabolism-related signalling molecules by RT-PCR and Western blot. Results: Acetic acid treatment increased AMPKα phosphorylation, which subsequently increased the expression and transcriptional activity of peroxisome proliferator-activated receptor α and upregulated the expression of lipid oxidation genes. These changes ultimate led to increasing levels of lipid oxidation in BRL-3A cells. Furthermore, elevated AMPKα phosphorylation reduced the expression and transcriptional activity of the sterol regulatory element-binding protein 1c, which reduced the expression of lipogenic genes, thereby decreasing lipid biosynthesis in BRL-3A cells. Consequently, triglyceride content in acetate-treated BRL-3A cells was significantly decreased. Conclusions: These results indicate that acetic acid activates the AMPKα signalling pathway, leading to increased lipid oxidation and decreased lipid synthesis in BRL-3A cells, thereby reducing liver fat accumulation in vitro.

show abstract

Exposure to bioaccumulative organochlorine compounds alters adipogenesis, fatty acid uptake, and adipokine production in NIH3T3-L1 cells

Cited by 103 publications

References 38 publications

Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers

Persistent organic pollutants and biomarkers of diabetes risk in a cohort of Great Lakes sport caught fish consumers

Adipose Tissue as a Site of Toxin Accumulation

Acetic Acid Influences BRL-3A Cell Lipid Metabolism via the AMPK Signalling Pathway

Contact Info

Product

Resources

About