BACKGROUND Decabromodiphenyl ether (BDE-209) is the most commonly used brominated flame retardant. Recently, BDE-209 has been suspected of being an environmental risk factor for metabolic diseases such as obesity, insulin resistance (IR), type 2 diabetes mellitus, and hypertension. AIM To investigate the effects of BDE-209 on IR and glucose and lipid metabolism in C57BL/6 mice. METHODS Adult male C57BL/6 mice were randomly divided into high, medium-high, medium, medium-low, and low dose BDE-209 groups, and a control group ( n = 6 per group), which received 1000, 800, 600, 450, 300, and 0 mg/kg BDE-209, respectively. After BDE-209 exposure for 60 d, the mice were fasted overnight, and then sacrificed to obtain tissues. An automatic biochemical analyzer was used to detect serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C); enzyme-linked immunosorbent assay kits were used to detect fasting serum insulin (FINS), leptin (LEP), and adiponectin (Adp) levels; a blood glucose meter was used to detect fasting blood glucose (FBG). Morphological changes of the liver were observed by hematoxylin and eosin staining. Real-time quantitative polymerase chain reaction and Western blot were used to determine the messenger ribonucleic acid (mRNA) and protein levels, respectively, of LEP, Adp, and peroxisome proliferators activated receptor-γ (PPARγ) in mouse liver and adipose tissues. RESULTS There was a statistically significant difference in the weight of mice in each group after 45 and 60 d of exposure ( P < 0.05). After 60 d of exposure, the weight of liver and adipose tissues in the exposure groups were greater than that of the control group ( P < 0.05). The liver tissue structure was disordered and the liver tissues were accompanied by local inflammatory cell infiltration in the high, medium-high, and medium dose BDE-209 groups. The levels of FINS, insulin sensitivity index, Adp, and HDL-C were decreased in the BDE-209 group compared with the control group, as were the mRNA and protein levels of Adp in liver and adipose tissues ( P < 0.05). Serum level of FBG and LEP were higher in the BDE-209 group than in controls. TC, TG, and LDL-C levels as well as the mRNA and protein expression of LEP and PPARγ in liver and adipose tissues were higher than those in the control group ( P < 0.05). Homeostatic assessment model of IR was higher in the medium and medium-low dose BDE-209 groups ( P < 0.05). CONCLUSION BDE-209 increases the body weight, fat and liver tissue weight, TC, TG, and LDL-C, reduces HDL-C, and causes IR in mice, which may be related to activating the PPARγ receptor.
Fatty acids are important components of the avocado mesocarp, so a better understanding of how their change during fruit development will contribute to improving the quality of avocado fruits and their nutritional value. The changes in fatty acids, lipid droplets, and expression of some key genes and regulators participating in late glycolysis and fatty acid biosynthesis were analyzed at different stages of the development of avocado mesocarp. The total fatty acid contents of the avocado mesocarp increased during fruit development, with an increase by a factor of seven (from 1,628.04 to 11,116.30 mg/100 g dry weight) in the late stage of fruit maturation, this was confirmed by the changes observed in the lipid droplets. The composition of the main fatty acids varied at four developmental stages of fruit development. Palmitic, palmitoleic, oleic, and linoleic acid contents generally increased during fruit development, reaching maxima at Harvest, with percentages of total fatty acids of 50%, 9%, 31%, and 8%, respectively. Meanwhile, the amount of PaWRI1, PaACP4-2, and PapPK-β1 expressed consistently increased by up to 4-fold during fruit development. This comprehensive analysis has indicated that the changes in the expressions of PaWRI1, PaACP4-2, and PapPK-β1 were consistent with those in the total fatty acid contents, so they might have key roles in the accumulation of oil in the avocado mesocarp.
Aryl hydrocarbon receptor (AHR) plays an important role in tumor development. However, its function in cervical cancer has not been fully elucidated. We evaluated the ten genes that are predicted to associate with AHR protein interaction. The comprehensive scores were: CYP1A1, ARNT2, HSP90AA1, ARNT, AIP, PTGES3, HSP90AB1, CYP1B1, ESR1, MAF, respectively. In addition, we showed that levels of AHR and its related genes were correlated with the immune infiltration and expression of immuno-regulators (immunoinhibitors, immunostimulators, MHC molecules) levels in cervical cancer. High expression of AHR, CYP1A1, HSP90AA1, and HSP90AB1 and low expression of ESR1 were negatively correlated with the prognoses of cervical cancer patients. The Cox multivariate regression showed that high expression of AHR ( HR = 1.874, 95% CI = 1.069–3.285, P = 0.028) and CYP1A1 ( HR = 1.822, 95%CI = 1.077–3.080, P = 0.025) were risk factors for prognosis in patients with cervical cancer. IHC results indicated that AHR and CYP1A1 were widely expressed in cervical cancer. These findings suggest that AHR and CYP1A1 may serve as prognostic biomarkers for determining prognosis and immune infiltration in cervical cancer.
Background: Environmental polybrominated diphenyl ether (PBDE) exposure may be associated with diabetes and obesity. 2,2′,4,4′,5,5′-Hexabromodiphenyl ether (BDE-153) is one of the most abundant and widely distributed homologs of PBDEs detected in humans. This study investigated the effects of BDE-153 on the expression of adipokines and glucose and lipid metabolism. Methods: Adult male C57BL/6 mice were divided into five BDE-153 groups and one control group. After BDE-153 exposure for 4 weeks, the levels of biochemical indexes and the mRNA and protein expression levels of leptin, adiponectin, peroxisome proliferators activated receptors gamma (PPARγ), and AMPKα were measured. The histomorphological changes of liver and pancreas tissues were observed. Results: After BDE-153 exposure, the weight of mice in the medium-high-dose group at different exposure times was lower than that in the control group (p all <0.05), and the body weight decreased slightly with the increase of the dose of BDE-153. BDE-153 caused the disorder of glucose and lipid metabolism in mice, the weight of liver and pancreas increased, lipid droplets accumulated in liver cells, and the positive rate of insulin staining increased in a dose-dependent manner. BDE-153 also interfered with the expression of PPARγ, AMPKα, and adipokines. The results of restrictive cubic splines (RCS) showed that there were a nonlinear dose-response relationship between the exposure dose of BDE-153 and the expression levels of PPARγ, AMPKα, and adipokines. Conclusion: Our results suggest that BDE-153 may interfere with the expression of adipokines and the secretion of insulin by affecting the expression of PPARγ and AMPKα, which play a key role in glucose and lipid metabolism, leading to the occurrence of glucose and lipid metabolism disorder.
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