Polychlorinated biphenyls exposure-induced insulin resistance is mediated by lipid droplet enlargement through Fsp27
العنوان: | Polychlorinated biphenyls exposure-induced insulin resistance is mediated by lipid droplet enlargement through Fsp27 |
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المؤلفون: | Hye Young Kim, Jong-Min Kim, Seung Hee Yoo, Ju Yong Bae, Young Hyun Yoo, Mi Hwa Lee, Woo Young Kwon, Yeon A Kim, Yoo Jin Oh |
المصدر: | Archives of Toxicology. 91:2353-2363 |
بيانات النشر: | Springer Science and Business Media LLC, 2016. |
سنة النشر: | 2016 |
مصطلحات موضوعية: | Blood Glucose, Male, 0301 basic medicine, medicine.medical_specialty, Health, Toxicology and Mutagenesis, medicine.medical_treatment, Intraperitoneal injection, Cell Culture Techniques, Adipose tissue, 010501 environmental sciences, Biology, Toxicology, 01 natural sciences, Mice, 03 medical and health sciences, chemistry.chemical_compound, fluids and secretions, Insulin resistance, In vivo, 3T3-L1 Cells, Internal medicine, Lipid droplet, Adipocyte, Adipocytes, medicine, Animals, Insulin, RNA, Small Interfering, reproductive and urinary physiology, Cell Size, 0105 earth and related environmental sciences, organic chemicals, Proteins, food and beverages, Cell Differentiation, Lipid Droplets, General Medicine, medicine.disease, Polychlorinated Biphenyls, In vitro, Mice, Inbred C57BL, stomatognathic diseases, 030104 developmental biology, Endocrinology, Adipose Tissue, chemistry, Insulin Resistance |
الوصف: | Although epidemiological and experimental studies demonstrated that polychlorinated biphenyls (PCBs) lead to insulin resistance, the mechanism underlying PCBs-induced insulin resistance has remained unsolved. In this study, we examined in vitro and in vivo effects of PCB-118 (dioxin-like PCB) and PCB-138 (non-dioxin-like PCB) on adipocyte differentiation, lipid droplet growth, and insulin action. 3T3-L1 adipocytes were incubated with PCB-118 or PCB-138 during adipocyte differentiation. For in vivo studies, C57BL/6 mice were administered PCB-118 or PCB-138 (37.5 mg/kg) by intraperitoneal injection and we examined adiposity and whole-body insulin action. PCB-118 and PCB-138 significantly promoted adipocyte differentiation and increased the lipid droplet (LD) size in 3T3-L1 adipocytes. In mice, both PCBs increased adipose mass and adipocyte size. Furthermore, both PCBs induced insulin resistance in vitro and in vivo. Expression of fat-specific protein 27 (Fsp27), which is localized to LD contact sites, was increased in PCB-treated 3T3-L1 adipocytes and mice. Depletion of Fsp27 by siRNA resulted in the inhibition of LD enlargement and attenuation of insulin resistance in PCB-treated 3T3-L1 adipocytes. An anti-diabetic drug, metformin, attenuated insulin resistance in PCB-treated 3T3-L1 adipocytes through the reduced expression of Fsp27 protein and LD size. This study suggests that PCB exposure-induced insulin resistance is mediated by LD enlargement through Fsp27. |
تدمد: | 1432-0738 0340-5761 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::089b31779930509783e6ea7099e6a1d9Test https://doi.org/10.1007/s00204-016-1889-2Test |
حقوق: | CLOSED |
رقم الانضمام: | edsair.doi.dedup.....089b31779930509783e6ea7099e6a1d9 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 14320738 03405761 |
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