Tags

Type your tag names separated by a space and hit enter

Protectin DX attenuates LPS-induced inflammation and insulin resistance in adipocytes via AMPK-mediated suppression of the NF-κB pathway.
Am J Physiol Endocrinol Metab. 2018 10 01; 315(4):E543-E551.AJ

Abstract

Several studies have demonstrated that protectins, ω-3 fatty acid-derived proresolution mediators, may ameliorate inflammation. Recently, protectin DX (PDX) was also reported to attenuate inflammation and insulin resistance in several cell types. However, the effects of PDX on inflammation in adipocytes remain ambiguous. In this study, we found that PDX treatment suppressed adipogenesis and lipid accumulation during 3T3-L1 differentiation. Treatment of differentiated 3T3-L1 cells with PDX stimulated AMP-activated protein kinase (AMPK) phosphorylation in a dose-dependent manner. PDX-induced AMPK phosphorylation blocked lipopolysaccharide (LPS)-induced secretion of proinflammatory cytokines, such as tumor necrosis factor-α and monocyte chemoattractant protein-1. Treatment of 3T3-L1 cells with PDX alleviated LPS-induced NF-κB and inhibitory factor κB phosphorylation. Furthermore, PDX treatment diminished LPS-induced impairment of insulin signaling and insulin-stimulated glucose uptake, as well as fatty acid oxidation. These effects were decreased by silencing AMPK expression with small-interfering RNA. In conclusion, the current findings suggest that PDX attenuates inflammation and insulin resistance in adipocytes via an AMPK-dependent pathway, which in turn provides evidence that PDX has anti-inflammatory and antidiabetic effects in adipocytes.

Authors+Show Affiliations

Research Administration Team, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.Department of Anatomy, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, Republic of Korea.Department of Pharmacology, Faculty of Veterinary Medicine, Cairo University , Giza , Egypt. Department of Medical Pharmacology, Medical Faculty, Ataturk University , Erzurum , Turkey.Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29584445

Citation

Jung, Tae Woo, et al. "Protectin DX Attenuates LPS-induced Inflammation and Insulin Resistance in Adipocytes Via AMPK-mediated Suppression of the NF-κB Pathway." American Journal of Physiology. Endocrinology and Metabolism, vol. 315, no. 4, 2018, pp. E543-E551.
Jung TW, Chung YH, Kim HC, et al. Protectin DX attenuates LPS-induced inflammation and insulin resistance in adipocytes via AMPK-mediated suppression of the NF-κB pathway. Am J Physiol Endocrinol Metab. 2018;315(4):E543-E551.
Jung, T. W., Chung, Y. H., Kim, H. C., Abd El-Aty, A. M., & Jeong, J. H. (2018). Protectin DX attenuates LPS-induced inflammation and insulin resistance in adipocytes via AMPK-mediated suppression of the NF-κB pathway. American Journal of Physiology. Endocrinology and Metabolism, 315(4), E543-E551. https://doi.org/10.1152/ajpendo.00408.2017
Jung TW, et al. Protectin DX Attenuates LPS-induced Inflammation and Insulin Resistance in Adipocytes Via AMPK-mediated Suppression of the NF-κB Pathway. Am J Physiol Endocrinol Metab. 2018 10 1;315(4):E543-E551. PubMed PMID: 29584445.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protectin DX attenuates LPS-induced inflammation and insulin resistance in adipocytes via AMPK-mediated suppression of the NF-κB pathway. AU - Jung,Tae Woo, AU - Chung,Yoon Hee, AU - Kim,Hyoung-Chun, AU - Abd El-Aty,A M, AU - Jeong,Ji Hoon, Y1 - 2018/03/27/ PY - 2018/3/28/pubmed PY - 2019/7/28/medline PY - 2018/3/28/entrez KW - adenosine 5′-monophosphate-activated protein kinase KW - adipocyte KW - lipopolysaccharide KW - nuclear factor-κB SP - E543 EP - E551 JF - American journal of physiology. Endocrinology and metabolism JO - Am J Physiol Endocrinol Metab VL - 315 IS - 4 N2 - Several studies have demonstrated that protectins, ω-3 fatty acid-derived proresolution mediators, may ameliorate inflammation. Recently, protectin DX (PDX) was also reported to attenuate inflammation and insulin resistance in several cell types. However, the effects of PDX on inflammation in adipocytes remain ambiguous. In this study, we found that PDX treatment suppressed adipogenesis and lipid accumulation during 3T3-L1 differentiation. Treatment of differentiated 3T3-L1 cells with PDX stimulated AMP-activated protein kinase (AMPK) phosphorylation in a dose-dependent manner. PDX-induced AMPK phosphorylation blocked lipopolysaccharide (LPS)-induced secretion of proinflammatory cytokines, such as tumor necrosis factor-α and monocyte chemoattractant protein-1. Treatment of 3T3-L1 cells with PDX alleviated LPS-induced NF-κB and inhibitory factor κB phosphorylation. Furthermore, PDX treatment diminished LPS-induced impairment of insulin signaling and insulin-stimulated glucose uptake, as well as fatty acid oxidation. These effects were decreased by silencing AMPK expression with small-interfering RNA. In conclusion, the current findings suggest that PDX attenuates inflammation and insulin resistance in adipocytes via an AMPK-dependent pathway, which in turn provides evidence that PDX has anti-inflammatory and antidiabetic effects in adipocytes. SN - 1522-1555 UR - https://www.unboundmedicine.com/medline/citation/29584445/Protectin_DX_attenuates_LPS_induced_inflammation_and_insulin_resistance_in_adipocytes_via_AMPK_mediated_suppression_of_the_NF_κB_pathway_ L2 - https://journals.physiology.org/doi/10.1152/ajpendo.00408.2017?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -