Leptin Activates NLRP3 Inflammasome-Associated with Type II Diabetes and Obesity
DOI:
https://doi.org/10.17140/aftnsoj-4-e016Abstract
Obesity is a major health problem worldwide and is often associated with leptin resistance and inflammation.1 In this editorial, we will briefly describe the leptin system and the (NOD)-like receptor protein 3 (NLRP3) inflammasome and dis-cuss recent discoveries related to their interaction and role in the development of metabolic disease mainly obesity and Time-divi-sion multiplexing (TDM).
References
Pan H, Guo J, Su Z. Advances in understanding the interrelations between leptin resistance and obesity. Pysiol Behav. 2014; 130: 157-169. doi: 10.1016/j.physbeh.2014.04.003
Allison MB, Myers MG. 20 Years or leptin: Connecting leptin signaling to biological function. J. Endrocrinol. 2014; 223(1): T25-T35. doi: 10.1530/JOE-14-0404
Drent ML, Klok MD, Jakobsdottir S. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: A review. Obes Rev. 2007; 8(1): 21-34. doi: 10.1111/j.1467- 789X.2006.00270.x
Iikuni N, Lam QLK, Lu L, et al. Leptin and Inflammation. Curr Immunol Rev. 2008; 4(2): 70-79. doi: 10.2174/157339508784325046
Groß CJ, Mishra R, Schneider KS, et al. K+ Efflux-Independent NLRP3 Inflammasome activation by small molecules targeting mitochondria. Immunity. 2016; 45: 761-773. doi: 10.1016/j.immuni.2016.08.010
Mortimer L,Moreau F, MacDonald JA, Chadee K. NLRP3 inflammasome inhibition is disrupted in a group of auto-inflammatory disease CAPS mutations. Nat Immunol. 2016; 17(10): 1176- 1186. doi: 10.1038/ni.3538
Shuttleworth S, Townsend P, Silva F, et al. Progress in the development of small molecule therapeutics targeting Th17 cell function for the treatment of immune-inflammatory diseases. Prog Med Chem. 2011; 50: 109-133. doi: 10.1016/B978-0-12-381290- 2.00003-3
Fu S, Xu L, Li S, et al. Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection. Vet Res. 2016; 47(1): 80. doi: 10.1186/s13567- 016-0359-4
De Rosa V, Procaccini VC, Cali G, et al. A key role of leptin in the control of regulatory T cell proliferation. Immunity. 2007; 26(2): 241-255. doi: 10.1016/j.immuni.2007.01.011
Reed JC, Doctor K, Rojas A, et al. Comparative analysis of apoptosis and inflammation genes of mice and humans. Genome Res. 2003; 13(6B): 1376-1388. doi: 10.1101/gr.1053803
Ting JP, Lovering RC, Alnemri ES, et al. The NLR gene family: A standard nomenclature. Immunity. 2008; 28(3): 285-287. doi: 10.1016/j.immuni.2008.02.005
Fu S, Lei L, Lei H, Yiyun Y. Leptin promotes IL-18 secretion by activating the NLRP3 inlammasome in RAW 264.7 cells. Mol Med Rep. 2017; 16(6): 9770-9776. doi: 10.3892/mmr.2017.7797
Zhong, Yifei, Anna Kinio, and Maya Saleh. Functions of NOD-like receptors in human disease. Front Immunol. 2013; 4: 333. doi: 10.3389/fimmu.2013.00333
Bo-Zong S, Zhe-Qi X, Bin-Ze H, et al. NLRP3 inflammasome and its inhibitors: A review. Front Pharmacol. 2015; 6: 262. doi: 10.3389/fphar.2015.00262
Franchi L, Eigenbrod T, Munoz-Panillo R, et al. Cytosolic double-stranded RNA activates the NLRP3 inflammasome via MAVSinduced membrane permeabilization and K+ efflux. J Immunol. 2014; 193(8): 4214-4222. doi: 10.4049/jimmunol.1400582
Ozaki E, Campbell M, Doyle SL. Targeting the NLRP3 inflammasome in chronic inflammatory diseases: Current perspectives. J Inflamm Res. 2015; 8: 15-27. doi: 10.2147/JIR.S51250
Schroder K. Tschopp J. The inflammasomes. Cell. 2010; 140(6): 821-832. doi: 10.1016/j.cell.2010.01.040
Gross O, Thomas CJ, Guarda G, Tschopp J. The inflammasome: An integrated view. Immunol Rev. 2011; 243(1): 136-151. doi: 10.1111/j.1600-065X.2011.01046.x Editorial | Volume 4 | Number 2| e15 Adv Food Technol Nutr Sci Open J. 2018; 4(2): e13-e16. doi: 10.17140/AFTNSOJ-4-e016 Dridi S, et al
De Zoete MR, Palm NW, Zhu S, Flavell RA. Inflammasomes. Cold Spring Harb Perspect Biol. 2014; 6(12): 1-22. doi: 10.1101/cshperspect.a016287
Masters SL, Dunne A, Subramanian SL, et al. Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes. Nat Immunol. 2010; 11(10): 897-904. doi: 10.1038/ni.1935
Stienstra R, Tack CJ, Kanneganti TD, et al. The Inflammasome Puts Obesity in the Danger Zone. Cell Metab. 2012; 15:10-18. doi: 10.1016/j.cmet.2011.10.011
Olefsky JM, Glass CK. Macrophages, inflammation, and insulin resistance. Annu Rev Physiol. 2010; 72: 219-246. doi: 10.1146/ annurev-physiol-021909-135846
Shoelson SE, L. Herrero, and A. Naaz. Obesity, inflammation, and insulin resistance. Gastroenterology. 2007; 132(6): 2169-2180. doi: 10.1053/j.gastro.2007.03.059
Jager, J, Gremeaux T, Cormont M, et al. Interleukin-1 betainduced insulin resistance in adipocytes through down-regulation of insulin receptor substrate-1 expression. Endocrinology. 2007; 148: 241-251 doi: 10.1210/en.2006-0692
Netea MG, Joosten LA, Lewis E, et al. Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance. Nat Med. 2006; 12(6): 650-656. doi: 10.1038/nm1415
Zorrilla EP, Sanchez-Alavez M, Sugama S, et al. Interleukin-18 controls energy homeostasis by suppressing appetite and feed ef ficiency. Proc Natl Acad Sci USA. 2007; 104(26): 11097-11102. doi: 10.1073/pnas.0611523104
Vandanmagsar B, Youm YH, Ravussin A, et al. The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance. Nat Med. 2011; 17(2): 179-188. doi: 10.1038/nm.2279
Rheinheimer J, De Souza BM, Cardoso NS, et al. Current role of the NLRP3 inflammasome on obesity and insulin resistance: A systemic review. Metabolism. 2017; 74: 1-9. doi: 10.1016/j.metabol.2017.06.002 Editorial | Volume 4 | Number 2|e16 Submit your article to this journal | https://openventio.org/submit-manuscript/
Published
How to Cite
Issue
Section
License

This work is licensed under a Creative Commons Attribution 4.0 International License.
All content published in Advances in Food Technology and Nutrition Sciences (AFTNS) is licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0). This license allows anyone to copy, distribute, transmit, and adapt the work — including for commercial purposes — provided appropriate credit is given to the original author(s) and source.