Korelacija GLUT4, LEPR i TNF-α sa endometrijskom recepcijom u ženama s policističnim jajničkim sindromom indukovanom nepristojenošću
Sažetak
Cilj: Analizirati korelaciju glukoznog transportera 4 (GLUT4), receptora leptina (LEPR) i faktora tumora nekroze-α (TNF-α) sa endometrijskim receptivom u pacijenata s policističnim jajničkim sindromom (PCOS)-indukovanom nepristojnošću, kako bi pružili klinički dokaz za buduću dijagnozu i liječenje nepristojnosti indukovane na PCOS-u.
Metode: 46 pacijenata s nepristojnošću indukovanih PCOS-a priznanih u našu bolnicu od juna 2020. do avgusta 2023 (istraživačka grupa), kao i 35 istovremenih slučajeva jednostavnih PCOS-a (kontrolne grupe) i 32 zdravih žena (normalne grupe) izabrani su kao učesnici istraživanja. U svim sudionicima je otkrivena periferalna krvna nivoa GLUT4, LEPR i TNF-α, a analizirana je dijagnostična vrijednost troje za PCOS u zdravim ženama i za nepristojnost indukovane na PCOS-u bolesnika PCOS-a. Osim toga, izmjerili su endometrijsku debljinu i indeks pulsiranja endometrijskog toka krvi (PI) i indeks otpora (RI) pacijenata u istraživačkoj grupi, a razgovarali su o korelaciji GLUT4, LEPR i TNF-α sa endometrijskom recepcijom. Rezultati: GLUT4 je bio niži u istraživačkoj skupini u usporedbi s kontrolom i normalnim grupama, dok su LEPR i TNF-α bili veći (P<0,05); the control group showed lower GLUT4 and higher LEPR and TNF-α levels than the normal group (P<0.05). Dijagnozna osjetljivost i specifičnost kombinovanog ispitivanja GLUT4, LEPR i TNF-α u ženama PCOS-indukovanoj nespoložnosti bila su 88,57% i 75,00%, a one za PCOS-e u zdravim ženama bile su 78,57% i 60,00%, odnosno (P<0,05). U istraživačkoj grupi, GLUT4 je pozitivno povezan sa endometrijskom debelom i negativno povezanom sa RI i PI-om; dok su LEPR i TNF-α negativno povezani sa endometrijskom debelom i pozitivno povezanim sa RI i PI (P<0,05). Zaključaci: GLUT4, LEPR i TNF-α su bliski povezani sa endometrijskom recepcijom u pacijenata s nepristojnošću indukovanih na PCOS-u, a njihovo kombinirano detektivo može efektivno proceniti pojavljivanje PCOS-a i nepristojnosti indukovanih na PCOS-u.
Reference
2. Siddiqui S, Mateen S, Ahmad R, Moin S. A brief insight into the etiology, genetics, and immunology of polycystic ovarian syndrome (PCOS). J Assist Reprod Genet. 2022;39(11):2439-73.
3. Garcia-Saenz MR, Ferreira-Hermosillo A, Lobaton-Ginsberg M. [Proinflammatory cytokines in polycystic ovarian syndrome]. Rev Med Inst Mex Seguro Soc. 2022;60(5):569-76. Citocinas proinflamatorias en el sindrome de ovario poliquistico.
4. Zhong P, Guan B, Lin Y, Zhang S. Changes in inflammatory factors, oxidative stress, glucose and lipid metabolism, and insulin resistance in patients with polycystic ovary syndrome. Cell Mol Biol (Noisy-le-grand). 2022;67(5):45-50.
5. Celik O, Aydin S, Celik N, Ugur K, Yavuzkir S, Hatirnaz S, et al. Molecular role of peptides/proteins in subfertility of polycystic ovarian syndrome. Cell Mol Biol (Noisy-le-grand). 2019;65(3):32-40.
6. Reynolds LJ, Pollack RI, Charnigo RJ, Rashid CS, Stromberg AJ, Shen S, et al. Increased birth weight is associated with altered gene expression in neonatal foreskin. J Dev Orig Health Dis. 2017;8(5):575-83.
7. Richter EA, Hargreaves M. Exercise, GLUT4, and skeletal muscle glucose uptake. Physiol Rev. 2013;93(3):993-1017.
8. Deng M, Guerrero-Juarez CF, Sheng X, Xu J, Wu X, Yao K, et al. Lepr(+) mesenchymal cells sense diet to modulate intestinal stem/progenitor cells via Leptin-Igf1 axis. Cell Res. 2022;32(7):670-86.
9. Zhang D, Lin W, Jiang S, Deng P, Liu L, Wang Q, et al. Lepr-Expressing PDLSCs Contribute to Periodontal Homeostasis and Respond to Mechanical Force by Piezo1. Adv Sci (Weinh). 2023;10(29):e2303291.
10. Horiuchi T, Mitoma H, Harashima S, Tsukamoto H, Shimoda T. Transmembrane TNF-alpha: structure, function and interaction with anti-TNF agents. Rheumatology (Oxford). 2010;49(7):1215-28.
11. Xiang S, Xia MF, Song JY, Liu DQ, Lian F. Effect of Electro-acupuncture on Expression of IRS-1/PI3K/GLUT4 Pathway in Ovarian Granulosa Cells of Infertile Patients with Polycystic Ovary Syndrome-Insulin Resistance of Phlegm-Dampness Syndrome. Chin J Integr Med. 2021;27(5):330-5.
12. Tu X, Yu C, Gao M, Zhang Y, Zhang Z, He Y, et al. LEPR gene polymorphism and plasma soluble leptin receptor levels are associated with polycystic ovary syndrome in Han Chinese women. Per Med. 2017;14(4):299-307.
13. Dabravolski SA, Nikiforov NG, Eid AH, Nedosugova LV, Starodubova AV, Popkova TV, et al. Mitochondrial Dysfunction and Chronic Inflammation in Polycystic Ovary Syndrome. Int J Mol Sci. 2021;22(8).
14. Mirza FG, Tahlak MA, Rjeili RB, Hazari K, Ennab F, Hodgman C, et al. Polycystic Ovarian Syndrome (PCOS): Does the Challenge End at Conception? Int J Environ Res Public Health. 2022;19(22).
15. Shahid R, Iahtisham Ul H, Mahnoor, Awan KA, Iqbal MJ, Munir H, et al. Diet and lifestyle modifications for effective management of polycystic ovarian syndrome (PCOS). J Food Biochem. 2022;46(7):e14117.
16. Liu S, Zhang Y, Yang F, Gu J, Zhang R, Kuang Y, et al. Modified Cangfu Daotan decoction ameliorates polycystic ovary syndrome with insulin resistance via NF-kappaB/LCN-2 signaling pathway in inflammatory microenvironment. Front Endocrinol (Lausanne). 2022;13:975724.
17. Li L, Lee KJ, Choi BC, Baek KH. Relationship between leptin receptor and polycystic ovary syndrome. Gene. 2013;527(1):71-4.
18. Zhai Y, Pang Y. Systemic and ovarian inflammation in women with polycystic ovary syndrome. J Reprod Immunol. 2022;151:103628.
19. Cui P, Li X, Wang X, Feng Y, Lin JF, Billig H, et al. Lack of cyclical fluctuations of endometrial GLUT4 expression in women with polycystic ovary syndrome: Evidence for direct regulation of GLUT4 by steroid hormones. BBA Clin. 2015;4:85-91.
20. Zheng L, Chen PF, Dai WC, Zheng ZQ, Wang HL. Curcumin Alleviates Hyperandrogenism and Promotes Follicular Proliferation in Polycystic Ovary Syndrome Rats: Insights on IRS1/PI3K/GLUT4 and PTEN Modulations. Chin J Integr Med. 2022;28(12):1088-95.
21. Samad MB, Mohsin M, Razu BA, Hossain MT, Mahzabeen S, Unnoor N, et al. [6]-Gingerol, from Zingiber officinale, potentiates GLP-1 mediated glucose-stimulated insulin secretion pathway in pancreatic beta-cells and increases RAB8/RAB10-regulated membrane presentation of GLUT4 transporters in skeletal muscle to improve hyperglycemia in Lepr(db/db) type 2 diabetic mice. BMC Complement Altern Med. 2017;17(1):395.
22. Siemian JN, Arenivar MA, Sarsfield S, Borja CB, Russell CN, Aponte Y. Lateral hypothalamic LEPR neurons drive appetitive but not consummatory behaviors. Cell Rep. 2021;36(8):109615.
23. Liu Y, Chen SQ, Jing ZH, Hou X, Chen Y, Song XJ, et al. Association of LEPR Gln223Arg polymorphism with T2DM: A meta-analysis. Diabetes Res Clin Pract. 2015;109(3):e21-6.
24. Daghestani MH, Daghestani MH, Daghistani MH, Bjorklund G, Chirumbolo S, Warsy A. The influence of the rs1137101 genotypes of leptin receptor gene on the demographic and metabolic profile of normal Saudi females and those suffering from polycystic ovarian syndrome. BMC Womens Health. 2019;19(1):10.
25. Trapali M, Houhoula D, Batrinou A, Kanellou A, Strati IF, Siatelis A, et al. Association of TNF-alpha 308G/A and LEPR Gln223Arg Polymorphisms with the Risk of Type 2 Diabetes Mellitus. Genes (Basel). 2021;13(1).
26. Xie Q, Hong W, Li Y, Ling S, Zhou Z, Dai Y, et al. Chitosan oligosaccharide improves ovarian granulosa cells inflammation and oxidative stress in patients with polycystic ovary syndrome. Front Immunol. 2023;14:1086232.
27. Orostica L, Astorga I, Plaza-Parrochia F, Vera C, Garcia V, Carvajal R, et al. Proinflammatory environment and role of TNF-alpha in endometrial function of obese women having polycystic ovarian syndrome. Int J Obes (Lond). 2016;40(11):1715-22.
Sva prava zadržana (c) 2024 Yan Dong, Wei Kong, Yifei Li, Yan Liu, Lin Li, Yan Li
Ovaj rad je pod Creative Commons Autorstvo 4.0 međunarodnom licencom.
The published articles will be distributed under the Creative Commons Attribution 4.0 International License (CC BY). It is allowed to copy and redistribute the material in any medium or format, and remix, transform, and build upon it for any purpose, even commercially, as long as appropriate credit is given to the original author(s), a link to the license is provided and it is indicated if changes were made. Users are required to provide full bibliographic description of the original publication (authors, article title, journal title, volume, issue, pages), as well as its DOI code. In electronic publishing, users are also required to link the content with both the original article published in Journal of Medical Biochemistry and the licence used.
Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.