Education, Science, Technology, Innovation and Life
Open Access
Sign In
  1. Home
  2. Journals
  3. MEDS Clinical Medicine
  4. Vol 5, Issue 2, 2024

Study on the Effect of Follicle Simulating Hormone on Lipid Metabolism in Postmenopausal T2DM and Potential Mechanisms

Download as PDF

DOI: 10.23977/medsc.2024.050203 | Downloads: 17 | Views: 108

Author(s)

Yining Gong 1, Qian Wang 1, Shulong Shi 2, Yongping Wang 1, Jian Li 3, Dandan Yin 1, Dehuan Kong 4, Yaping Liu 2

Affiliation(s)

1 Jining Medical University, Jining, 272000, China
2 Department of Endocrinology, Jining No. 1 People's Hospital, Jining, Shandong, 272000, China
3 Department of Osteoarticular Surgery, Jining No. 1 People's Hospital, Jining, Shandong, 272000, China
4 Department of Diabetes and Metabolic Diseases, The Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, 271000, China

Corresponding Author

Dehuan Kong

ABSTRACT

The purpose of our study was to analyze the relationship between serum FSH levels and TC, TG, LDL-C, HDL-C in postmenopausal T2DM patients and further explore the potential molecular mechanisms of FSH affecting lipid metabolism in postmenopausal T2DM via data mining online databases for associations between FSH and Dyslipidemia. Methods used in this paper. The first was a retrospective study of 279 postmenopausal patients with natural gestational type 2 diabetes mellitus (T2DM) admitted to the Department of Endocrinology of the First People's Hospital of Jining City from October 2020 to October 2022. Secondly, target genes for postmenopausal T2DM and lipid metabolism complications were retrieved from GeneCard, OMIM and GEO databases. Compound-target, protein-protein interaction (PPI) and compound-target-pathway networks were created using Cytoscape software. GO and KEGG pathway analyses were also performed to identify possible enrichment of genes with specific biological themes. The results obtained in this study are the age group of 50 to 60 years was demonstrated to have the most significant FSH levels in postmenopausal T2DM patients. Compared with the low FSH group, the TG level in the high FSH group significantly increased (P<0.05). The GeneCards database selected 2,113 pathogenic targets for T2DM, 878 targets for the postmenopausal period, and 335 pathogenic targets for dyslipidemia. Among them, INS, ALB, IL-6, TNF, PPARG, LEP, ADIPOQ, APOE, CRP, and APOB ranked in the top 10 nodes in terms of degree value and the AGE-RAGE signaling pathway dominated the KEGG signaling pathway. Further investigation in postmenopausal T2DM patients aged 50 to 60 years demonstrated a favorable connection between serum TG, FSH, IL-6.We conclude that, first, The FSH level reaches its peak secretion period in postmenopausal T2DM patients aged 50-60 years. Second, Serum TG levels in postmenopausal T2DM patients aged 50-60 are positively correlated with FSH. Third, FSH may exacerbate lipid metabolism disorders in postmenopausal T2DM patients aged 50-60 by activating the inflammatory cytokine IL-6.Fourth, AGE-RAGE, AMPK, and TNF signaling pathways may lead to abnormal blood lipids in postmenopausal T2DM.

KEYWORDS

Follicle-Stimulating Hormone, Dyslipidemia, T2DM (Diabetes Mellitus Type 2), Bioinformatics Analysis, Molecular Mechanism

CITE THIS PAPER

Yining Gong, Qian Wang, Shulong Shi, Yongping Wang, Jian Li, Dandan Yin, Dehuan Kong, Yaping Liu, Study on the Effect of Follicle Simulating Hormone on Lipid Metabolism in Postmenopausal T2DM and Potential Mechanisms. MEDS Clinical Medicine (2024) Vol. 5: 16-29. DOI: http://dx.doi.org/10.23977/medsc.2024.050203.

REFERENCES

[1] Magliano DJ, Boyko EJ; IDF Diabetes Atlas 10th edition scientific committee . IDF DIABETES ATLAS. 10th ed. Brussels: International Diabetes Federation; 2021.
[2] Zheng, Y., S.H. Ley, and F.B. Hu, Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nat Rev Endocrinol, 2018. 14(2): p. 88-98.
[3] Wang, H.Q., et al., Advances in the Regulation of Mammalian Follicle-Stimulating Hormone Secretion. Animals (Basel), 2021. 11(4).
[4] Zhao Caixia, Liu Peng. New metabolic regulatory functions of follicle-stimulating hormone and its effects on aging [J]. Journal of Physiology,2021,73(05):755-760.
[5] Sun, L., et al., FSH directly regulates bone mass. Cell, 2006. 125(2): p. 247-260.
[6] Wang, N., et al., Follicle-Stimulating Hormone, Its Association with Cardiometabolic Risk Factors, and 10-Year Risk of Cardiovascular Disease in Postmenopausal Women. J Am Heart Assoc, 2017. 6(9).
[7] Serviente, C., et al., Follicle-stimulating hormone is associated with lipids in postmenopausal women. Menopause, 2019. 26(5): p. 540-545.
[8] Guo Y, Zhao M, Bo T, et al. Blocking FSH inhibits hepatic cholesterol biosynthesis and reduces serum cholesterol. Cell Res. 2019,29(2):151-166.
[9] Bhartiya D, Patel H. An overview of FSH-FSHR biology and explaining the existing conundrums. J Ovarian Res. 2021,14(1):144.
[10] Cui, H., et al., FSH stimulates lipid biosynthesis in chicken adipose tissue by upregulating the expression of its receptor FSHR. J Lipid Res, 2012. 53(5): p. 909-917.
[11] Liu, X. M., et al., FSH regulates fat accumulation and redistribution in aging through the Gαi/Ca2+/CREB pathway. Aging Cell, 2015. 14(3): p. 409-420.
[12] Liu Y, Zhang M, Kong D, et al. High follicle-stimulating hormone levels accelerate cartilage damage of knee osteoarthritis in postmenopausal women through the PI3K/AKT/NF-κB pathway. FEBS Open Bio. 2020,10(10):2235-2245.
[13] Jung, E.S., et al., Serum Follicle-Stimulating Hormone Levels Are Associated with Cardiometabolic Risk Factors in Post-Menopausal Korean Women. J Clin Med, 2020. 9(4).
[14] Song, Y., et al., Follicle-Stimulating Hormone Induces Postmenopausal Dyslipidemia Through Inhibiting Hepatic Cholesterol Metabolism. J Clin Endocrinol Metab, 2016. 101(1): p. 254-263.
[15] Wu M, Cao A, Dong B, et al. Reduction of serum free fatty acids and triglycerides by liver-targeted expression of long chain acyl-CoA synthetase 3. Int J Mol Med. 2011,27(5):655-662.
[16] Rohm TV, Meier DT, Olefsky JM, Donath MY. Inflammation in obesity, diabetes, and related disorders. Immunity. 2022; 55(1):31-55.
[17] Sharif, S., et al., Low-grade inflammation as a risk factor for cardiovascular events and all-cause mortality in patients with type 2 diabetes. Cardiovasc Diabetol, 2021. 20(1): p. 220.
[18] Chen Lingxia, Miao Yide. Study on the correlation of C-reactive protein, interleukin-6 and tumor necrosis factor α with abnormal blood lipids in type 2 glycosuria disease [J]. Chinese Journal of General Medicine,2004, (13):956-957.
[19] Akash, M.S.H., et al., Biochemical investigation of gender-specific association between insulin resistance and inflammatory biomarkers in types 2 diabetic patients. Biomed Pharmacother, 2018. 106: p. 285-291.
[20] Pouresmaeil, V., S. Mashayekhi, and M. Sarafraz Yazdi, Investigation of serum level relationship anti-glutamic acid decarboxylase antibody and inflammatory cytokines (IL1-beta, IL-6) with vitamins D in type 2 diabetes. J Diabetes Metab Disord, 2022. 21(1): p. 181-187.
[21] Hassan, W., et al., Interleukin-6 signal transduction and its role in hepatic lipid metabolic disorders. Cytokine, 2014. 66(2): p. 133-142.
[22] Uciechowski, P. and W.C.M. Dempke, Interleukin-6: A Masterplayer in the Cytokine Network. Oncology, 2020. 98(3): p. 131-137.
[23] Kraakman MJ, Allen TL, Whitham M, et al. Targeting gp130 to prevent inflammation and promote insulin action. Diabetes Obes Metab. 2013,15 Suppl 3:170-175.
[24] Hyo-Jeong Kim, Takamasa Higashimori, So-Young Park, et al. Differential Effects of Interleukin-6 and -10 on Skeletal Muscle and Liver Insulin Action In Vivo. Diabetes 1 April 2004, 53 (4):1060–1067
[25] McNeilly, A.D., et al., Central deficiency of IL-6Ra in mice impairs glucose-stimulated insulin secretion. Mol Metab, 2022. 61: p. 101488.
[26] Yamaguchi, K., et al., Blockade of interleukin 6 signalling ameliorates systemic insulin resistance through upregulation of glucose uptake in skeletal muscle and improves hepatic steatosis in high-fat diet fed mice. Liver Int, 2015. 35(2): p. 550-561.

Subscription
E-Mail Alert
Most popular papers
Call for Special Issue
Publication Ethics & OA Statement
Plagiarism Policy
Contact Us
Downloads: 4556
Visits: 197252

Sponsors, Associates, and Links

All published work is licensed under a Creative Commons Attribution 4.0 International License.

Copyright © 2016 - 2031 Clausius Scientific Press Inc. All Rights Reserved.