Menopause, Sindroma Metabolik dan Terapi Hormon
Menopause, Metabolic Syndrome and Hormone Therapy
DOI:
https://doi.org/10.35473/ijm.v8i1.3778Keywords:
Estrogen, Resistensi Insulin, Sindroma Metabolik, Terapi HormonAbstract
Estrogens play a crucial role in protecting against insulin resistance (IR) by regulating metabolic processes that govern energy balance and mitigating inflammation. In postmenopausal women, the decline in estrogen levels significantly increases the risk of developing insulin resistance. This decline leads to impaired insulin action and secretion, paving the way for persistent hyperglycemia, hyperlipidemia, hypertension, and obesity—key components of metabolic syndrome (MetS). These factors not only elevate the risk of cardiometabolic disorders but also substantially increase the likelihood of developing Type 2 Diabetes Mellitus (T2DM) and cardiovascular disease (CVD). The protective benefits of estrogen against insulin resistance are critical, especially as these benefits diminish with menopause. However, they can be restored through hormone replacement therapy, presenting an effective strategy for mitigating these health risks. This review underscores the vital protective role of estrogen regarding insulin resistance as part of metabolic syndrome and emphasizes the importance of hormone therapy in developing proactive preventive strategies. To build on this understanding, a comprehensive search was conducted across PubMed, using MeSH terms like “Metabolic Syndrome,” “Estrogen,” “Menopause,” “Insulin Resistance,” “Type 2 Diabetes Mellitus,” “Cardiovascular,” “Dyslipidemia,” and “Hormone Therapy.” Out of 200 articles, 168 were identified as relevant to the topic, focusing on studies published between 2015 and 2025, ultimately narrowing down to 102 significant articles. This extensive research lays the groundwork for enhancing preventive measures in women’s health.
Abstrak
Estrogen dapat melindungi dari perkembangan resistensi insulin (IR) dengan memodulasi proses metabolisme yang terlibat dalam keseimbangan energi dan menurunkan regulasi dan/atau menekan peradangan. Kadar estrogen yang berkurang pada wanita pascamenopause meningkatkan resiko IR. Gangguan kerja insulin dan/atau sekresi insulin berkontribusi terhadap perkembangan dan keberlanjutan hiperglikemia, hiperlipidemia, hipertensi, dan obesitas, yang merupakan ciri khas sindroma metabolik (MetS), dengan konsekuensi utama berkembangnya gangguan kardiometabolik, berupa peningkatan resiko yang signifikan terhadap perkembangan diabetes mellitus tipe 2 (DMT2) dan/atau penyakit kardiovaskuler (PKV). Perlindungan terhadap IR ini didorong oleh hormon estrogen, yang cenderung menghilang dengan timbulnya menopause tetapi dapat dibangun kembali dengan terapi penggantian hormon. Tinjauan ini mengevaluasi pengetahuan terkini tentang peran protektif estrogen terkait dengan IR yang merupakan komponen dari suatu kondisi yang dikenal sebagai MetS dan kaitannya dengan terapi hormon untuk mendorong pengembangan strategi pencegahan yang lebih efektif. Sebanyak 200 artikel PubMed dipilih menggunakan istilah MeSH seperti: “Sindrom Metabolik”, “Estrogen”, “Menopause”, “Resistensi Insulin”, “Diabetes Melitus tipe 2”, “Kardiovaskuler”. “Dislipidemia” dan “Terapi Hormon”. Seleksi relevansi dengan topik 168 artikel, seleksi tahun terbit (2015 – 2025) terpilih 102 artikel
Downloads
References
Abbasian M, Ebrahimi H, Delvarianzadeh M, Norouzi P, & Fazli M. 2016. Association between serum uric acid (SUA) levels and metabolic syndrome (MetS) components in personnel of Shahroud University of Medical Sciences. Diabetes Metab Syndr, 10(3), 132–136.
Ali Hamza, M., Abdulhameed, A., & Ali Mansour, A. 2022. Total Testosterone to Estradiol Ratio as a Predictor Marker of Metabolic Syndrome in Males. Arch Razi Inst, 77(1), 351–357.
Ambikairajah A., Walsh E, & Cherbuin N. 2019. Lipid Profile Differences during Menopause: a Review with Meta-Analysis. Menopause 26 (11), 1327–1333.
Amitay, E. L., Niedermaier, T., Alwers, E., Chang-Claude, J., Hoffmeister, M., & Brenner, H. 2022. Reproductive Factors and Colorectal Cancer Risk: A Population-Based Case-Control Study. JNCI Cancer Spectrum, 6(4), Pkac042.
Anagnostis, P., & Goulis, D. G. 2019. Menopause and its Cardiometabolic Consequences: Current Perspectives. Curr Vasc Pharmacol, 17(6), 543–545.
Anagnostis, P., Paschou, S. A., Katsiki, N., Krikidis, D., Lambrinoudaki, I., & Goulis, D. G. 2019. Menopausal Hormone Therapy and Cardiovascular Risk: Where are we Now?. Curr Vasc Pharmacol, 17(6), 564–572.
Anagnostis, P., Stevenson, J. C., Crook, D., Johnston, D. G., & Godsland, I. F. 2016. Effects of gender, age and menopausal status on serum apolipoprotein concentrations. Clin Endocrinol, 85(5), 733–740.
Anagnostis P, Bitzer J, Cano A, Ceausu I, Chedraui P, Durmusoglu F, et al. 2020. Menopause symptom management in women with dyslipidemias: An EMAS clinical guide,. Maturitas, 135, 82-88.
Barton M. 2013. Cholesterol and atherosclerosis: modulation by oestrogen. Curr Opin Lipidol, 24(3), 214–220.
Berezin AE, Berezin AA, & Lichtenauer, M. 2020. Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus. Front Cardiovasc Med, 7, 583175.
Bhardwaj, P., Au, C. C., Benito-Martin, A., Ladumor, H., Oshchepkova, S., Moges, R., et al 2019. Estrogens and breast cancer: Mechanisms involved in obesity-related development, growth and progression. J Steroid Biochem Mol Biol, 189, 161–170.
Bielecka-Dabrowa, A., Bartlomiejczyk, M. A., Sakowicz, A., Maciejewski, M., & Banach, M. 2020. The Role of Adipokines in the Development of Arterial Stiffness and Hypertension. Angiology, 71(8), 754–761.
Downloads
Published
How to Cite
Issue
Section
License
Copyright notice:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- 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.
