The research team, led by W. Aidan Martel, S. Bradley King, and senior author Rebecca V. Mountain, set out to answer two questions that previous work had left open. First, do the sex differences seen in isolation-induced bone loss simply reflect different timelines, with females eventually succumbing to the same damage if given enough time? Second, what role do the sex steroid hormones estrogen and testosterone play in mediating the skeletal response? To address these questions, the investigators housed 16-week-old C57BL/6J mice either in groups of four per cage or alone, one mouse per cage, for periods of 2, 4, or 8 weeks, and then subjected their bones to detailed structural, biomechanical, and molecular analysis.

The results were unambiguous for the males. Single housing significantly reduced bone parameters across every treatment length tested. On average, isolated male mice showed a 20 percent reduction in trabecular bone volume fraction, a key measure of the spongy, metabolically active bone found inside the ends of long bones and vertebrae. Cortical thickness, the measure of the dense outer shell of bone that provides most of a skeleton’s resistance to bending and fracture, fell by an average of 8 percent. Critically, these changes appeared remarkably fast: trabecular bone was measurably affected after as little as two weeks of isolation, suggesting that the male skeleton responds to the loss of social contact with surprising speed.

Structure alone does not determine whether a bone will break, so the team also tested mechanical performance. Bones are not simply mineral scaffolds; their ability to absorb energy and resist fracture depends on the interplay of material quality and architecture. When the researchers subjected the femurs to biomechanical testing, they found that isolation degraded the mechanical properties of the bone in male mice but not in females. In practical terms, the isolated males were left with femurs that were thinner, less dense, and weaker, a combination that in a living animal would translate into a substantially elevated fracture risk.

The females told a very different story. Across all three treatment durations, the overall bone phenotype of isolated female mice was essentially unaffected. Trabecular and cortical parameters held steady, and biomechanical performance remained comparable to that of group-housed controls, even after eight weeks of single housing. This finding rules out the simplest explanation for the sexual dimorphism, namely that females merely respond more slowly. Whatever protects the female skeleton from the consequences of social isolation, it is not a matter of delayed onset but of a fundamentally different biological response.

Yet the female skeleton was not entirely silent. When the researchers measured bone turnover markers, the biochemical signals of bone formation and bone resorption that circulate in the blood, they found that isolated females showed an increase after just two weeks of isolation. Bone remodeling is a continuous process in which osteoclasts break down old bone and osteoblasts lay down new bone, and shifts in turnover markers indicate that the cellular machinery had been perturbed even though the net structure remained intact. The authors interpret this as evidence that isolated females experienced changes in bone remodeling dynamics that somehow resolved without producing measurable bone loss, a decoupling that may itself hold clues to the protective mechanism.

The search for a hormonal explanation produced one of the study’s most intriguing results. In male mice isolated for four or eight weeks, the researchers observed alterations in the expression of estrogen-related genes, even though circulating estrogen levels themselves were unchanged. This dissociation between gene expression and circulating hormone concentration suggests that the skeletal response to isolation may be mediated locally, at the level of the bone tissue itself, rather than through systemic changes in sex steroid availability. It also raises the possibility that estrogen signaling, traditionally studied in the context of female physiology, plays an underappreciated role in the male skeleton’s response to psychological stress.

The clinical resonance of these findings is considerable. Social isolation and loneliness affect a large and growing share of the human population, particularly older adults, and epidemiological studies have associated them with elevated risks of numerous chronic conditions. If a sexually dimorphic relationship between social contact and bone health exists in humans, as the murine data suggest it might, then men who are socially isolated could represent an unrecognized population at elevated risk of osteoporosis and fragility fracture. Osteoporosis is already underdiagnosed in men, in part because the disease is often perceived as a condition of postmenopausal women, and a psychosocial contribution to male bone loss could sharpen both screening and prevention strategies.

The study also sounds a cautionary note for the research community. Single housing is a routine practice in biomedical research, whether for experimental necessity, behavioral phenotyping, or animal management, and the new data show that this housing condition is not physiologically neutral, at least for male rodents. Any study using individually housed male mice as a baseline could be inadvertently measuring the skeletal consequences of isolation superimposed on the experimental variable of interest. The authors note that these findings have important implications for pre-clinical rodent models utilizing single housing, and the rapid two-week onset of bone changes suggests that even short housing periods may be sufficient to confound skeletal endpoints.

Many questions remain. The precise mechanism linking social isolation to osteoclast and osteoblast activity is still unknown, as is the identity of the factor that shields female bone. The role of testosterone, which the study set out to examine, and the functional significance of the altered estrogen-related gene expression in males, will require further investigation. What is already clear, however, is that the skeleton listens to the social environment, and that it does so differently in males and females. As loneliness becomes an increasingly prominent public health concern, this work suggests that its costs may be written not only in the brain and the heart, but in the very architecture of bone, and that sex must be part of any equation that seeks to predict who pays the price.

Subject of Research: Sex-dependent effects of social isolation on bone health in adult mice

Article Title: Short- and long-term effects of social isolation on adult murine bone are sex-dependent

Article References: Martel, W. A., King, S. B., Buchanan, E., Merrill, B. M., Stohn, J. P., Brooks, D. J., Barlow, D., Motyl, K. J., & Mountain, R. V. (2026). Short- and long-term effects of social isolation on adult murine bone are sex-dependent. Biology of Sex Differences. https://doi.org/10.1186/s13293-026-00995-6

Image Credits: AI Generated

DOI: 10.1186/s13293-026-00995-6

Keywords: social isolation, bone health, sexual dimorphism, osteoporosis, trabecular bone, cortical bone, bone turnover, estrogen, testosterone, murine model, loneliness, biomechanics

The researchers began from a metabolic observation that has been gaining traction across vascular biology. When blood vessels grow abnormally, the endothelial cells that line them shift their energy production toward glycolysis, the rapid, oxygen-independent breakdown of glucose. The enzyme PFKFB3, an allosteric activator of the glycolytic pathway, is central to this switch. Earlier studies showed that blocking PFKFB3 even partially reduces pathological vessel sprouting, and that endothelial cells lacking it cannot form vessels efficiently. What remained unclear was how PFKFB3 protein levels are controlled in the endothelial cells infiltrating endometriotic lesions.

To answer that question, the team examined vascular endothelial cells in ectopic endometrial tissue taken from both human patients and mouse models. In both species, they found that PFKFB3 was significantly upregulated, and that this elevation tracked closely with increased expression of YTHDF3, a member of the YTH domain family of proteins. These proteins are known as readers of N6-methyladenosine, or m6A, the most abundant internal chemical modification in eukaryotic messenger RNA. The m6A mark does not change the genetic code; instead, it influences the fate of each transcript, dictating whether it is translated into protein, degraded, or stored.

The causal importance of YTHDF3 became clear in genetic experiments. When the researchers specifically deleted the Ythdf3 gene in endothelial cells of mice, PFKFB3 protein levels dropped and angiogenesis within the ectopic endometrial lesions was suppressed. Notably, the manipulation targeted the translation step rather than the abundance of the mRNA itself. This distinction matters because it points to a regulatory layer that most existing therapies never touch: the efficiency with which a stable message is actually converted into functional protein.

Delving into the mechanism, the team focused on endometrial microvascular endothelial cells, where the PFKFB3 messenger RNA carried increased m6A modifications. The writer of those marks is METTL3, the catalytic core of the enzyme complex that installs m6A on transcripts. According to the study, METTL3 enhances m6A modification of the PFKFB3 mRNA, and YTHDF3 then recognizes these modified sites, promoting the translation of PFKFB3 and thereby raising glycolytic activity within the cells. The metabolic boost translates directly into cellular behavior: ovarian microvascular endothelial cells showed enhanced tube formation, migration and proliferation when the pathway was active.

The m6A system has been implicated in metabolism and angiogenesis before. Previous work showed that the modification regulates glycolysis in cancer cells through enzymes such as PDK4, and reviews have catalogued multiple RNA modifications shaping vessel growth. YTHDF3 itself has a colorful track record: it has been shown to promote the translation of m6A-enriched transcripts in breast cancer brain metastasis, to modulate antiviral interferon responses through FOXO3, and to assist translation by recruiting initiation factors. The new study extends this translation-enhancing role into a gynecological disease context, linking it to a hormone-driven pathology.

That hormonal link is perhaps the most clinically provocative element of the findings. Endometriosis is an estrogen-dependent disease, and the researchers found that estrogen upregulates both METTL3 and PFKFB3 through the estrogen receptor ERα. In other words, the very hormone that drives the growth of endometrial tissue also appears to arm the vessel-feeding machinery that sustains it, by amplifying the RNA-modification writer and the metabolic target it acts upon. This creates a coherent loop in which hormonal signaling, epitranscriptomic regulation and endothelial metabolism converge to support lesion establishment and expansion.

Angiogenesis has long been recognized as a requirement for endometriotic lesions to survive and grow after they are seeded within the pelvic cavity, and anti-angiogenic strategies have been proposed as adjunct therapies for years. The difficulty has been specificity: vessels in healing wounds and normal tissues also depend on glycolytic endothelial cells, so systemic blockade of PFKFB3 carries risks. The YTHDF3-m6A-PFKFB3 axis offers a more layered target. Interfering with the reader protein or with the estrogen-driven upregulation of METTL3 could, in principle, blunt pathological vessel growth in lesions while sparing some of the baseline vascular functions that depend on other regulators.

The study’s authors, led by Xiaosa Li, Jiale Wang and Liang Yuan as co-first authors under the direction of senior investigators including Xiaodong Fu, Huiping Lin and Junxiu Liu, argue that their findings establish the YTHDF3-m6A-PFKFB3 pathway as a critical driver of angiogenesis in endometriosis and suggest that targeting this pathway represents a promising therapeutic strategy. The work was supported by the National Natural Science Foundation of China and by a research fund from Guangzhou, and the authors declare no competing interests.

As with any mechanistic study, the road from molecular circuit to clinic is long. Animal models and cell culture systems capture only part of the human disease, and m6A readers act on many transcripts at once, so systemic interventions would need careful dosing and delivery strategies. Still, the study adds endometriosis to a growing list of conditions in which chemical tags on RNA, rather than changes in the genes themselves, determine whether disease-associated cells thrive. For millions of patients whose pain and fertility struggles have outpaced available treatments, the idea that a single reader protein controls the fuel supply of the vessels feeding their lesions is a compelling new lead, and one that researchers are likely to pursue with urgency.

Subject of Research: m6A reader YTHDF3 promotes angiogenesis in endometriosis by enhancing PFKFB3 translation

Article Title: YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3

Article References: Li, X., Wang, J., Yuan, L., Wang, Y., Wei, J., Li, P., Wang, R., Xu, X., Mai, Q., Liu, J., Lin, H., & Fu, X. (2026). YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3. Angiogenesis, 29(4), Article 70. https://doi.org/10.1007/s10456-026-10095-z

Image Credits: AI Generated

DOI: 10.1007/s10456-026-10095-z

Keywords: endometriosis, angiogenesis, YTHDF3, m6A, PFKFB3, METTL3, glycolysis, endothelial cells, estrogen, translation, PFKFB3 mRNA, vascular biology

The study, published as an open-access research article in BMC Endocrine Disorders, drew on the Korea National Health and Nutrition Examination Survey, known as KNHANES, specifically the fourth wave conducted between 2007 and 2009. The investigators, led by Ziran Qiu of the Department of Breast and Thyroid Surgery at Loudi Central Hospital in Hunan, China, together with colleagues including corresponding author Na Jin, focused on postmenopausal women, a group in which both menopausal hormone therapy and thyroid disease converge with unusual frequency. Thyroid disorders, which range from underactive and overactive gland function to nodules and autoimmune inflammation, are markedly more common in women than in men, and their prevalence rises with age, making the postmenopausal population a natural setting for asking whether exogenous hormones tip the balance.

The analytical sample comprised 3,974 postmenopausal women, of whom 582 reported a history of using female hormone medication. The exposure was deliberately simple: a questionnaire item recording whether the participant had ever taken female hormone drugs. Importantly, the survey did not capture whether use was current, which formulation was taken, at what dose, or for how long, a limitation that shapes how the results can be interpreted. The outcomes were equally grounded in self-report: thyroid disorders diagnosed by a doctor served as the primary endpoint, while current thyroid disorder, lifetime thyroid disorder, and currently treated thyroid disorder served as secondary endpoints. This reliance on questionnaire-defined disease means the study measures the burden of recognized and recorded thyroid illness rather than laboratory-confirmed thyroid dysfunction in the moment.

The headline numbers are striking. Weighted prevalence of doctor-diagnosed thyroid disorder was 10.87 percent among women with a hormone therapy history versus 6.87 percent among women without one. Current thyroid disorder showed a similar gap, 6.79 percent versus 3.79 percent, as did lifetime thyroid disorder at 10.95 percent versus 6.96 percent and treated thyroid disorder at 4.88 percent versus 2.95 percent. In every case, women reporting prior hormone medication use carried roughly a one-and-a-half to nearly two-fold heavier burden of thyroid disease on the raw, survey-weighted scale.

Because raw differences in observational data can easily reflect age, body weight, income, reproductive history, or the simple fact of seeing doctors more often, the team turned to survey-weighted logistic regression, the standard tool for estimating associations in complex national surveys. Their models adjusted for demographic, socioeconomic, metabolic, reproductive, and survey-year factors. To guard against the statistical trap of cherry-picking significant results across multiple tests, they applied Benjamini-Hochberg correction, computing q values that control the expected proportion of false discoveries across the four outcomes. After adjustment, a history of female hormone therapy remained associated with doctor-diagnosed thyroid disorder with an adjusted odds ratio of 1.52 and a 95 percent confidence interval of 1.06 to 2.16, with a q value of 0.031. The estimate for current thyroid disorder was even stronger, at an odds ratio of 1.75 with a confidence interval of 1.09 to 2.83, and lifetime thyroid disorder yielded an odds ratio of 1.50 with a confidence interval of 1.06 to 2.14, both also surviving the false discovery correction at q equal to 0.031. The estimate for currently treated thyroid disorder was directionally similar but less statistically secure, at an odds ratio of 1.60 with a confidence interval spanning 0.96 to 2.68 and a q value of 0.071.

Recognizing that any single modeling choice can swing results, the researchers ran an unusually thorough battery of sensitivity analyses. When they expanded the covariate set further, the primary estimate attenuated to an odds ratio of 1.38 with a confidence interval of 0.96 to 2.00, no longer excluding the possibility of no association. When they adjusted for healthcare contact, an attempt to account for the possibility that hormone therapy users simply interact with the medical system more and therefore get diagnosed more often, the association held at an odds ratio of 1.46 with a confidence interval of 1.01 to 2.10. Restricting the analysis to narrower age bands, however, produced estimates that crossed the null, suggesting the signal may be sensitive to the age composition of the sample. Adding gravidity, the number of times a woman had been pregnant, to the adjustment left the estimate essentially unchanged at an odds ratio of 1.52 with a confidence interval of 1.05 to 2.20. Exploratory analyses of treatment duration returned heterogeneous results, offering no consistent picture of whether longer exposure carried greater risk.

What might connect ovarian hormone preparations and the thyroid gland biologically? The mechanistic story is plausible but unresolved. Estrogen influences thyroid physiology in several documented ways: it can stimulate thyroglobulin, the protein scaffold on which thyroid hormones are synthesized, and it modulates immune activity in a gland where autoimmune disease, particularly Hashimoto’s thyroiditis, is disproportionately common in women. Hormone therapy could also plausibly promote thyroid growth or nodule formation in a gland already rich in estrogen receptors. Conversely, the association could run in the opposite causal direction: women with thyroid symptoms such as fatigue, weight change, or mood disturbance might seek menopausal symptom relief through hormone therapy, or their thyroid conditions might simply be diagnosed around the same life stage. Residual confounding by health-seeking behavior, physician vigilance, or unmeasured metabolic traits remains a live possibility in any cross-sectional design.

The authors are explicit about the limits of their evidence. Because the exposure and outcomes were both self-reported and captured at a single point in time, the study cannot establish temporality, let alone causality. It cannot distinguish whether hormone therapy preceded the thyroid disorder, followed it, or merely co-occurred with it. The questionnaire also could not identify current users or treatment details, blurring any dose or duration effects. Yet the consistency of the association across three of four endpoints, its survival of false discovery correction, and its persistence under healthcare-contact adjustment give the finding enough weight that it should not be dismissed as statistical noise. At the same time, the attenuation under expanded adjustment and the null results in age-restricted analyses are honest reminders that the true effect, if any, is likely modest and context-dependent.

For clinicians and the millions of postmenopausal women weighing hormone therapy, the practical takeaway is one of measured vigilance rather than alarm. The study’s authors state plainly that their findings do not support universal thyroid screening for women with a hormone therapy history, nor do they justify changing menopausal hormone therapy decisions solely on the basis of that history. Standard practice, in which thyroid function is evaluated when symptoms or clinical findings warrant it, remains the appropriate course. What the research does provide is a well-powered, nationally representative East Asian data point in a literature long dominated by Western cohorts, and a clear template for the kind of study needed next: prospective, longitudinal designs with pharmacy-verified hormone exposure, laboratory-measured thyroid function, and careful sequencing of treatment and diagnosis. Until such evidence arrives, the association between hormone therapy history and thyroid disorder burden in postmenopausal Korean women stands as an intriguing signal, a question mark that modern endocrinology will now be pressed to resolve.

Subject of Research: The association between self-reported menopausal hormone therapy history and thyroid disorder prevalence among postmenopausal Korean women in the KNHANES IV survey.

Article Title: Self-reported female hormone therapy history and thyroid disorder burden among postmenopausal Korean women: a cross-sectional KNHANES IV study

Article References: Qiu, Z., Long, H., Li, R., Yang, J., Cao, W., Chen, S., & Jin, N. (2026). Self-reported female hormone therapy history and thyroid disorder burden among postmenopausal Korean women: a cross-sectional KNHANES IV study. BMC Endocrine Disorders. https://doi.org/10.1186/s12902-026-02540-3

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02540-3

Keywords: menopausal hormone therapy, thyroid disorder, postmenopausal women, KNHANES, cross-sectional study, South Korea, endocrinology, odds ratio, thyroid screening, estrogen, women's health, observational study

Type 2 diabetes is among the most consequential public health challenges of the twenty-first century, ranking as the eighth leading cause of death and disability worldwide. The burden is unevenly distributed, not only between countries but between the sexes, and the reasons are deeply tied to biology. Before menopause, women tend to enjoy a metabolic advantage that men do not, largely because estrogen enhances insulin sensitivity, supports glucose-stimulated insulin secretion, and protects insulin-producing beta cells from apoptosis. After menopause, that advantage erodes. Estrogen levels fall, insulin resistance rises, and body fat shifts toward the abdomen in an androgenic pattern, all of which converge to raise diabetes risk in older women above that of men in the same age groups. Epidemiological evidence reinforces this picture: women who reach menopause before the age of forty, or who lose their ovaries surgically, face markedly higher diabetes rates than those who reach menopause after fifty, a pattern attributed primarily to prolonged estrogen deficiency.

While the influence of individual reproductive factors, such as breastfeeding, parity, age at menarche, and age at menopause, has been studied extensively, the results have often been contradictory. Breastfeeding appears protective, abortion may raise risk, and findings on menarche and menopause timing conflict across studies. What researchers behind the new study argued was missing was a unified metric: the total duration over which a woman is exposed to estradiol-dominant menstrual cycles across her reproductive life. To their knowledge, no prior investigation had examined how this cumulative exposure relates to the incidence of type 2 diabetes, despite earlier work by the same group linking estrogen exposure duration to fractures, chronic kidney disease, cardiovascular outcomes, and hypertension.

To address the gap, the team turned to the Tehran Lipid and Glucose Study, a population-based cohort launched in 1998 with 15,005 participants aged three and older, selected through multistage cluster sampling and followed at three-year intervals across seven completed study phases. From this resource, the researchers identified 6,273 postmenarchal women aged twenty or older who had at least one follow-up visit. After excluding women with prevalent diabetes, insufficient follow-up, hormone replacement therapy use, surgical menopause, or incomplete data, the analytic sample comprised 3,411 women, of whom 1,053 developed type 2 diabetes over a median follow-up of approximately 17.6 years. Diabetes was defined rigorously according to American Diabetes Association criteria, using fasting plasma glucose of 126 mg/dL or higher, two-hour plasma glucose of 200 mg/dL or higher during an oral glucose tolerance test, or the use of antidiabetic medication.

The study’s central methodological innovation lay in how exposure was quantified. Endogenous estrogen exposure duration was defined as the interval between menarche and whichever came first: natural menopause, the onset of diabetes, or the end of follow-up. Critically, the investigators subtracted periods during which the estradiol-dominant follicular phase was absent, including pregnancies calculated at forty weeks per birth and twenty weeks per abortion, hormonal contraceptive use, months of breastfeeding per child, and the roughly two-week progesterone-dominant luteal phase of each menstrual cycle. This refinement aimed to isolate the estrogen-dominant portions of reproductive life, producing a z-score that could be entered into Cox proportional hazards regression models, adjusted first for age and body mass index and then for a fuller set of covariates including cholesterol fractions, triglycerides, physical activity, prediabetes, family history of diabetes, and gestational diabetes history.

The results were consistent across both models. In the fully adjusted analysis, each one-standard-deviation increase in the estrogen exposure z-score was associated with a 10 percent lower hazard of developing type 2 diabetes, a highly significant effect. The relationship was most pronounced among premenopausal women, who made up nearly 81 percent of the sample. In that subgroup, the age- and BMI-adjusted hazard ratio indicated a 16 percent risk reduction per standard deviation of longer exposure, and the fully adjusted estimate of 0.87 remained significant. Among the 657 postmenopausal women, the association was directionally similar and of comparable magnitude, with a fully adjusted hazard ratio of 0.88, but the wider confidence interval that touched 1.0 meant the finding fell just short of conventional statistical significance, likely reflecting the smaller subgroup size.

The baseline data contextualize these findings. Women who went on to develop diabetes were older, heavier, and had a less favorable lipid profile, with higher total cholesterol and triglycerides and lower HDL cholesterol. They also carried a substantially higher burden of prediabetes, affecting 39.5 percent of future cases compared with 11.7 percent of those who remained diabetes-free, along with more frequent histories of gestational diabetes and family history of the disease. Yet the protective association between estrogen exposure and diabetes incidence persisted after adjustment for all of these factors, suggesting the relationship was not merely an artifact of baseline metabolic differences. Adjusted survival curves also revealed that postmenopausal women showed consistently lower cumulative diabetes-free survival than premenopausal women, with the gap widening over time.

The biology underlying the association is increasingly well understood. Oestrogen receptors are expressed in the brain, liver, skeletal muscle, adipose tissue, and pancreatic beta cells, and activation of these receptors modulates glucose balance across multiple tissues simultaneously. Estrogen suppresses hepatic gluconeogenesis through transcriptional mechanisms involving Foxo1, curbs low-grade inflammation linked to insulin resistance, and influences energy equilibrium and body composition, with menopausal loss of these effects promoting visceral fat accumulation and further insulin resistance. Interestingly, the authors caution that estrogen’s metabolic actions are not universally beneficial: evidence from type 1 diabetes and insulin-deficient animal models suggests that in autoimmune, insulin-deficient contexts, estrogen can worsen vascular and metabolic instability. The protective association observed in this cohort, they argue, likely reflects estrogen’s favorable role in the insulin-resistant physiology that defines type 2 diabetes, a fundamentally different metabolic environment.

The study’s strengths are considerable: its long follow-up, large sample size, objective laboratory-based diabetes ascertainment repeated across seven phases, and careful statistical modeling of confounders. Limitations remain, however. Reproductive histories, including ages at menarche and menopause and durations of breastfeeding and contraceptive use, were self-reported and therefore vulnerable to recall bias, although three-yearly reassessment in the cohort supports consistency. The subtraction of a uniform two-week luteal phase is an approximation, fasting insulin data were unavailable precluding HOMA-IR analysis, the cohort was urban, and the observational design means the findings establish association rather than causation.

Even so, the implications are striking. If cumulative estrogen exposure can be incorporated into diabetes screening tools, clinicians may be able to identify women with short reproductive life spans, early menopause, or surgically induced menopause as candidates for intensified monitoring and personalized prevention. With Iranian diabetes prevalence at 15.14 percent among adults aged 25 and older and projections approaching 9.2 million cases without effective intervention, and with women worldwide shouldering rising risk after menopause while often receiving less guideline-recommended treatment than men, the study underscores the need for sex-specific approaches to diabetes prevention. Future research, the authors conclude, should clarify precisely how estrogen exposure duration shapes metabolic trajectories and translate that knowledge into targeted primary prevention strategies for the women at greatest risk.

Subject of Research: The association between cumulative endogenous estrogen exposure duration and the incidence of type 2 diabetes in women

Article Title: Diabetes Type 2 in Women: The Impact of EndogenousOestrogen, A Population‐Based Study With About 2 Decades of Follow‐Up

Article References: Ramezani Tehrani, F., Mousavi, M., Farhadi‐Azar, M., Mahboobifard, F., Azizi, F., & Farahmand, M. (2026). Diabetes Type 2 in Women: The Impact of EndogenousOestrogen, A Population‐Based Study With About 2 Decades of Follow‐Up. Endocrinology, Diabetes & Metabolism, 9(5), Article e70267. https://doi.org/10.1002/edm2.70267

Image Credits: AI Generated

DOI: 10.1002/edm2.70267

Keywords: type 2 diabetes, endogenous estrogen exposure, menopause, women's health, insulin resistance, reproductive factors, cohort study, Tehran Lipid and Glucose Study, estrogen, diabetes risk, hormonal exposure, epidemiology