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International Medical Scientific Journal       Issue-2 
10.5281/zenodo.5563473 

197 

  



Art of Medicine           Volume-1 

International Medical Scientific Journal       Issue-2 
10.5281/zenodo.5563473 

198 

 

Art of Medicine International Medical Scientific journal 

 

Founder and Publisher Pascual Izquierdo-Egea 

Published science may 2021 year. Issued Quarterly.  

Internet address: http://artofmedicineimsj.us 

E-mail: info@artofmedicineimsj.us 

11931 Barlow Pl Philadelphia, PA 19116, USA +1 (929) 266-0862 

 

 

 

  



Art of Medicine           Volume-1 

International Medical Scientific Journal       Issue-2 
10.5281/zenodo.5563473 

199 

 

Obesity and uterine fibroids 

I.M. Tojieva
1
, Z.Yu. Khalimova

1
, Sh.A. Zufarova

2
  

 

Republican Specialized Scientific and Practical Medical Center of Endocrinology 

named after Y. H. Turakulova 

Republican Center for Reproductive Health of the Population 

 

Abstract: The review is devoted to the role of metabolic syndrome in the 

development of good-quality hyperplastic myometrial lesion. Obesity is a potent 

potentiating endocrine factor in uterine diseases. Modern correction of endocrine-

metabolic disorders is a key component of complex treatment and prevention of 

hyperplastic diseases of the uterus. 

Keywords: uterine fibroids; dyslipidemia; metabolic endocrine diseases; 

metabolic syndrome 

 

Uterine fibroids (UF) is a benign monoclonal tumor made up of smooth muscle 

cells and connective tissue that develops in the wall of the uterus. Also known as 

uterine leiomyoma, UF is one of the most coUFon pelvic tumors, affecting over 70% 

of women of reproductive and premenopausal age [1]. Leiomyoma can be 

asymptomatic, but at the same time it is the main reason for hospitalization. Because 

most patients with UFs remain asymptomatic, the actual incidence of UFs is assumed 

to be much higher than that reported. Based on the ultrasound screening, the 

incidence for UFs is reported to be 1.278% in Asia and 3.745% in African- American 

women per year [2]. UFs may be responsible for a wide range of severe and chronic 

symptoms (heavy menstrual bleeding, anemia, pelvic pressure, bladder/bowel 

dysfunction, pelvic non-cyclic pain, dyspareunia, infertility, pregnancy 

complications) [3] with a deep impact on patients quality-of-life [4]. 

Many risk factors have been identified, such as a positive family history for UFs,  

combined oral contraceptive use or the use of an intrauterine device, low parity, early 

onset of menarche, unhealthy lifestyle and, more recently, obesity [3]. Although the 

etiology is largely unknown, leiomyomas are estrogen- and progesterone-dependent 

tumors characterized by an increased and disorganized proliferation of smooth 

muscle cells with an over-production of extracellular matrix (ECM). 

A study showed that obesity leads to changes in endocrine system function, 

affects the levels of blood sex hormones and alters the secrete modes and metabolic 

pathways of hormones and their roles in target organs [5]. Furthermore, some current 

studies have proved that obesity is one of the risk factors for uterine fibroids. 



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However, studies on the risk of uterine fibroids in women with central obesity, 

especially those with relatively large visceral fat area (VFA), are rare. 

Obesity is able to cause metabolic disorders, making local tissues to form an 

abnormally high estrogen environment. The mechanism includes: 1) androstenedione 

secreted by adrenal glands can be converted into estrone by aromatase in adipose 

tissues, and the level of estrone in plasma is increased with elevated adipose tissues 

and strengthened conversion ability, thus leading to persistent estrogen effect; 2) 

obesity leads to the lack of periodic regulation of progesterone, so that the 

endometrium is in an environment of over stimulation from no estrogen antagonistic 

progesterone for a long time [6,7] 3. Systemic inflaUFation: Excessive fat 

accumulation is associated with increased production of adipokines and inflaUFatory 

cytokines, which can lead to increased levels of reactive oxygen species (ROS). ROS 

are capable of stimulating cell proliferation, inhibiting cell apoptosis, and promoting 

the deposition of ECM, which is a key event in the emergence of UF [8]. In addition, 

in vitro studies have shown that UF cells have defective antioxidant enzymatic 

activity with reduced expression of catalase and superoxide dismutase, thus 

increasing the effect of ROS on smooth muscle cells [9]. 4.  Decreased production of 

sex hormone binding globulin (SHBG): Overweight women are more likely to have 

decreased production of SHBG by the liver, resulting in more unbound levels of 

circulating estrogen [10]. Low SHBG concentration has been shown to be associated 

with increased insulin resistance [11,12] 

There are no definitive conclusions about a possible correlation between obesity 

and UF. Several studies have been published on this topic with conflicting results. 

Some authors found a positive correlation [13-15] or inverse correlation [16-18], 

while others reported no association [19-21]. A possible explanation for the inverse 

correlation may be related to the fact that women with high obesity have lower levels 

of sex hormones due to anovulation and a decrease in the number of menstrual 

cycles, which are often observed in such patients. 

Decreased physical activity, diet and weight changes can also be considered 

modifiable risk factors for UF. Feedback has been reported between exercise and UF 

risk. Indeed, regular physical activity is responsible for increasing SHBG levels and 

lowering insulin and sex hormones. In addition, a diet rich in fruits, green vegetables, 

and fish also appears to play a protective role against leiomyomas [22]. Only a few 

studies have examined the relationship between weight change in adulthood and the 

risk of UF. A study by Terry et al. [19] found no association between childhood / 

adolescence weight and risk of UF. Similar results were obtained in a recent study: 

data presented by Lee et al. [23] show that weight gain in adulthood (starting at age 



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18), rather than current BMI, is associated with a higher risk of developing 

leiomyomas. 

Insulin resistance (IR) following hyperglycemic status is coUFon in patients with 

metabolic syndrome, and hyperinsulinemia caused by IR may provide a possible 

biological link underlying the relationship between UF and metabolic syndrome. 

Indeed, insulin appears to have a direct, specific effect on the ovaries. Through 

insulin receptors or insulin-like growth factor-1 receptors, insulin can promote the 

secretion of ovarian hormones and can also reduce their binding to globulins, 

ultimately increasing the total level of unbound circulating sex steroid hormones [24]. 

In addition, insulin has been observed to enhance the proliferation and mitosis of 

vascular smooth cells (animal model) and promote the growth of UF cells (in vitro 

studies) by altering the tyrosine kinase signaling pathway [24]. However, the 

relationship between UF and IR is still debated, given the conflicting results obtained 

in various experimental studies [25-26]. 

Regarding the relationship between dyslipidemia and UF, it is well known that 

estrogens affect several aspects of lipid metabolism (HDL and triglyceride levels, 

lipoprotein lipase expression) [27]. Given the fact that UF are estrogen-dependent 

tumors, it seems plausible to hypothesize a link between leiomyomas and the 

development of metabolic diseases. However, reports on this issue differ [28,29], and 

further research is required. 

In conclusion, obesity is one of the risk factors for uterine fibroids, and increased 

body fat (especially abdominal visceral fat) is capable of raising the risk of uterine 

fibroids. Meanwhile, providing nutrition guidance and changing diet and exercise 

habits are important measures to prevent the development of uterine fibroids. Further 

research is needed to elucidate the biology and natural history of leiomyomas in order 

to identify modifiable risk factors and to identify effective prevention and treatment 

strategies.  

 

  



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Experimental and therapeutic medicine  18:  404-410,  2019.404 

 


