Kim Tae Hoon, Bae Nayoung, Kim Taeho, Hsu Albert L, Hunter Mark I, Shin Jung-Ho, Jeong Jae-Wook
Department of Obstetrics, Gynecology & Reproductive Biology, Michigan State University, Grand Rapids, MI 49534, USA.
Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, Guro Hospital, Korea University Medical Center, Seoul 02841, Korea.
Biomedicines. 2022 Sep 1;10(9):2160. doi: 10.3390/biomedicines10092160.
Endometriosis is a chronic inflammatory condition in women, and obesity leads to an inflammatory condition that is directly involved in the etiology of endometriosis. However, observational studies have shown an inverse correlation between endometriosis and a low body mass index (BMI). Obesity does not protect against endometriosis, and on the contrary, an increased BMI may lead to more severe forms of the disease. To determine the effect of obesity on endometriosis, diet-induced and genetically engineered obese mouse models were integrated with endometriosis mouse models with fluorescence-tagged ectopic lesions. High-fat diet-induced obese mice revealed a significant increase in endometriosis development compared with regular-diet control mice. However, obese recipient mice with leptin deficiency and leptin receptor deficiency showed suppressed endometriosis development compared with control mice. Furthermore, donor uterine tissues with leptin deficiency and leptin receptor deficiency suppressed endometriosis development compared with control donor in control recipient mice. Importantly, we revealed that aberrant high levels of leptin concentration significantly increased endometriosis development compared with vehicle treatment group in control mice with normal body weight. Our results suggest that leptin and its receptor are critical for endometriosis development.
子宫内膜异位症是一种女性慢性炎症性疾病，肥胖会导致一种直接参与子宫内膜异位症病因的炎症状态。然而，观察性研究表明子宫内膜异位症与低体重指数（BMI）之间存在负相关。肥胖并不能预防子宫内膜异位症，相反，BMI升高可能导致该疾病更严重的形式。为了确定肥胖对子宫内膜异位症的影响，将饮食诱导和基因工程肥胖小鼠模型与带有荧光标记异位病变的子宫内膜异位症小鼠模型相结合。与常规饮食对照小鼠相比，高脂饮食诱导的肥胖小鼠的子宫内膜异位症发展显著增加。然而，与对照小鼠相比，缺乏瘦素和瘦素受体的肥胖受体小鼠的子宫内膜异位症发展受到抑制。此外，与对照受体小鼠中的对照供体相比，缺乏瘦素和瘦素受体的供体子宫组织抑制了子宫内膜异位症的发展。重要的是，我们发现与体重正常的对照小鼠中的载体治疗组相比，异常高水平的瘦素浓度显著增加了子宫内膜异位症的发展。我们的结果表明，瘦素及其受体对子宫内膜异位症的发展至关重要。
