Leptin Stimulates Endometriosis Development in Mouse Models.
Leptin Stimulates Endometriosis Development in Mouse Models.
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DOI：
10.3390/biomedicines10092160
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发表时间：
2022-09-01
期刊：
影响因子：
4.7
通讯作者：
中科院分区：
文献类型：
--
作者：
子宫内膜异位症是女性的一种慢性炎症性疾病，肥胖导致的炎症性疾病直接参与子宫内膜异位症的病因学。然而，观察性研究表明子宫内膜异位症与低体重指数（BMI）之间呈负相关。肥胖并不能预防子宫内膜异位症，相反，体重指数增加可能会导致更严重的疾病。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的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，高脂肪饮食诱导的肥胖小鼠子宫内膜异位症的发展显着增加。然而，与对照小鼠相比，瘦素缺乏和瘦素受体缺乏的肥胖受体小鼠表现出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，具有瘦素缺陷和瘦素受体缺陷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，与正常体重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着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于子宫内膜异位症的发展至关重要。
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.
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影响因子：
6.1
作者：
Johnson, Neil P.;Hummelshoj, Lone
通讯作者：
Hummelshoj, Lone
DOI：
10.1016/j.ejogrb.2004.11.019
发表时间：
2005-07-01
期刊：
EUROPEAN JOURNAL OF OBSTETRICS GYNECOLOGY AND REPRODUCTIVE BIOLOGY
影响因子：
--
作者：
Ferrero, S;Anserini, P;Ragni, N
通讯作者：
Ragni, N
DOI：
10.1177/2284026518773939
发表时间：
2018-06-01
影响因子：
0.5
作者：
Holdsworth-Carson, Sarah J.;Dior, Uri P.;Girling, Jane E.
通讯作者：
Girling, Jane E.
影响因子：
--
作者：
Liu, Yong;Zhang, Weiyuan
通讯作者：
Zhang, Weiyuan
影响因子：
3.8
作者：
Cummings, AM;Metcalf, JL;Birnbaum, L
通讯作者：
Birnbaum, L