Lopez Fontana Constanza M, Maselli Artola Maria E, Di Milta Monaco Nicolas, Recalde Rincon Gabriela M, Vanrell Rodriguez Maria C, Uvilla Recupero Ana, Messina Lombino Diego, Perez Elizalde Rafael F, Lopez Laur Jose Daniel
Metabolic and Cancer Laboratory, Faculty of Pharmacy and Biochemistry, University Juan Agustin Maza, Argentina.
Arch Esp Urol. 2009 Mar;62(2):103-8. doi: 10.4321/s0004-06142009000200003.
Many studies have investigated the association between obesity, adipose tissue-derived factors (leptin and adiponectin) and prostate cancer (CaP) but the results are still inconsistent.
The aim of this study was to carry out a comprehensive review of the existing evidence about the role of leptin and adiponectin in prostate carcinogenesis and to provide an overview of it.
Recent evidence suggests that leptin may play a rol in prostate cancer progression, while adiponectin may act as an "antiprostatic cancer" adipokine.
Obesity may promote the progression of established prostate cancer and and adipokines may provide a molecular mechanism whereby obesity exerts its effects on prostate tumour biology.
许多研究调查了肥胖、脂肪组织衍生因子(瘦素和脂联素)与前列腺癌(CaP)之间的关联,但结果仍不一致。
本研究的目的是对关于瘦素和脂联素在前列腺癌发生中作用的现有证据进行全面综述,并提供一个概述。
最近的证据表明,瘦素可能在前列腺癌进展中起作用,而脂联素可能作为一种“抗前列腺癌”脂肪因子发挥作用。
肥胖可能促进已确诊前列腺癌的进展,脂肪因子可能提供一种分子机制,通过该机制肥胖对前列腺肿瘤生物学产生影响。