作者: Shannon J. Graewin , James M. Kiely , Debao Lu , Carol L. Svatek , Hayder H. Al-Azzawi
DOI: 10.1016/J.JAMCOLLSURG.2007.09.015
关键词:
摘要: Background Little is known about the genetic factors that cause alterations in gallbladder motility, cholesterol crystal nucleation, biliary lipids, and, ultimately, gallstones. Obese, leptin-deficient (Lepob) mice have large volumes with decreased contraction vitro and are predisposed to formation. Leptin administration these causes weight loss restores function. We hypothesize of leptin Lepob would loss, decrease volume, change genes related nucleating factors, lipid metabolism. Study Design Twenty-four 8-week-old were fed a nonlithogenic diet for 4 weeks. Twelve received daily IP saline injections, 12 5 μg/g recombinant leptin. Gallbladder mRNA was pooled analyzed on murine genome microarray chips. Selected confirmed by real-time polymerase chain reaction (PCR) second group treated same protocol. Results Leptin-deficient given had significant reductions volume. These upregulation receptor (p = 0.007; PCR=1.1-fold increase) but downregulation 0.003; PCR=13.5-fold decrease). upregulated cholecystokinin A Conclusions modulates obesity regulates gallstone pathogenesis.