Abstract
Abstract Introduction: We have demonstrated that leptin deficiency and leptin resistance are associated with abnormal motility in the gallbladder. In addition, we have shown that serum glucose and insulin are inversely correlated with biliary motility and that administration of leptin to deficient mice normalizes gallbladder function. Thus, leptin administration may be therapeutic for biliary dyskinesia. However, no data are available on biliary leptin receptor levels. Therefore, we hypothesized that leptin receptors would be abundant in the gallbladder. Methods: 11 week old female lean control (C57Bl/6J, n = 12), leptin-deficient obese/diabetic (Lepob, n = 8), leptin-resistant obese/diabetic (Lepdb, n = 8) and non-obese, diabetic (NOD/LtJ, n = 8) mice were fasted overnight. The next day alimentary tissues including stomach, duodenum/jejunum, ileum, colon, gallbladder, liver and spleen were removed, and leptin receptor (Ob-Rb, long form) protein levels were determined by ELISA. Data were analyzed by Two-way and One-way ANOVA and by Student-Newman-Keuls for pair-wise multiple comparisons. Results: Leptin receptors were similarly abundant in the gallbladder of each strain (p ∗ . C57BI/6J Lepob Lepdb NOD Leptin receptors 22.6 ± 4.9 23.8 ± 3.5 24.6 ± 4.0 35.5 ± 8.3 ∗ ∗ p Conclusions: These data suggest that leptin receptors 1) are found most commonly in the gallbladder and 2) are increased in the gallbladder of non-obese diabetic mice. We conclude that alimentary leptin receptors are most abundant in the gallbladder and that leptin provides a link among obesity, diabetes, and gallstone formation.
Published Version
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