Resistin-like molecule alpha reduces gallbladder optimal tension.

INTRODUCTION: Insulin resistance is associated with increased gallbladder volume and impaired gallbladder emptying. Resistin and resistin-like molecule alpha (RELM-alpha) are adipose-derived hormones that are believed to mediate insulin resistance. Therefore, we tested the hypothesis that administration of resistin or RELM-alpha would cause insulin resistance and diminish gallbladder contractility.
METHODS: In two sequential studies 40 eight-week-old nondiabetic lean mice were fed a chow diet for 4 weeks. In Study A, 10 mice received 20 microg of resistin IP, while in Study B 10 mice received 20 microg of RELM-alpha IP for seven days. In each study, 10 control mice received an equal volume of saline IP for seven days. At 12 weeks animals were fasted and underwent cholecystectomy, and in vitro gallbladder response to neurotransmitters was determined. Serum resistin, RELM-alpha, glucose, and insulin levels were measured. HOMA index, a measure of insulin resistance, was calculated.
RESULTS: RELM-alpha significantly increased HOMA index. RELM-alpha decreased gallbladder optimal tension, but did not alter responses to neurotransmitters. Resistin had no effect on HOMA index or on gallbladder optimal tension or response.
CONCLUSION: These data suggest that in nondiabetic lean mice: 1) resistin does not alter insulin resistance or gallbladder optimal tension, but 2) RELM-alpha increases insulin resistance and reduces gallbladder optimal tension. Therefore, we concluded that RELM-alpha may play a role in insulin-resistance mediated gallbladder dysmotility.