This study was designed to evaluate whether or not continuous intracerebroventricular infusion of leptin (1.5 microg/rat/24 h, for 28 days) produced different regional response on the skeleton of growing rats. Leptin reduce the accretion of total femoral bone mineral content (BMC) and density (BMD). This effect was related to a reduction of metaphyseal femur as no changes were detected in the diaphysis. Despite the reduced accretion in the volumetric of both femur and tibia compared to controls, leptin had no significant effects on the lumbar vertebrae. Urine deoxypyrydinoline and serum osteocalcin remained more elevated in the leptin-treated group as compared to controls. The results demonstrate that long-term central infusion of leptin activates bone remodeling with a negative balance. Leptin induces distinct responses in the different structure of bone and in the axial and appendicular skeleton.
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http://dx.doi.org/10.1016/j.peptides.2005.10.014 | DOI Listing |
Placenta
December 2024
Department of Physiology, Development & Neuroscience, University of Cambridge, UK; Centre for Trophoblast Research, University of Cambridge, UK; BHF Cardiovascular Centre for Research Excellence, University of Cambridge, UK; Strategic Research Initiative in Reproduction, University of Cambridge, UK. Electronic address:
Introduction: Preeclamptic patients, both lean and obese, present with elevated leptin levels which are associated with the development of maternal endothelial dysfunction and adverse fetal outcomes, such as growth restriction, leading to low birth weight. Recent studies in pregnant mice demonstrate that mid-late gestation leptin infusion induces clinical characteristics of preeclampsia, including elevated maternal blood pressure, maternal endothelial dysfunction and fetal growth restriction. However, whether leptin triggers placental stress responses that contribute to adverse fetal outcomes as in preeclampsia is unknown.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2024
Department of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, Mississippi, United States.
Sci Rep
September 2024
Institute for Translational Medicine, Medical School, University of Pécs, 12 Szigeti street, Pécs, 7624, Hungary.
Middle-aged obesity and aging anorexia with muscle loss (sarcopenia) of old people present public health burden. These alterations may appear both in humans and rodents suggesting the role for regulatory alterations. Previously, we demonstrated that biphasic changes in the weight-reducing (catabolic) effects of neuropeptides of the hypothalamus-adipose tissue axis (e.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
December 2024
Division of Pediatric Nephrology, Rady Children's Hospital, University of California, San Diego, La Jolla, CA, USA.
Background: The CTNS gene mutation causes infantile nephropathic cystinosis (INC). Patients with INC develop Fanconi syndrome and chronic kidney disease (CKD) with significant bone deformations. C57BL/6 Ctns mice are an animal model for studying INC.
View Article and Find Full Text PDFBiomolecules
August 2024
Biochemistry Section, Faculty of Sciences and Chemical Technologies, University of Castilla-La Mancha, Avda. Camilo José Cela 10, 13071 Ciudad Real, Spain.
Leptin, acting centrally or peripherally, has complex effects on cardiac remodeling and heart function. We previously reported that central leptin exerts an anti-hypertrophic effect in the heart via cardiac PPARβ/δ activation. Here, we assessed the impact of central leptin administration and PPARβ/δ inhibition on cardiac function.
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