ECE2013 Poster Presentations Diabetes (151 abstracts)
Heterozygous deficiency of endoglin decreases insulin and hepatic triglyceride levels during high fat diet
Daniel Beiroa 1 , Romero-Picó Amparo 1 , Langa Carmen 2 , Bernabeu Carmelo 2 , Lopez Miguel 1 , Jose M Lopez-Novoa 3 , Nogueiras Ruben 1 & Dieguez Carlos 1
1Department of Physiology, Instituto de Investigaciones Sanitarias (IDIS), CIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), School of Medicine-CIMUS, Santiago de Compostela, Spain; 2Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC), and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain; 3Renal and Cardiovascular Physiopathology Unit, Department of Physiology and Pharmacology, University of Salamanca and Instituto de Investigaciones Biomédicas de Salamanca (IBSAL), Salamanca, Spain.
Introduction: Endoglin is a transmembrane auxiliary receptor for transforming growth factor-β (TGF-β) that is predominantly expressed on proliferating endothelial cells. It plays a wide range of physiological roles but its importance on energy balance or insulin sensitivity has been unexplored.
Material and methods: Heterozygous deficient mice (HZ) were fed standard chow or high fat diet during 16 weeks. Blood glucose levels were measured after an i.p. injection of either D-glucose or insulin. Western blots were performed to measure the protein levels. Liver triglyceride levels was measured using colorimetric methods.
Results: Here we report for first time that heterozygous endoglin deficiency in mice decreases high fat diet-induced hepatic triglyceride content and insulin levels these effects are independent of changes in body weight or adiposity. At molecular level, we failed to detect relevant changes in the insulin signalling pathway.We found decreased triglyceride content in the liver of endoglin heterozygous mice fed a high fat diet.
Conclusion: Our findings indicate that endoglin is a potentially important physiological mediator of insulin levels and hepatic lipid metabolism.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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