4 results match your criteria: "a Center for Molecular and Vascular Biology[Affiliation]"
Adipocyte
December 2019
a Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences , KU Leuven , Leuven , Belgium.
Obesity has become a global health-threat for every age group. It is well known that young mice (10-12 weeks of age) fed a western-type diet (WD) become obese and develop higher cholesterol levels and liver steatosis whereas insulin sensitivity is reduced. Less is known, however, about the effect of a WD on advanced-age mice.
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September 2019
a Center for Molecular and Vascular Biology, KU Leuven , Leuven , Belgium.
Intestinal alkaline phosphatase 3 (AKP3) is an enzyme that was reported to play a role in lipid metabolism and to prevent high fat diet-induced metabolic syndrome in mice. To investigate a potential functional role of AKP3 in diet-induced adiposity and metabolic health, we have kept male and female wild-type or AKP3 deficient mice on a high fat diet for 15 weeks to induce obesity and compared those with mice kept on standard fat diet. Body weight as well as adipose tissue mass were statistically significantly higher upon high fat diet feeding for mice of both genders and genotypes.
View Article and Find Full Text PDFPlatelets
June 2016
a Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences , KU Leuven , Leuven , Belgium.
Unlabelled: Dextran sulfate (DxS; Mr 500 kD) induces fibrinogen receptor (αIIbβ3) activation via CLEC-2/Syk signaling and via a Syk-independent SFK/PI3K/Akt-dependent tyrosine kinase pathway in human and murine platelets. The platelet surface receptor, responsible for the DxS-induced Syk-independent Akt-activation, has hitherto not been identified. We found that DxS elicited a concentration-dependent aggregation of human platelets resulting from direct PEAR1 activation by DxS.
View Article and Find Full Text PDFCrit Rev Microbiol
November 2016
a Center for Molecular and Vascular Biology, KU Leuven , Leuven , Belgium.
Both coagulation and fibrinolysis are tightly connected with the innate immune system. Infection and inflammation cause profound alterations in the otherwise well-controlled balance between coagulation and fibrinolysis. Many pathogenic bacteria directly exploit the host's hemostatic system to increase their virulence.
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