ICAM-1 and beta2 integrin deficiency impairs fat oxidation and insulin metabolism during fasting |
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Authors: | Babic Aleksandar M Wang Hong-Wei Lai Margaret J Daniels Thomas G Felbinger Thomas W Burger Peter C Stricker-Krongrad Alain Wagner Denisa D |
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Institution: | The CBR Institute for Biomedical Research, Boston, Massachusetts 02115, USA. |
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Abstract: | Intercellular adhesion molecule 1 (ICAM-1) and beta2 integrins play critical roles in immune responses. ICAM-1 may also participate in regulation of energy balance because ICAM-1-deficient mice become obese on a high-fat diet. We show that mice deficient in these adhesion receptors are unable to respond to fasting by up-regulation of fatty acid oxidation. Normal mice, when fasted, exhibit reduced circulating neutrophil counts and increased ICAM-1 expression and neutrophil recruitment in liver. Mice lacking ICAM-1 or beta2 integrins fail to show these responses--instead they become hypoglycemic with steatotic livers. Fasting ICAM-1-deficient mice reduce insulin more slowly than wild-type mice. This produces fasting hyperinsulinemia that prevents activation of adenosine mono-phosphate (AMP)-activated protein kinase in muscles and liver, which results in decreased import of long chain fatty acids into mitochondria. Thus, we show a new role for immune cells and their adhesion receptors in regulating metabolic response to fasting. |
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