ICAM-1 and β2 integrin deficiency impairs fat oxidation and insulin metabolism during fasting

摘要: Intercellular adhesion molecule 1 (ICAM-1) and beta2 integrins play critical roles in immune responses. ICAM-1 may also participate regulation of energy balance because ICAM-1-deficient mice become obese on a high-fat diet. We show that deficient these receptors are unable to respond fasting by up-regulation fatty acid oxidation. Normal mice, when fasted, exhibit reduced circulating neutrophil counts increased expression recruitment liver. Mice lacking or fail responses--instead they hypoglycemic with steatotic livers. Fasting reduce insulin more slowly than wild-type mice. This produces hyperinsulinemia prevents activation adenosine mono-phosphate (AMP)-activated protein kinase muscles liver, which results decreased import long chain acids into mitochondria. Thus, we new role for cells their regulating metabolic response fasting.