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Reduced stress- and cold-induced increase in energy expenditure in interleukin-6-deficient mice.

Journal article
Authors Ingrid Wernstedt
Amanda Edgley
Anna Berndtsson
Jenny Fäldt
Göran Bergström
Ville Wallenius
John-Olov Jansson
Published in American journal of physiology. Regulatory, integrative and comparative physiology
Volume 291
Issue 3
Pages R551-7
ISSN 0363-6119
Publication year 2006
Published at Wallenberg Laboratory
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages R551-7
Language en
Links dx.doi.org/10.1152/ajpregu.00514.20...
Keywords Animals, Cold Temperature, Energy Metabolism, genetics, physiology, Female, Interleukin-6, deficiency, genetics, metabolism, Male, Mice, Mice, Knockout, Norepinephrine, blood, Stress, Physiological, physiopathology, Thermogenesis, physiology
Subject categories Physiology

Abstract

Interleukin-6 (IL-6) deficient (-/-) mice develop mature onset obesity. Pharmacological studies have shown that IL-6 has direct lipolytic effects and when administered centrally increases sympathetic outflow. However, the metabolic functions of endogenous IL-6 are not fully elucidated. We aimed to investigate the effect of IL-6 deficiency with respect to cold exposure and cage-switch stress, that is, situations that normally increase sympathetic outflow. Energy metabolism, core temperature, heart rate, and activity were investigated in young preobese IL-6-/- mice by indirect calorimetry together with telemetry. Baseline measurements and the effect of cage-switch stress were investigated at thermoneutrality (30 degrees C) and at room temperature (20 degrees C). The effect of cold exposure was investigated at 4 degrees C. At 30 degrees C, the basal core temperature was 0.6 +/- 0.24 degrees C lower in IL-6-/- compared with wild-type mice, whereas the oxygen consumption did not differ significantly. The respiratory exchange ratio at 20 degrees C was significantly higher and the calculated fat utilization rate was lower in IL-6-/- mice. In response to cage-switch stress, the increase in oxygen consumption at both 30 and 20 degrees C was lower in IL-6-/- than in wild-type mice. The increase in heart rate was lower in IL-6-/- mice at 30 degrees C. At 4 degrees C, both the oxygen consumption and core temperature were lower in IL-6-/- compared with wild-type mice, suggesting a lower cold-induced thermogenesis in IL-6-/- mice. The present results indicate that endogenous IL-6 is of importance for stress- and cold-induced energy expenditure in mice.

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