Csf1 Haploinsufficiency Triggers Hepatic Steatosis, But Does Not Protect From Obesity-induced Insulin Resistance In Mice | 25264
Journal of Gastrointestinal & Digestive System
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Background: Macrophages have been implicated in obesity-related pathologies through their role in inflammation. Colony
stimulating factor (Csf1) mediates macrophage development and function, and mice haploinsufficient for Csf1 (Csf1op/+)
are protected against atherosclerosis. However, its role in the pathogenesis of obesity-related disorders has never been
experimentally addressed. It was hypothesized that Csf1op/+ mice show decreased hepatic inflammation, thereby protecting
against fatty liver disease and insulin resistance.
Results: Csf1+/+ and Csf1op/+ mice fed a chow or high-fat cholesterol (HFC) diet were studied. Although body weight did not
differ between genotypes, Csf1op/+ mice showed a reduced lean body mass and an increased fat mass compared to controls. In
line with this, indirect calorimetric analysis revealed a lower metabolic rate in Csf1op/+ mice compared to Csf1+/+ mice. Hepatic,
adipose tissue and systemic inflammation were reduced in Csf1op/+ compared to Csf1+/+ mice. Hepatic cell fractionations
indicated that the Kupffer cells are responsible for the differences in liver inflammation. Moreover, Csf1 haploinsufficiency
resulted in increased fasting-induced hepatic steatosis. This hepatic steatosis could be partly explained by a reduced VLDL-TG
synthesis and secretion in Csf1op/+ mice, whereas no differences were found in de novo lipogenesis between genotypes. Despite
reduced inflammation, whole-body glucose tolerance and fasting insulin levels did not differ between the genotypes.
Conclusion: Obtained data point towards a beneficial role of Csf1 in the control of lipid metabolism in the liver, but it does not
affect the development of systemic insulin resistance in mice.
Debby P Y Koonen is an Assistant Professor in the Laboratory of Molecular Genetics, at the University Medical Center Groningen, Groningen, NL. She has completed
her PhD (Physiology) at Maastricht University in the Netherlands and received Postdoctoral fellowship training at the University of Alberta in Edmonton, Alberta,
Canada. She has specific interest in obesity, metabolic disease and aging in relation to the development and progression of non-alcoholic fatty liver disease (NAFLD).
Her research is focused on the pathogenesis of obesity at the crossroads of inflammation and lipid metabolism. She has published 25 papers in reputed journals.
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