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A I Martín Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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E Castillero Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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M Granado Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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M López-Menduiña Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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M A Villanúa Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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A López-Calderón Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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Adjuvant-induced arthritis is a model of rheumatoid arthritis that induces cachexia. In other cachectic situations, there is an increase in lipolysis resulting in a loss of adipose tissue mass. The aim of this work was to analyse the effect of chronic arthritis, induced by adjuvant injection, on white adipose tissue (WAT). For this purpose, rats were killed 10 days after adjuvant injection, when the first external symptoms appeared, on days 15 and 22 when the external signs of the illness reach their severest level. As arthritis decreases food intake, a pair-fed group was also included. Serum concentrations of insulin, leptin, adiponectin, glycerol and nitrites, as well as gene expression of leptin, adiponectin, hormone-sensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor α and zinc-α2-glycoprotein (ZAG) were determined. Arthritis decreased food intake between days 5 and 16, but not during the last 5 days of the experiment. There was a marked decrease in relative adipose tissue weight and in serum leptin and adiponectin as well as in their gene expression in WAT in arthritic rats. Arthritis decreased the gene expression of FAS in the WAT. However, none of these effects was found in pair-fed rats. Arthritis did not increase lipolysis, since arthritic rats have lower serum concentrations of glycerol, HSL mRNA in WAT, as well as liver ZAG mRNA than the pair-fed or control rats. These data suggest that in chronic arthritis the decrease in white adipose mass is secondary to a reduced adipose lipogenesis, and this effect is not mainly due to the decrease in food intake.

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A I Martín Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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M López-Menduiña Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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E Castillero Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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M Granado Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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M A Villanúa Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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A López-Calderón Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 28040 Madrid, Spain

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The aim of this work was to analyse the role of cyclooxygenase-2 (Ptgs2) in endotoxin-induced decrease in Igf1 and Igf binding protein-3 (Igfbp3). For this purpose, male Wistar rats were injected with lipolysaccharide (LPS) and/or the Ptgs2 inhibitor meloxicam. LPS induced a significant decrease (P<0.01) in serum concentrations of Igf1 and Igfbp3 and their mRNAs in the liver. Meloxicam administration prevented the inhibitory effect of LPS injection on serum Igf1 and its liver mRNA. By contrast, meloxicam administration was unable to modify the inhibitory effect of LPS on Igfbp3. LPS injection also induced a decrease in GH receptor (Ghr) mRNA in the liver, and meloxicam attenuated this effect. In order to elucidate a direct action of the Ptgs2 inhibitor on the liver cells, the effect of LPS and/or meloxicam was studied in primary cultures of hepatocytes with non-parenchymal cells. LPS decreased Igf1 and Ghr but not Igfbp3 gene expression in liver cells in culture. Meloxicam administration attenuated the inhibitory effect of LPS on Igf1 mRNA, whereas it did not modify the decrease in Ghr mRNA after LPS. The effect of meloxicam on the LPS response does not seem to be mediated by changes in nitric oxide or tumour necrosis factor (Tnf) production, since meloxicam did not modify the stimulatory effect of LPS on nitric oxide or Tnfα gene expression both in vivo and in vitro. All these data suggest that LPS-induced Ptgs2 activation decreases Igf1 gene expression in liver cells.

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