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- Author: Jin-Woo Park x
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Dermcidin (DCD), an antimicrobial peptide that is secreted by sweat glands, is reportedly a human homolog of mouse proteolysis-inducing factor. This study was conducted to investigate the effect of DCD on body fat mobilization. The expression level of DCD in the livers of Ad-DCD-injected mice was higher than in those of Ad-β-galactosidase (Ad-β-gal)-injected mice 7 days after injection. In addition, injection with the Ad-DCD virus led to decreased body weight and epididymal fat mass when compared with controls. The plasma triglyceride level was decreased, whereas the free fatty acid and glycerol levels were increased in the Ad-DCD-injected group. Epididymal adipose tissues obtained from Ad-DCD-injected mice consisted of smaller adipocytes than tissues obtained from Ad-β-gal-injected mice. The gene expression profiles revealed an upregulation of hormone-sensitive lipase and adipose fatty acid-binding protein, both of which are involved in adipocyte lipolysis, in Ad-DCD-injected mice, and this lipolytic effect of DCD paralleled the increase of circulating tumor necrosis factor-α (TNF-α) level that was observed. The perilipin levels in adipose tissue were decreased in Ad-DCD-injected mice when compared with those of the control mice. Taken together, these results suggest that DCD-mediated body fat reduction might occur as a result of TNF-α-induced downregulation of perilipin in adipose tissue.
Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea
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Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea
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Isoeugenol exerts various beneficial effects on human health. However, the mechanisms underlying these effects are poorly understood. In this study, we observed that isoeugenol activated AMP-activated protein kinase (AMPK) and increased glucose uptake in rat L6 myotubes. Isoeugenol-induced increase in intracellular calcium concentration and glucose uptake was inhibited by STO-609, an inhibitor of calcium/calmodulin-dependent protein kinase kinase (CaMKK). Isoeugenol also increased the phosphorylation of protein kinase C-α (PKCα). Chelation of calcium with BAPTA-AM blocked isoeugenol-induced AMPK phosphorylation and glucose uptake. Isoeugenol stimulated p38MAPK phosphorylation that was inhibited after pretreatment with compound C, an AMPK inhibitor. Isoeugenol also increased glucose transporter type 4 (GLUT4) expression and its translocation to the plasma membrane. GLUT4 translocation was not observed after the inhibition of AMPK and CaMKK. In addition, isoeugenol activated the Akt substrate 160 (AS160) pathway, which is downstream of the p38MAPK pathway. Knockdown of the gene encoding AS160 inhibited isoeugenol-induced glucose uptake. Together, these results indicate that isoeugenol exerts beneficial health effects by activating the AMPK/p38MAPK/AS160 pathways in skeletal muscle.
Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Department of Internal Medicine, Biomedical Research Center, Department of Biological Sciences, University of Ulsan College of Medicine, 88 Olympic‐ro 43‐gil, Songpa‐gu, Seoul 138‐736, Korea
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Mitochondrial dysfunction in hypertrophic adipocytes can reduce adiponectin synthesis. We investigated whether 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression is increased in hypertrophic adipocytes and whether this is responsible for mitochondrial dysfunction and reduced adiponectin synthesis. Differentiated 3T3L1 adipocytes were cultured for up to 21 days. The effect of AZD6925, a selective 11β-HSD1 inhibitor, on metabolism was examined. db/db mice were administered 600 mg/kg AZD6925 daily for 4 weeks via gastric lavage. Mitochondrial DNA (mtDNA) content, mRNA expression levels of 11 β -H sd1 and mitochondrial biogenesis factors, adiponectin synthesis, fatty acid oxidation (FAO), oxygen consumption rate and glycolysis were measured. Adipocyte hypertrophy in 3T3L1 cells exposed to a long duration of culture was associated with increased 11 β -Hsd1 mRNA expression and reduced mtDNA content, mitochondrial biogenesis factor expression and adiponectin synthesis. These cells displayed reduced mitochondrial respiration and increased glycolysis. Treatment of these cells with AZD6925 increased adiponectin synthesis and mitochondrial respiration. Inhibition of FAO by etomoxir blocked the AZD6925-induced increase in adiponectin synthesis, indicating that 11β-HSD1-mediated reductions in FAO are responsible for the reduction in adiponectin synthesis. The expression level of 11 β -Hsd1 was higher in adipose tissues of db/db mice. Administration of AZD6925 to db/db mice increased the plasma adiponectin level and adipose tissue FAO. In conclusion, increased 11β-HSD1 expression contributes to reduced mitochondrial respiration and adiponectin synthesis in hypertrophic adipocytes.
