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Increased levels of acylation-stimulating protein in interleukin-6-deficient (IL-6(-/-)) mice

Artikel i vetenskaplig tidskrift
Författare Ingrid Wernstedt
Bob Olsson
Margareta Jernås
S. Paglialunga
Lena M S Carlsson
Ulf Smith
K. Cianflone
Kristina Wallenius
Ville Wallenius
Publicerad i Endocrinology
Volym 147
Nummer/häfte 6
Sidor 2690-5
ISSN 0013-7227 (Print)
Publiceringsår 2006
Publicerad vid Wallenberglaboratoriet
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 2690-5
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adipocytes/pathology, Adipose Tissue/metabolism, Animals, Body Weight, Complement C3/metabolism, Complement C3a/*analysis/metabolism, Fatty Acids, Nonesterified/blood, Female, Interleukin-6/*physiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Prealbumin/genetics, Properdin/genetics, Triglycerides/biosynthesis
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

IL-6-deficient (IL-6(-/-)) mice develop obesity at 6-7 months of age. To elucidate the mechanisms of this mature-onset obesity, global gene expression profiles of 3-month-old preobese IL-6(-/-) were compared with those of IL-6(+/+) mice using DNA arrays. Genes that were up-regulated in IL-6(-/-) mice included the factors transthyretin and properdin in white adipose tissue and adipsin in muscle. These factors have been shown to influence the formation of acylation-stimulating protein (ASP), a cleavage product of complement C3. ASP stimulates the synthesis of triacylglycerol in adipocytes, and ASP-deficient mice are resistant to diet-induced obesity. In line with the increases in transthyretin, properdin, and adipsin, ASP levels in serum were increased by 31-54% in IL-6(-/-) compared with IL-6(+/+) mice. Furthermore, IL-6 replacement treatment in IL-6(-/-) mice decreased ASP levels significantly by 25-60%. In conclusion, ASP levels are increased in preobese IL-6(-/-) mice. This increase may result in increased triacylglycerol formation and uptake in IL-6(-/-) adipocytes and thereby contribute to the development of obesity in IL-6(-/-) mice.

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