Effect of conditioned media from mature human adipocytes on insulin-stimulated Akt/PKB phosphorylation in human skeletal muscle cells: role of BMI and fat cell size.

T. Skurk, C. Alberti-Huber, H. Hauner

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Obesity is associated with chronic low-grade inflammation. It is currently hypothesized that products secreted from fat cells not only cause this proinflammatory condition but may also have a direct impact on the development of insulin resistance in skeletal muscle. The aim of this study was to investigate if adipocyte-conditioned media interfere with insulin-stimulated Akt/PKB phosphorylation in in vitro differentiated human skeletal muscle cells. Primary human skeletal muscle cells were exposed to adipocyte-conditioned media from subjects with a wide range of BMI. Insulin-induced phosphorylation of the signaling proteins Akt/PKB and ERK-2 was analyzed using a bead-based fluorescence detection system and was correlated to BMI and fat cell size. Adipocyte-conditioned media reduced insulin-stimulated Akt/PKB phosphorylation in a manner depending on BMI and fat cell volume. This inhibition in serine phosphorylation was comparable to that observed in TNF-alpha-treated control cultures. Conditioned media from omental adipocytes reduced Akt/PKB phosphorylation moderately to a greater extent compared to media from subcutaneous fat cells from the same donors (p<0.05). Furthermore, there were significant associations between the concentration of selected adipokines and Akt/PKB phosphorylation. These data provide first direct evidence that secreted factors from freshly isolated mature fat cells separated according fat cell size reduce insulin-stimulated Akt/PKB phosphorylation in human skeletal muscle cells and may contribute to the pathogenesis of obesity-associated insulin resistance.

Original languageEnglish
Pages (from-to)190-196
Number of pages7
JournalHormone and Metabolic Research
Volume41
Issue number3
DOIs
StatePublished - Mar 2009
Externally publishedYes

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