Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation
Munukka, E., Wiklund, P., Partanen, T., Välimäki, S., Laakkonen, E., Lehti, M., Fischer-Posovzsky, P., Wabitsch, M., Cheng, S., Huovinen, P., & Pekkala, S. (2016). Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation. PLoS ONE, 11(4), Article e0152786. https://doi.org/10.1371/journal.pone.0152786
Julkaistu sarjassa
PLoS ONETekijät
Päivämäärä
2016Oppiaine
Gerontologia ja kansanterveysLiikuntalääketiedeGerontology and Public HealthSports and Exercise MedicineTekijänoikeudet
© 2016 Munukka et al. This is an open
access article distributed under the terms of the
Creative Commons Attribution License.
2016:26 | 2017:160 | 2018:260 | 2019:110 | 2020:98 | 2021:77 | 2022:60 | 2023:58 | 2024:68 | 2025:6
While the role of both elevated levels of circulating bacterial cell wall components and adipose
tissue in hepatic fat accumulation has been recognized, it has not been considered that the
bacterial components-recognizing adipose tissue receptors contribute to the hepatic fat content.
In this study we found that the expression of adipose tissue bacterial flagellin (FLG)-recognizing
Toll-like receptor (TLR) 5 associated with liver fat content (r = 0.699, p = 0.003) and
insulin sensitivity (r = -0.529, p = 0.016) in humans (n = 23). No such associations were found
for lipopolysaccharides (LPS)-recognizing TLR4. To study the underlying molecular mechanisms
of these associations, human HepG2 hepatoma cells were exposed in vitro to the
conditioned culture media derived from FLG or LPS-challenged human adipocytes. The adipocyte-mediated
effects were also compared to the effects of direct HepG2 exposure to FLG
and LPS. We found that the media derived from FLG-treated adipocytes stimulated fat accumulation
in HepG2 cells, whereas either media derived from LPS-treated adipocytes or direct
FLG or LPS exposure did not. This is likely due to that FLG-treatment of adipocytes increased
lipolysis and secretion of glycerol, which is known to serve a substrate for triglyceride synthesis
in hepatocytes. Similarly, only FLG-media significantly decreased insulin signaling-related
Akt phosphorylation, IRS1 expression and mitochondrial respiratory chain ATP5A. In conclusion,
our results suggest that the FLG-induced TLR5 activation in adipocytes increases glycerol
secretion from adipocytes and decreases insulin signaling and mitochondrial functions,
and increases fat accumulation in hepatocytes. These mechanisms could, at least partly,
explain the adipose tissue TLR5 expression associated with liver fat content in humans.
...
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