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题名:Alarmin High-Mobility Group B1 (HMGB1) is regulated in human adipocytes in insulin resistance and influences insulin secretion in beta-cells.
作者:GUZMAN-RUIZ R; ORTEGA F; RODRIGUEZ A; VAZQUEZ-MARTINEZ R; DIAZ-RUIZ A; GARCIA-NAVARRO S; GIRALT M; GARCIA-RIOS A; COBO-PADILLA D; TINAHONES FJ; LOPEZ-MIRANDA J; VILLARROYA F; FRUHBECK G; FERNANDEZ-REAL JM; MALAGON MM;
来源:Int J Obes (Lond). 2014 Feb 28. doi: 10.1038/ijo.2014.36. [ IF= 0.00 ] ]
URL :10.1038/ijo.2014.36
日期:20140317
摘要:BackgroundThe nuclear protein high-mobility group box 1 (HMGB1) can be passively
released by necrotic cells or secreted actively by several cell types to regulate
immune and inflammatory responses as well as tissue remodelling. We herein aimed
to characterize the effect of insulin resistance on HMGB1 in adipose tissue and
to examine its potential role as a metabolic regulator in beta-pancreatic
cells.DesignPlasma HMGB1 concentration and adipose HMGB1 expression were assessed
in relation to obesity and insulin resistance. Cultured adipocytes from lean and
obese patients were used to investigate the intracellular distribution and
factors regulating HMGB1 release, as well as to test its effects on adipogenesis
and lipid metabolism. A regulatory role for HMGB1 in insulin secretion was also
investigated.ResultsCirculating HMGB1 was positively associated with BMI, while
adipose HMGB1 mRNA levels correlated with the expression of inflammatory markers.
Insulin resistance modified the intracellular distribution of HMGB1 in human
adipocytes with HMGB1 being predominantly nuclear in lean and obese normoglycemic
individuals, while localized to the cytosol in obese patients with type 2
diabetes. Adipocytes from lean individuals exposed to conditioned media from
LPS-stimulated macrophages induced HMGB1 redistribution to the cytoplasm and
release. HMGB1 treatment had no effect on differentiation and lipid metabolism in
adipocytes. However, HMGB1, whose circulating levels correlated with post-load
insulin concentration, increased both insulin release and intracellular Ca2+
concentration in INS-1 cells.ConclusionsThese findings show, for the first time,
that HMGB1 expression and release by human adipocytes is altered by inflammatory
conditions, as those imposed by obesity and insulin resistance. Our data reveal a
novel role for HMGB1 as a stimulatory factor of insulin secretion of
beta-pancreatic cells.International Journal of Obesity accepted article preview
online, 28 February 2014; doi:10.1038/ijo.2014.36.

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