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Krill Oil Reverses White Adipose Tissue Dysfunction by Inhibiting Macrophage M1 Polarization in Mice With Type 2 Diabetes
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DOI：10.1002/mnfr.70215.png)
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Abstract
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White adipose tissue (WAT) dysfunction is a crucial contributor to insulin resistance (IR), which is the key cause for type 2 diabetes mellitus (T2DM). Macrophage infiltration and M1 polarization induce WAT dysfunction. Krill oil (KO) possesses anti-inflammation activity, but its effect on WAT dysfunction under T2DM remained unclear. To this end, T2DM was established in mice followed by a 6-month KO supplementation, showing that KO significantly lowered fasting blood glucose level, mitigated insulin resistance, and improved WAT dysfunction. Notably, KO decreased the number of infiltrated M1-polarized macrophages in the WAT. Moreover, lipolysis and insulin signaling impairment of the WAT were inhibited by KO. In vitro, KO blunted lipopolysaccharide-induced macrophage M1 polarization. Furthermore, in co-culture experiments, these KO-treated macrophages resulted in a less expression of inflammatory factors and resistin, an elevation of adiponection level, as well as an enhanced lipid storage capacity in adipocytes. In summary, the current study found that KO might improve adipocyte dysfunction and insulin resistance by inhibiting macrophage M1 polarization, providing a potential approach for T2DM intervention.
Keywords:
diabetes
krill oil
macrophage
T2DM
white adipose tissue
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