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Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;49(12): e5826, 2016. graf
Article in English | LILACS | ID: biblio-828173

ABSTRACT

Glucagon-like peptide 1 (GLP-1), a kind of gut hormone, is used in the treatment of type 2 diabetes (T2D). Emerging evidence indicates that GLP-1 has anti-inflammatory activity. Chronic inflammation in the adipose tissue of obese individuals is a cause of insulin resistance and T2D. We hypothesized that GLP-1 analogue therapy in patients with T2D could suppress the inflammatory response of macrophages, and therefore inhibit insulin resistance. Our results showed that GLP-1 agonist (exendin-4) not only attenuated macrophage infiltration, but also inhibited the macrophage secretion of inflammatory cytokines including TNF-β, IL-6, and IL-1β. Furthermore, we observed that lipopolysaccharide (LPS)-induced macrophage conditioned media could impair insulin-stimulated glucose uptake. This effect was compensated by treatment with the conditioned media from macrophages treated with the combination of LPS and exendin-4. It was also observed that exendin-4 directly inhibited the activation of NF-κB in macrophages. In conclusion, our results indicated that GLP-1 improved inflammatory macrophage-derived insulin resistance by inhibiting NF-κB pathway and secretion of inflammatory cytokines in macrophages. Furthermore, our observations suggested that the anti-inflammatory effect of GLP-1 on macrophages can contribute to GLP-1 analogue therapy of T2D.


Subject(s)
Humans , Animals , Mice , Glucagon-Like Peptide 1/pharmacology , Inflammation Mediators/pharmacology , Inflammation/drug therapy , Insulin Resistance , Macrophages/drug effects , Peptides/pharmacology , Venoms/pharmacology , Adipose Tissue/metabolism , Cell Migration Assays , Inflammation/metabolism , Macrophages/metabolism
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