Galectin-3 is a regulator of metaflammation in adipose tissue and pancreatic islets

The cells of the innate and adaptive immune systems have been implicated in the development of obesity-induced metaflammation and metabolic disorders including type 2 diabetes. Galectin-3, a β-galactoside-binding lectin, modulates immune/inflammatory responses and specifically binds to advanced glyc...

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Vydáno v:Adipocyte Ročník 2; číslo 4; s. 266 - 271
Hlavní autoři: Pejnovic, Nada N, Pantic, Jelena M, Jovanovic, Ivan P, Radosavljevic, Gordana D, Djukic, Aleksandar Lj, Arsenijevic, Nebojsa N, Lukic, Miodrag L
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Taylor & Francis 22.10.2013
Informa UK Limited
Landes Bioscience
Témata:
Commentary
galectin-3
IL-1β
inflammation
insulin resistance
NFκB
NLRP3 inflammasome
obesity
type 2 diabetes
type 2 diabetes
NFκB
inflammation
IL-1β
NLRP3 inflammasome
galectin-3
insulin resistance
obesity
ISSN:2162-3945, 2162-397X
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Shrnutí:The cells of the innate and adaptive immune systems have been implicated in the development of obesity-induced metaflammation and metabolic disorders including type 2 diabetes. Galectin-3, a β-galactoside-binding lectin, modulates immune/inflammatory responses and specifically binds to advanced glycation end products (AGE), modified lipoproteins, and endotoxin. In the recently published study we demonstrate proinflammatory changes in the visceral adipose tissue and pancreatic islets in galectin-3-deficient mice fed high-fat diet which also exhibited excess adiposity, hyperglycemia, insulin resistance and systemic inflammation compared with their diet matched wild-type controls. This was associated with the increased incidence of Type-1 T and NKT cells and pro-inflammatory CD11c + CD11b + macrophages in the visceral adipose tissue. Severe insulitis, infiltration of macrophages expressing NLRP3 inflammasome and IL-1β, and enhanced accumulation of AGE were present within the pancreatic islets in obese LGALS3 −/− mice. Moreover, increased caspase-1 dependent IL-1β secretion with increased expression of NLRP3 inflammasome and phospho-NFκBp65 were observed in LGALS3 −/− peritoneal macrophages stimulated in vitro by lipopolysaccharide and/or saturated fatty acid palmitate. The amplified high-fat diet-induced obesity and hyperglycemia and exacerbated inflammation in adipose tissue and pancreatic islets in LGALS3 −/− mice suggest an important role for galectin-3 in the regulation of adiposity, metaflammation and type 2 diabetes.
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ISSN:2162-3945
2162-397X
DOI:10.4161/adip.24881