Hematopoietic-Derived Galectin-3 Causes Cellular and Systemic Insulin Resistance

In obesity, macrophages and other immune cells accumulate in insulin target tissues, promoting a chronic inflammatory state and insulin resistance. Galectin-3 (Gal3), a lectin mainly secreted by macrophages, is elevated in both obese subjects and mice. Administration of Gal3 to mice causes insulin r...

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Vydané v:Cell Ročník 167; číslo 4; s. 973
Hlavní autori: Li, Pingping, Liu, Shuainan, Lu, Min, Bandyopadhyay, Gautum, Oh, Dayoung, Imamura, Takeshi, Johnson, Andrew M F, Sears, Dorothy, Shen, Zhufang, Cui, Bing, Kong, Lijuan, Hou, Shaocong, Liang, Xiao, Iovino, Salvatore, Watkins, Steven M, Ying, Wei, Osborn, Olivia, Wollam, Joshua, Brenner, Martin, Olefsky, Jerrold M
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 03.11.2016
Predmet:
Adipocytes - metabolism
Adipocytes - pathology
Animals
Chemotaxis
Diabetes Mellitus, Type 2 - drug therapy
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - pathology
Galectin 3 - antagonists & inhibitors
Galectin 3 - blood
Galectin 3 - genetics
Galectin 3 - metabolism
Hepatocytes - metabolism
Hepatocytes - pathology
Humans
Insulin - blood
Insulin Resistance
Macrophages - immunology
Macrophages - pathology
Mice
Mice, Knockout
Muscle Cells - metabolism
Muscle Cells - pathology
Obesity - immunology
Obesity - metabolism
Obesity - pathology
inflammation
galectin-3
insulin resistance
ISSN:1097-4172, 1097-4172
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Popis
Shrnutí:In obesity, macrophages and other immune cells accumulate in insulin target tissues, promoting a chronic inflammatory state and insulin resistance. Galectin-3 (Gal3), a lectin mainly secreted by macrophages, is elevated in both obese subjects and mice. Administration of Gal3 to mice causes insulin resistance and glucose intolerance, whereas inhibition of Gal3, through either genetic or pharmacologic loss of function, improved insulin sensitivity in obese mice. In vitro treatment with Gal3 directly enhanced macrophage chemotaxis, reduced insulin-stimulated glucose uptake in myocytes and 3T3-L1 adipocytes and impaired insulin-mediated suppression of glucose output in primary mouse hepatocytes. Importantly, we found that Gal3 can bind directly to the insulin receptor (IR) and inhibit downstream IR signaling. These observations elucidate a novel role for Gal3 in hepatocyte, adipocyte, and myocyte insulin resistance, suggesting that Gal3 can link inflammation to decreased insulin sensitivity. Inhibition of Gal3 could be a new approach to treat insulin resistance.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1097-4172
1097-4172
DOI:10.1016/j.cell.2016.10.025