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PI3Kγ activity in leukocytes promotes adipose tissue inflammation and early-onset insulin resistance during obesity.

Artikel i vetenskaplig tidskrift
Författare Ludovic Breasson
Barbara Becattini
Claudia Sardi
Angela Molinaro
Fabio Zani
Romina Marone
Fabrizio Botindari
Mélanie Bousquenaud
Curzio Ruegg
Matthias P Wymann
Giovanni Solinas
Publicerad i Science signaling
Volym 10
Nummer/häfte 488
ISSN 1937-9145
Publiceringsår 2017
Publicerad vid Wallenberglaboratoriet
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Språk en
Länkar dx.doi.org/10.1126/scisignal.aaf296...
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adipose Tissue, pathology, Animals, Class Ib Phosphatidylinositol 3-Kinase, physiology, Diet, High-Fat, adverse effects, Gene Expression Profiling, Inflammation, etiology, prevention & control, Insulin Resistance, Leukocytes, enzymology, pathology, Lipid Metabolism, Macrophages, pathology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Obesity, complications, physiopathology, Phosphorylation, Proto-Oncogene Proteins c-akt, metabolism
Ämneskategorier Annan hälsovetenskap, Cell- och molekylärbiologi, Fysiologi

Sammanfattning

The phosphoinositide 3-kinase γ (PI3Kγ) plays a major role in leukocyte recruitment during acute inflammation and has been proposed to inhibit classical macrophage activation by driving immunosuppressive gene expression. PI3Kγ plays an important role in diet-induced obesity and insulin resistance. In seeking to determine the underlying molecular mechanisms, we showed that PI3Kγ action in high-fat diet-induced inflammation and insulin resistance depended largely on its role in the control of adiposity, which was due to PI3Kγ activity in a nonhematopoietic cell type. However, PI3Kγ activity in leukocytes was required for efficient neutrophil recruitment to adipose tissue. Neutrophil recruitment was correlated with proinflammatory gene expression in macrophages in adipose tissue, which triggered insulin resistance early during the development of obesity. Our data challenge the concept that PI3Kγ is a general suppressor of classical macrophage activation and indicate that PI3Kγ controls macrophage gene expression by non-cell-autonomous mechanisms, the outcome of which is context-dependent.

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