Matches in SemOpenAlex for { <https://semopenalex.org/work/W2753070699> ?p ?o ?g. }
Showing items 1 to 77 of
77
with 100 items per page.
- W2753070699 endingPage "150" @default.
- W2753070699 startingPage "150" @default.
- W2753070699 abstract "An influx of lipid-loaded macrophages characterizes visceral adipose tissue (VAT) inflammation, which is an important factor in the development of insulin resistance (IR) in obesity. Depletion of macrophage lipids accompanies increased whole body insulin sensitivity, but the underlying mechanism is unknown. Deficiency of autophagy protein ATG16L1 is associated with increases in inflammatory diseases and lipid metabolism, but the connection between ATG16L1, IR, and obesity remains elusive. We hypothesize that myeloid ATG16L1 contributes to lipid loading in macrophages and to IR.Wild-type (WT) bone marrow derived macrophages (BMDMs) were treated with fatty acids and assessed for markers of autophagy. Myeloid-deficient Atg16l1 and littermate control male mice were fed high fat diet (HFD) or low fat diet (LFD) for 3 months starting at 8 weeks of age. Mice were assessed for body mass, fat and lean mass, glucose and insulin sensitivity, food consumption and adipose inflammation. Fluorescence-activated cell sorted VAT macrophages were assessed for lipid content and expression of autophagy related genes.VAT and VAT macrophages from HFD-fed WT mice did not show differences in autophagy protein and gene expression compared to tissue from LFD-fed mice. Fatty acid-treated BMDMs increased neutral lipid content but did not change autophagy protein expression. HFD-fed Atg16l1 myeloid-deficient and littermate mice demonstrated no differences in body mass, glucose or insulin sensitivity, food consumption, fat or lean mass, macrophage lipid content, or adipose tissue inflammation.ATG16L1 does not contribute to obesity, IR, adipose tissue inflammation or lipid loading in macrophages in mice fed HFD." @default.
- W2753070699 created "2017-09-15" @default.
- W2753070699 creator A5000263041 @default.
- W2753070699 creator A5008264999 @default.
- W2753070699 creator A5011712738 @default.
- W2753070699 creator A5025080569 @default.
- W2753070699 creator A5060102632 @default.
- W2753070699 date "2017-09-01" @default.
- W2753070699 modified "2023-09-25" @default.
- W2753070699 title "Discovery of microRNAs regulating complement-dependent cytotoxicity" @default.
- W2753070699 doi "https://doi.org/10.1016/j.molimm.2017.06.104" @default.
- W2753070699 hasPublicationYear "2017" @default.
- W2753070699 type Work @default.
- W2753070699 sameAs 2753070699 @default.
- W2753070699 citedByCount "0" @default.
- W2753070699 crossrefType "journal-article" @default.
- W2753070699 hasAuthorship W2753070699A5000263041 @default.
- W2753070699 hasAuthorship W2753070699A5008264999 @default.
- W2753070699 hasAuthorship W2753070699A5011712738 @default.
- W2753070699 hasAuthorship W2753070699A5025080569 @default.
- W2753070699 hasAuthorship W2753070699A5060102632 @default.
- W2753070699 hasConcept C126322002 @default.
- W2753070699 hasConcept C134018914 @default.
- W2753070699 hasConcept C151955695 @default.
- W2753070699 hasConcept C171089720 @default.
- W2753070699 hasConcept C17675752 @default.
- W2753070699 hasConcept C185592680 @default.
- W2753070699 hasConcept C190283241 @default.
- W2753070699 hasConcept C203522944 @default.
- W2753070699 hasConcept C25095133 @default.
- W2753070699 hasConcept C2776914184 @default.
- W2753070699 hasConcept C2777391703 @default.
- W2753070699 hasConcept C2778004101 @default.
- W2753070699 hasConcept C2779306644 @default.
- W2753070699 hasConcept C2994476132 @default.
- W2753070699 hasConcept C4733338 @default.
- W2753070699 hasConcept C55493867 @default.
- W2753070699 hasConcept C71924100 @default.
- W2753070699 hasConcept C86803240 @default.
- W2753070699 hasConceptScore W2753070699C126322002 @default.
- W2753070699 hasConceptScore W2753070699C134018914 @default.
- W2753070699 hasConceptScore W2753070699C151955695 @default.
- W2753070699 hasConceptScore W2753070699C171089720 @default.
- W2753070699 hasConceptScore W2753070699C17675752 @default.
- W2753070699 hasConceptScore W2753070699C185592680 @default.
- W2753070699 hasConceptScore W2753070699C190283241 @default.
- W2753070699 hasConceptScore W2753070699C203522944 @default.
- W2753070699 hasConceptScore W2753070699C25095133 @default.
- W2753070699 hasConceptScore W2753070699C2776914184 @default.
- W2753070699 hasConceptScore W2753070699C2777391703 @default.
- W2753070699 hasConceptScore W2753070699C2778004101 @default.
- W2753070699 hasConceptScore W2753070699C2779306644 @default.
- W2753070699 hasConceptScore W2753070699C2994476132 @default.
- W2753070699 hasConceptScore W2753070699C4733338 @default.
- W2753070699 hasConceptScore W2753070699C55493867 @default.
- W2753070699 hasConceptScore W2753070699C71924100 @default.
- W2753070699 hasConceptScore W2753070699C86803240 @default.
- W2753070699 hasLocation W27530706991 @default.
- W2753070699 hasOpenAccess W2753070699 @default.
- W2753070699 hasPrimaryLocation W27530706991 @default.
- W2753070699 hasRelatedWork W2099352432 @default.
- W2753070699 hasRelatedWork W2113795181 @default.
- W2753070699 hasRelatedWork W2123508173 @default.
- W2753070699 hasRelatedWork W2146053648 @default.
- W2753070699 hasRelatedWork W2771652879 @default.
- W2753070699 hasRelatedWork W2888559361 @default.
- W2753070699 hasRelatedWork W2919868591 @default.
- W2753070699 hasRelatedWork W3129269856 @default.
- W2753070699 hasRelatedWork W3129382605 @default.
- W2753070699 hasRelatedWork W3022047353 @default.
- W2753070699 hasVolume "89" @default.
- W2753070699 isParatext "false" @default.
- W2753070699 isRetracted "false" @default.
- W2753070699 magId "2753070699" @default.
- W2753070699 workType "article" @default.