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Title:
Loss of Lkb1 in CD11c+ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance | Cellular and Molecular Life Sciences
Description:
Adipose tissue CD11c+ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in CD11c+ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in CD11c+ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and CD11c− macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat CD11c+ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity.
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Keywords {🔍}
mice, cells, lkbff, pubmed, article, adipose, hfd, lkb, tissue, google, scholar, cdccrelkbff, cdc, fig, cas, expression, vat, atdc, cell, obesity, ifnγ, ila, analysis, glucose, insulin, immune, metabolic, tregs, statistical, central, cdccre, results, representative, dendritic, nfd, atm, higher, weight, splenic, adipocytes, fat, levels, dio, feeding, lower, preadipocytes, model, fed, resistance, role,
Topics {✒️}
il-17a/il-17ra/p-stat3/fabp4 axis high-fat-diet-induced hepatic steatosis creb/ppar-γ/cd36 pathway lkb1 tips il-17a/ifn-γ rorγt-mediated il-17a production 50-ng/ml ifn-γ group cd45+mhc-ii+cd11chi cells ifn-γ-free control group article download pdf il-17a/ifn-γ balance liver kinase b1 high-fat diet-fed mice metabolic-immune vicious cycle adipose-tissue immune profile specific pathogen-free barrier diet-induced weight gain ifn-γ-free group ifn-γ remarkably tips distinctive fat-treg phenotype high-fat diet exposure cell-abundant immune profile il-17a-free group abolishes diet-induced thermogenesis ifn-γ-free medium 50 ng/ml ifn-γ 50-ng/ml ifn-γ 50 ng/ ml ifn-γ 50 ng/ml ifn-γ mir-27b-5p regulation liver/body weight ratio il-17/ifn-γ imbalance preserve systemic insulin sensitivity il-17a/ifn-γ diet-induced obesity model il-17a imbalance existed il-17a directly promotes 50 mg adipose tissue/sample ifn-γ promotes apoptosis amp-activated protein kinase obesity-induced insulin resistance pro-inflammatory cells ifn-γ promoted apoptosis adiponectin limits ifn-γ serine-threonine kinase pe-cy7-ifn-γ high-fat diet fatty acids [62] lower adipose-weight gain real-time qpcr analysis performed real-time qpcr
Questions {❓}
- Pessin JE, Kwon H (2012) How does high-fat diet induce adipose tissue fibrosis?
- Stolarczyk E (2017) Adipose tissue inflammation in obesity: a metabolic or immune response?
- Epicardial adipose tissue: What do we know?
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headline:Loss of Lkb1 in CD11c+ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance
description:Adipose tissue CD11c+ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in CD11c+ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in CD11c+ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and CD11c− macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat CD11c+ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity.
datePublished:2023-02-13T00:00:00Z
dateModified:2023-02-13T00:00:00Z
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Visceral adipose tissue
Dendritic cells
Macrophages
T cells
IL-17A
IFN-γ
Liver kinase B1
High-fat-diet-induced obesity
Cell Biology
Biomedicine
general
Life Sciences
Biochemistry
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headline:Loss of Lkb1 in CD11c+ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance
description:Adipose tissue CD11c+ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in CD11c+ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in CD11c+ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and CD11c− macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat CD11c+ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity.
datePublished:2023-02-13T00:00:00Z
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keywords:
Visceral adipose tissue
Dendritic cells
Macrophages
T cells
IL-17A
IFN-γ
Liver kinase B1
High-fat-diet-induced obesity
Cell Biology
Biomedicine
general
Life Sciences
Biochemistry
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