Dataset Information

Gene expression in the GWAT of ob/ob and ob/ob/Fsp27-/- mice

ABSTRACT: GWAT store most of the TAG in mice, ob/ob mice is an obese mice. Ob/ob/Fsp27-/- mice are lean when compared with ob/ob mice. The GWAT weight was dramatically reduced in ob/ob/Fsp27-/- mice. We next extract the total RNA from the GWAT of ob/ob and ob/ob/Fsp27-/- mice, to perform microaary analysis using Mouse Genome 430 2.0 arrays, Affymetrix. We then analysised the up-regulated and down regulated pathways. We extract the RNA of GWAT from 4 month old mice and hybridization on Affymetrix microarrays. We then analysis the data.

OTHER RELATED OMICS DATASETS IN: PRJNA256296

ORGANISM(S): Mus musculus

SUBMITTER: Xiayu Xia Linkang Zhou

PROVIDER: E-GEOD-59807 | ArrayExpress | 2015-04-17

SECONDARY ACCESSION(S): GSE59807PRJNA256296

REPOSITORIES: GEO, ArrayExpress

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Publications

Insulin resistance and white adipose tissue inflammation are uncoupled in energetically challenged Fsp27-deficient mice.

Zhou Linkang L Park Shi-Young SY Xu Li L Xia Xiayu X Ye Jing J Su Lu L Jeong Kyeong-Hoon KH Hur Jang Ho JH Oh Hyunhee H Tamori Yoshikazu Y Zingaretti Cristina M CM Cinti Saverio S Argente Jesús J Yu Miao M Wu Lizhen L Ju Shenghong S Guan Feifei F Yang Hongyuan H Choi Cheol Soo CS Savage David B DB Li Peng P

Nature communications 20150107

Fsp27 is a lipid droplet-associated protein almost exclusively expressed in adipocytes where it facilitates unilocular lipid droplet formation. In mice, Fsp27 deficiency is associated with increased basal lipolysis, 'browning' of white fat and a healthy metabolic profile, whereas a patient with congenital CIDEC deficiency manifested an adverse lipodystrophic phenotype. Here we reconcile these data by showing that exposing Fsp27-null mice to a substantial energetic stress by crossing them with ob ...[more]

PMID: 25565658

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Project description:OBJECTIVE:Obesity increases morbidity and resource utilization in sepsis patients. Sepsis transitions from early/hyper-inflammatory to late/hypo-inflammatory phase. Majority of sepsis-mortality occurs during the late sepsis; no therapies exist to treat late sepsis. In lean mice, we have shown that sirtuins (SIRTs) modulate this transition. Here, we investigated the role of sirtuins, especially the adipose-tissue abundant SIRT-2 on transition from early to late sepsis in obese with sepsis. METHODS:Sepsis was induced using cecal ligation and puncture (CLP) in ob/ob mice. We measured microvascular inflammation in response to lipopolysaccharide/normal saline re-stimulation as a "second-hit" (marker of immune function) at different time points to track phases of sepsis in ob/ob mice. We determined SIRT-2 expression during different phases of sepsis. We studied the effect of SIRT-2 inhibition during the hypo-inflammatory phase on immune function and 7-day survival. We used a RAW264.7 (RAW) cell model of sepsis for mechanistic studies. We confirmed key findings in diet induced obese (DIO) mice with sepsis. RESULTS:We observed that the ob/ob-septic mice showed an enhanced early inflammation and a persistent and prolonged hypo-inflammatory phase when compared to WT mice. Unlike WT mice that showed increased SIRT1 expression, we found that SIRT2 levels were increased in ob/ob mice during hypo-inflammation. SIRT-2 inhibition in ob/ob mice during the hypo-inflammatory phase of sepsis reversed the repressed microvascular inflammation in vivo via activation of endothelial cells and circulating leukocytes and significantly improved survival. We confirmed the key finding of the role of SIRT2 during hypo-inflammatory phase of sepsis in this project in DIO-sepsis mice. Mechanistically, in the sepsis cell model, SIRT-2 expression modulated inflammatory response by deacetylation of NF?Bp65. CONCLUSION:SIRT-2 regulates microvascular inflammation in obese mice with sepsis and may provide a novel treatment target for obesity with sepsis.

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