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CSE-induced hydorogen sulfide improves glucose homeostasis and inhibits beta-cell failure in high-fat diet mice

ABSTRACT: CSE knockout (CSE-KO)mice at age 6 months were fed a high fat diet (HFD) for 8 weeks.we determined the effects of CSE knockdown on beta-cell function and mass in islets from the mice. After 8 weeks of the HFD,blood glucose levels were drasically increaced in CSE-KO mice compared with WT mice. To assess the effect of HFD on gene expression in CSE-KO mice,we performed a comparative DNA microarray analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE50458 | GEO | 2013/09/02

SECONDARY ACCESSION(S): PRJNA217517

REPOSITORIES: GEO

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CSE-induced hydorogen sulfide improves glucose homeostasis and inhibits beta-cell failure in high-fat diet mice

Project description:CSE knockout (CSE-KO)mice at age 6 months were fed a high fat diet (HFD) for 8 weeks.we determined the effects of CSE knockdown on beta-cell function and mass in islets from the mice. After 8 weeks of the HFD,blood glucose levels were drasically increaced in CSE-KO mice compared with WT mice. To assess the effect of HFD on gene expression in CSE-KO mice,we performed a comparative DNA microarray analysis 2 samples analysis.control is CSE-WT(HFD+)

2013-09-02 | E-GEOD-50458 | biostudies-arrayexpress

Cdh13 null mice isolated islets RNAseq

Project description:The pancreas islets RNA expressions were compared between WT (exon2 floxed) mice and Cdh13 KO (exon2 deleted) mice. The islets were isolated from the mice at 8wks old, 14wks old under normal chow diet, and 14wks old under HFD conditions.

2022-12-09 | GSE186944 | GEO

Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis

Project description:The ubiquitous gasotransmitter hydrogen sulfide (H2S) has been recognised to play a crucial role in human health. However, a role for host H2S in pathogenesis has not yet been demonstrated. Using cystathionine -lyase (CSE) deficient mice, we demonstrated an unexpected role of H2S in Mtb pathogenesis. We showed that Mtb-infected CSE-/- mice survive longer than wild-type mice, and support reduced pathology and lower bacterial burdens in the lung, spleen and liver. Similarly, in vitro Mtb infection of macrophages resulted in reduced colony forming units (CFUs) in CSE-/-cells. Chemical complementation of infected wild-type and CSE-/-macrophages using the slow H2S releaser GYY3147 and the CSE inhibitor DL-propargylglycine demonstrated that H2S is the effector molecule regulating Mtb survival in macrophages. Furthermore, we demonstrate that CSE promotes an excessive innate immune response, suppresses the adaptive immune response and reduces circulating IL1β, IL-6, TNFα, and IFN-γ levels in response to Mtb infection. Notably, Mtb infected CSE-/- macrophages show increased flux through glycolysis and the pentose phosphate pathway thereby establishing a critical link between H2S and central metabolism. Our data suggest that excessive H2S produced by the infected wild type mice reduce HIF-1α levels, thereby suppressing glycolysis and production of IL-1β, IL-6 and IL-12, and increasing bacterial burden. Clinical relevance was demonstrated by the spatial distribution of H2S producing enzymes in human necrotic, non-necrotic and cavitary pulmonary TB lesions. In summary, CSE exacerbates TB pathogenesis by altering immunometabolism in mice and inhibiting CSE or modulating glycolysis are potential targets for host-directed TB control.

2020-04-06 | GSE143619 | GEO

Transcriptome data on gene expression in Drosophila strains with deletions of sulfur metabolism genes: CBS and CSE

Project description:To reveal the role of sulfur metabolism genes in memory formation processes, transcriptome libraries were obtained from the heads of 5-day-old naive males. The libraries were generated from Drosophila strains created in our laboratory with deleted cbs genes ( CBS-/-(5) and CBS-/-(8), cse (CSE-/-) and strains with double deletion of cbs and cse genes (CBS-/-,CSE-/-(1) and (CBS-/-,CSE-/-(2). Strain 58492, in which deletions were introduced by the CRISP/CAS9 method, was used as a control strain.

2022-04-14 | GSE200397 | GEO

Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet B-cell Endoplasmic Reticulum Stress and Proliferation

Project description:Sphingosine-1-phosphate (S1P) is a sphingolipid metabolite that regulates basic cell functions through metabolic and signaling pathways. Intracellular metabolism of S1P is controlled, in part, by two homologous S1P phosphatases, 1 and 2, which are encoded by Sgpp1 and Sgpp2, respectively. S1P phosphatase activity is needed for efficient recycling of sphingosine into the sphingolipid synthesis pathway. S1P phosphatase 1 is important for skin homeostasis, but little is known about the functional role of S1P phosphatase 2. To identify the functions of S1P phosphatase 2 in vivo, we studied mice with the Sgpp2 gene deleted. In contrast to Sgpp1-/- mice, Sgpp2-/- mice had normal skin and were viable into adulthood. Unexpectedly, WT mice expressed Sgpp2 mRNA at high levels in pancreatic islets when compared with other tissues. Sgpp2-/- mice had normal blood insulin levels and pancreatic islet size; however, Sgpp2-/- mice treated with a high-fat diet (HFD) had significantly lower blood insulin levels and smaller pancreatic islets compared with WT mice. The smaller islets in the HFD-treated Sgpp2-/- mice had a significantly lower adaptive B-cell proliferation rate in response to the diet compared with HFD-treated WT mice. Importantly, B-cells from Sgpp2-/- mice fed a normal diet showed significantly increased expression of proteins characteristic of the endoplasmic reticulum (ER) stress response compared with B-cells from WT mice. Our results suggest that Sgpp2 deletion causes B-cell ER stress, which is a known cause of B-cell dysfunction, and reveal a novel juncture in the sphingolipid recycling pathway that could impact the development of diabetes. Three replications of Mouse (WT vs KO) that were treated with with Normal and HFD foods.

2016-07-25 | E-GEOD-73131 | biostudies-arrayexpress

Hepatic gene expression profiling in AHNAK KO mice

Project description:To identify molecular mechanism underlying the protection from diet-induced hepatic steatosis in AHNAK deficiency mice, we examined microarray analysis with liver sample from HFD-fed AHNAK KO and WT mice. Two-condition experiment, regular chow (CD) -fed WT vs. CD-fed AHNAK KO and High fat diet(HFD)-fed WT vs. HFD-fed AHNAK KO mice. Biological replicates: 3 control, One replicate per array.

2015-06-23 | E-GEOD-70119 | biostudies-arrayexpress

Hepatic gene expression profiles after long-term high-fat diet feeding in wild type and Nrf2 knock-out mice.

Project description:To assess the role of the transcription factor NFE2 related factor 2 like 2 ( Nrf2) in the development of high-fat diet (HFD)-induced obesity and non-alcoholic HFD-induced fatty liver disease, 8 wild type (WT) and 8 Nrf2 knock-out (Nrf2-KO) C57BL6J male mice (obtained from Riken BRC, Tsukuba, Japan and originally developed by Prof. M. Yamamoto) were fed an HFD (60 kcal % fat) for 180 days. Whole genome microarray expression profiling was performed in pooled liver samples of WT and Nrf2-KO mice to identify genes that are differentially expressed between WT and Nrf2-KO mice under the stress conditions of HFD-induced obesity. Liver samples were taken from 8 wild type (WT) and 8 Nrf2 knock-out (Nrf2-KO) male mice on high-fat diet (60 kcal % fat) for 180 days. Total RNA was isolated from pooled liver samples from WT or Nrf2-KO mice to produce 4 samples each using the guanidinium thiocyanate method.

2011-11-30 | E-GEOD-33575 | biostudies-arrayexpress

Gene expression profile at single cell level of islet cells from CD and HFD mice

Project description:High-throughput scRNA-seq transcriptionally profiled an estimated 15093 cells from CD islets and 18906 from HFD islets. The mean number of reads per sequenced cell was 43,301 for CD islets and 33,867 for HFD islets, while the median number of genes per sequenced cell was 2105 and 1775, respectively.

2022-11-30 | GSE203376 | GEO

Hepatic gene expression profiles after long-term high-fat diet feeding in wild type and Nrf2 knock-out mice.

2011-11-30 | GSE33575 | GEO

Divergent Compensatory Responses to High Fat Diet Between C57BL6/J and C57BLKs/J Inbred Mouse Strains

Project description:To assess whether changes in islet gene expression contribute to differences in phenotypes in response to high fat diet or tretament with pioglitazone, Agilent Whole Mouse Genome Oligo Microarrays were performed on RNA isolated from islets of 4 mice per each treatment group for discovery analysis of gene expression. Male 8 week-old BL6 and BLKS mice were fed normal chow (18% kcal from fat), HFD (42% kcal from fat), or HFD supplemented with the PPAR-Î³ agonist pioglitazone (PIO) (140 mg PIO/kg diet) for 16 weeks.

2013-09-21 | E-GEOD-51055 | biostudies-arrayexpress

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