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Insulin response in mouse liver

ABSTRACT: Proteomics of mouse liver over a period of four hours after insulin administration. It is part of a larger project that contains multi-omic datasets.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Fumiko Matsuzaki

LAB HEAD: Hiroyuki Kubota

PROVIDER: PXD022728 | Pride | 2021-08-25

REPOSITORIES: Pride

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			Action	DRS
	ExperimentalDesignTemplate_proteomics.txt	Txt
	checksum.txt	Txt
	modificationSpecificPeptides.txt	Txt
	orb_151028_AB-FM-7_No1.raw	Raw
	orb_151028_AB-FM-7_No10.raw	Raw

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Publications

An extensive and dynamic trans-omic network illustrating prominent regulatory mechanisms in response to insulin in the liver.

Matsuzaki Fumiko F Uda Shinsuke S Yamauchi Yukiyo Y Matsumoto Masaki M Soga Tomoyoshi T Maehara Kazumitsu K Ohkawa Yasuyuki Y Nakayama Keiichi I KI Kuroda Shinya S Kubota Hiroyuki H

Cell reports 20210801 8

An effective combination of multi-omic datasets can enhance our understanding of complex biological phenomena. To build a context-dependent network with multiple omic layers, i.e., a trans-omic network, we perform phosphoproteomics, transcriptomics, proteomics, and metabolomics of murine liver for 4 h after insulin administration and integrate the resulting time series. Structural characteristics and dynamic nature of the network are analyzed to elucidate the impact of insulin. Early and promine ...[more]

PMID: 34433063

Similar Datasets

Insulin response in mouse liver

Project description:Phosphoproteomics of mouse liver over a period of four hours after insulin administration. It is part of a larger project that contains multi-omic datasets.

2021-08-25 | PXD022823 | Pride

Insulin response in mouse liver

Project description:An effective combination of multi-omic datasets can enhance our understanding of complex biological phenomena. To build a context-dependent network with multiple omic layers, i.e., a trans-omic network, we performed phosphoproteomics, transcriptomics, proteomics, and metabolomics of murine liver for 4 h after insulin administration and integrated the time series. Structural characteristics and dynamic nature of the network were analyzed to elucidate the impact of insulin. Early and prominent changes in protein phosphorylation and persistent and asynchronous changes in mRNA and protein levels through non-transcriptional mechanisms indicate enhanced crosstalk between phosphorylation-mediated signaling and protein expression regulation. Metabolic response shows different temporal regulation with transient increases at early time points across categories and enhanced response in the amino acid and nucleotide categories at later time points due to process convergence. This extensive and dynamic view of the trans-omic network elucidates prominent regulatory mechanisms that drive insulin responses through intricate interlayer coordination.

2021-08-24 | GSE166336 | GEO

Gene expression profile in the liver of insulin-deficient mice with icv leptin administration

2013-09-03 | GSE48598 | GEO

Gene expression profile in the liver of insulin-deficient mice with icv leptin administration

Project description:Analysis of gene expression in the liver of insulin-deficient mice regulated by icv leptin administration. Control group received icv PBS administration. Icv leptin administration ameliorates hyperglycemia in insulin-deficient mice. Our transcriptome data provides important aspects of the leptin’s anti-type 1 diabetes action. Mice were harvested 10 days after icv leptin administration (25ng/0.11uL/hour). Liver samples were quickly removed, frozen in liquid nitrogen and subsequently stored at –80ºC. RNAs were extracted by Qiagen mRNA extract kits (RNeasy plus). gDNA was eliminated in this procedure by gDNA eliminator column, which is included in Qiagen mRNA extract kits. Genomics and Microarray Core Facility at UT-Southwestern (http://microarray.swmed.edu/) checked RNA quality with Bioanalyzer Chip and processed the samples for hybridization with Illumina Mouse-6 V2 BeadChip (Illumina Inc., San Diego, CA).

2013-09-03 | E-GEOD-48598 | biostudies-arrayexpress

Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

Project description:Glucagon and insulin are counter-regulatory pancreatic hormones that precisely control blood glucose homeostasis1. Type 2 diabetes mellitus (T2DM) is characterized by inappropriately elevated blood glucagon2-5 levels as well as insufficient glucose stimulated insulin secretion (GSIS) by pancreatic ß-cells6. Early in the pathogenesis of T2DM, hyperglucagonemia is observable antecedent to ß-cell dysfunction7-9; and in mice, liver-specific activation of glucagon receptor-dependent signaling results in impaired GSIS10. However, the mechanistic relationship between hyperglucagonemia, hepatic glucagon action, and ß-cell dysfunction remains poorly understood. Here we show that glucagon action stimulates hepatic production of the neuropeptide kisspeptin1, which acts in an endocrine manner on ß-cells to suppress GSIS. In vivo glucagon administration acutely stimulates hepatic kisspeptin1 production, and kisspeptin1 is increased in livers from humans with T2DM and from mouse models of diabetes mellitus. Synthetic kisspeptin1 potently suppresses GSIS in vivo and in vitro from normal isolated islets, which express the kisspeptin1 receptor Kiss1R. Administration of a Kiss1R antagonist in diabetic Leprdb/db mice potently augments GSIS and reduces glycemia. Our observations indicate in the pathogenesis of T2DM an endocrine mechanism sequentially linking hyperglucagonemia via hepatic kisspeptin1 production to impaired insulin secretion. In addition, our findings suggest Kiss1R antagonism as a therapeutic avenue to improve ß-cell function in T2DM. Total RNA from L-Δprkar1a KO mice compared to control D-glucose mice

2014-04-01 | E-GEOD-48815 | biostudies-arrayexpress

Transcriptional alterations in response to insulin and glucagon in the murine liver

Project description:The analysis identified 122 genes displaying responses to insulin and/or glucagon administration in the liver of WT male mice. Of 122 genes, 75 genes responded in a insulin-selected manner, 29 genes in a glucagon-selected manner, and 18 genes were regulated by both of insulin and glucagon 60 min after stimulation with each hormone. Insulin upregulated expression of 45 genes including Btg2, Ddit4, and Rasgef1b, downregulated 30 genes such as Arrdc3 Rgs16, and Txnip. Glucagon upregulated expression of 15 genes including Chordc1 and Gck, and downregulated expression of 14 genes such as Mt2 and Lcn2. Seventeen genes showed transcriptional upregulation in response to both insulin and glucagon including Hspa1b, Nr4a1 Trp53inp1, and one gene, Orm2, displayed downregulation after stimulation of insulin or glucagon.

2018-03-06 | GSE111407 | GEO

Deletion of the mitochondrial peptidase miPEP in adipose tissue protects against obesity and insulin resistance by increasing adaptive thermogenesis

Project description:Mitochondria are pivotal for cellular metabolism, serving as sources and targets of nutrient intermediates from converging metabolic pathways. Here, we demonstrate that insulin resistance leads to a marked alteration in the mitochondrial proteome of adipocytes. Analysis across multiple insulin resistance models revealed a consistent decrease in the level of the mitochondrial processing peptidase miPEP, suggesting a potential role for miPEP in the aetiology of insulin resistance. Adipocyte specific miPEP knockout mice demonstrated a strong phenotype marked by a browning-independent increment in energy expenditure, enhanced insulin sensitivity, and reduced adiposity, despite normal food intake and physical activity. These phenotypes vanished when mice were housed at thermoneutrality suggesting that miPEP deletion triggers a compensatory enhancement in thermogenesis protecting against metabolic dysfunction. Tissue specific analysis of miPEP deficient mice revealed a selective increment in muscle metabolism evidenced by increased basal and insulin induced glucose uptake and upregulation of the protein Fbp2, involved in energy wasting via futile cycling. These findings suggest that miPEP deletion initiates a compensatory increase in thermogenesis, acting as a protective mechanism against diet-induced insulin resistance.

2024-08-10 | PXD051606 | Pride

RNA-seq of precision cut liver slice (PCLS) culture treated with increasing amounts of alpha-linolenic acid and insulin

Project description:This experiment was designed to test the effect of alpha-linolenic acid (ALA) and insulin on liver slices prepared from Atlantic salmon. Liver slices were incubated with increasing concentrations of ALA and insulin from 20µM to 100µM and 10nM to 100nM, respectively. RNA was subsequently sequenced and response was evaluated and compared to the expected response from Atlantic salmon feeding trials. The purpose of this was to evaluate liver slice culture as a cell culture system for studying lipid metabolism in Atlantic salmon.

2019-05-08 | E-MTAB-7366 | biostudies-arrayexpress

Quantitative proteomics of intestinal mucosa from male mice lacking intestinal epithelial insulin receptors

Project description:The goal of the present study was to determine whether loss of the insulin receptor alters the molecular landscape of the intestinal mucosa, using intestinal-epithelial insulin receptor knockout (IE-irKO) mice and both genetic (IRfl/fl and Villin-cre) controls. Quantitative proteomic analysis by Liquid Chromatography Mass Spectrometry (LC-MS) was deployed on jejunal and colonic mucosa from mice fed a chow- or Western diet (WD). Jejunal mucosa from IE-irKO mice demonstrated alterations in all intestinal cell linages, Paneth, goblet, absorptive and enteroendocrine cells, whereas only goblet and absorptive cells were affected in the colon. There was also a significant effect of the WD on the gut proteome. A significant reduction was detected in Paneth cell proteins with anti-microbial activity, including lysozyme C-1, angiogenin-4, cryptdin-related sequence1C-3 and -2, a-defensin 17 and intelectin-1a. The key protein expressed by goblet cells, mucin-2, was also reduced in the IE-irKO mice. Proteins involved in lipid metabolism, including aldose reductase-related protein 1, 15-hydroxyprostaglandin dehydrogenase [NAD(+)], apolipoprotein A-II and pyruvate dehydrogenase kinase isozyme 4, were increased in the mucosa of WD-fed IE-irKO mice as compared to controls. In contrast, expression of the nutrient-responsive gut hormones, glucose-dependent insulinotropic polypeptide and neurotensin, was reduced in the jejunal mucosa of IE-irKO mice, and there was a reduction in proteins of the P-type ATPases and the solute carrier-transporter family in the colon of WD-fed IE-irKO mice. In conclusion, IE-irKO mice display a distinct molecular phenotype, suggesting a biological role of insulin and its receptor in determining differentiated cell-specificity in the intestinal epithelium.

2017-08-18 | PXD005932 | Pride

RNA-seq of precision cut liver slice (PCLS) culture before slicing and up to 9 days after slicing, changing media either every day or every 3 days, with insulin

Project description:This experiment is designed to test the effect of culture time, media change regime, and insulin on liver slices. Samples were taken before slicing and 3, 4, 5, 6, 7, 8, and 9 days after slicing. Samples had media changed either every day or every three days and insulin was included in the media at 20nM concentration.

2019-05-08 | E-MTAB-7367 | biostudies-arrayexpress

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