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Insulin response in mouse liver

ABSTRACT: 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.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Fumiko Matsuzaki

LAB HEAD: Hiroyuki Kubota

PROVIDER: PXD022823 | Pride | 2021-08-25

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	ExperimentalDesignTemplate_phosphoproteomics.txt	Txt
	PhosphoSTYSites.txt	Txt
	checksum.txt	Txt
	modificationSpecificPeptides.txt	Txt
	orb_160427_AB-FM_1-1.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

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Insulin response in mouse liver

Project description: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.

2021-08-25 | PXD022728 | 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

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Phosphoproteomics of consecuively active AKT in liver and Insulin stimulated primary Hepatocytes

Project description:Liver mitochondria play a central role in metabolic adaptations to changing nutritional states, yet their dynamic regulation upon anticipated changes in the energy state has remained unaddressed. Here, we show that sensory food perception rapidly induces mitochondrial fission in the liver via protein kinase B/AKT-dependent phosphorylation of serine 131 of the Mitochondrial fission factor (MFFS131), a response mediated via activation of hypothalamic Pro-opiomelanocortin (POMC)-expressing neurons. A non-phosphorylatable MFFS131G knock-in mutation abrogates AKT-induced mitochondrial fragmentation in vitro. In vivo, MFFS131G knock-in mice display altered liver mitochondrial dynamics upon refeeding and impaired insulin stimulated suppression of gluconeogenesis. Collectively, we reveal a critical role for rapid activation of a hypothalamic/liver axis to adapt mitochondrial function to anticipated changes of nutritional state in control of hepatic glucose metabolism. R26-fl-Akt-C mice Mice carrying a conditional myristoylation tagged Akt-C transgene in the ROSA26 locus were used to activate AKT in the liver with a liver specific Cre-dependent virus. The generation of this line has been described previously (V. Kohlhaas et al, 2021) For AAV mediated liver-specific delivery of Cre, R26-fl-Akt-C or control mice were injected with a AAV8-TBG-iCre virus (VB1724, Vector Biolabs). This repository contains two experiments a) Liver of liver active Akt-CA and b) Insulin stimulation of primary heptocytes. Please note that replicate one of the hepatocyte dataset have been removed from the analysis due to the limited number of posphosites compared to others.

2024-03-28 | PXD049957 | Pride

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

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

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

Insulin-administrated phosphorylation of the CNS proteins in Lymnaea

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