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Search

Probes for INSULIN

ACD can configure probes for the various manual and automated assays for INSULIN for RNAscope Assay, or for Basescope Assay compatible for your species of interest.

Your search for "insulin" returned results. Search for our Top genes LGR5, vglut2, gad67, brca1

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    Gene

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    Category

    • Publications (3) Apply Publications filter
    VEGF-B ablation in pancreatic?-cells upregulates insulin expression without affecting glucose homeostasis or islet lipid uptake

    Sci Rep

    2020 Jan 22

    Ning FC1, Jensen N1, Mi J1, Lindstr�m W1, Balan M1, Muhl L1, Eriksson U1, Nilsson I1, Nyqvist D2.
    PMID: 31969592 | DOI: 10.1038/s41598-020-57599-2

    Type 2 diabetes mellitus (T2DM) affects millions of people and is linked with obesity and lipid accumulation in peripheral tissues. Increased lipid handling and lipotoxicity in insulin producing ?-cells may contribute to ?-cell dysfunction in T2DM. The vascular endothelial growth factor (VEGF)-B regulates uptake and transcytosis of long-chain fatty acids over the endothelium to tissues such as heart and skeletal muscle. Systemic inhibition of VEGF-B signaling prevents tissue lipid accumulation, improves insulin sensitivity and glucose tolerance, as well as reduces pancreatic islet triglyceride content, under T2DM conditions. To date, the role of local VEGF-B signaling in pancreatic islet physiology and in the regulation of fatty acid trans-endothelial transport in pancreatic islet is unknown. To address these questions, we have generated a mouse strain where VEGF-B is selectively depleted in ?-cells, and assessed glucose homeostasis, ?-cell function and islet lipid content under both normal and high-fat diet feeding conditions. We found that Vegfb was ubiquitously expressed throughout the pancreas, and that ?-cell Vegfb deletion resulted in increased insulin gene expression. However, glucose homeostasis and islet lipid uptake remained unaffected by ?-cell VEGF-B deficiency
    Reducing VEGF-B Signaling Ameliorates Renal Lipotoxicity and Protects against Diabetic Kidney Disease.

    Cell Metab.

    2017 Feb 01

    Falkevall A, Mehlem A, Palombo I, Heller Sahlgren B, Ebarasi L, He L, Ytterberg AJ, Olauson H, Axelsson J, Sundelin B, Patrakka J, Scotney P, Nash A, Eriksson U.
    PMID: 28190774 | DOI: 10.1016/j.cmet.2017.01.004

    Diabetic kidney disease (DKD) is the most common cause of severe renal disease, and few treatment options are available today that prevent the progressive loss of renal function. DKD is characterized by altered glomerular filtration and proteinuria. A common observation in DKD is the presence of renal steatosis, but the mechanism(s) underlying this observation and to what extent they contribute to disease progression are unknown. Vascular endothelial growth factor B (VEGF-B) controls muscle lipid accumulation through regulation of endothelial fatty acid transport. Here, we demonstrate in experimental mouse models of DKD that renal VEGF-B expression correlates with the severity of disease. Inhibiting VEGF-B signaling in DKD mouse models reduces renal lipotoxicity, re-sensitizes podocytes to insulin signaling, inhibits the development of DKD-associated pathologies, and prevents renal dysfunction. Further, we show that elevated VEGF-B levels are found in patients with DKD, suggesting that VEGF-B antagonism represents a novel approach to treat DKD.

    Hypothalamic POMC or MC4R deficiency impairs counterregulatory responses to hypoglycemia in mice.

    Molecular Metabolism

    2018 Nov 20

    Tooke BP, Yu H, Adams JM, Jones GL, Sutton-Kennedy T, Mundada L, Qi NR, Low MJ, Chhabra KH.
    PMID: - | DOI: 10.1016/j.molmet.2018.11.004

    Abstract

    Objective

    Life-threatening hypoglycemia is a major limiting factor in the management of diabetes. While it is known that counterregulatory responses to hypoglycemia are impaired in diabetes, molecular mechanisms underlying the reduced responses remain unclear. Given the established roles of the hypothalamic proopiomelanocortin (POMC)/melanocortin 4 receptor (MC4R) circuit in regulating sympathetic nervous system (SNS) activity and the SNS in stimulating counterregulatory responses to hypoglycemia, we hypothesized that hypothalamic POMC as well as MC4R, a receptor for POMC derived melanocyte stimulating hormones, is required for normal hypoglycemia counterregulation.

    Methods

    To test the hypothesis, we induced hypoglycemia or glucopenia in separate cohorts of mice deficient in either POMC or MC4R in the arcuate nucleus (ARC) or the paraventricular nucleus of the hypothalamus (PVH), respectively, and measured their circulating counterregulatory hormones. In addition, we performed a hyperinsulinemic-hypoglycemic clamp study to further validate the function of MC4R in hypoglycemia counterregulation. We also measured Pomc and Mc4r mRNA levels in the ARC and PVH, respectively, in the streptozotocin-induced type 1 diabetes mouse model and non-obese diabetic (NOD) mice to delineate molecular mechanisms by which diabetes deteriorates the defense systems against hypoglycemia. Finally, we treated diabetic mice with the MC4R agonist MTII, administered stereotaxically into the PVH, to determine its potential for restoring the counterregulatory response to hypoglycemia in diabetes.

    Results

    Stimulation of epinephrine and glucagon release in response to hypoglycemia or glucopenia was diminished in both POMC- and MC4R-deficient mice, relative to their littermate controls. Similarly, the counterregulatory response was impaired in association with decreased hypothalamic Pomc and Mc4r expression in the diabetic mice, a phenotype that was not reversed by insulin treatment which normalized glycemia. In contrast, infusion of an MC4R agonist in the PVH restored the counterregulatory response in diabetic mice.

    Conclusion

    In conclusion, hypothalamic Pomc as well as Mc4r, both of which are reduced in type 1 diabetic mice, are required for normal counterregulatory responses to hypoglycemia. Therefore, enhancing MC4R function may improve hypoglycemia counterregulation in diabetes.

    X
    Description
    sense
    Example: Hs-LAG3-sense
    Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe.
    Intron#
    Example: Mm-Htt-intron2
    Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection
    Pool/Pan
    Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G)
    A mixture of multiple probe sets targeting multiple genes or transcripts
    No-XSp
    Example: Hs-PDGFB-No-XMm
    Does not cross detect with the species (Sp)
    XSp
    Example: Rn-Pde9a-XMm
    designed to cross detect with the species (Sp)
    O#
    Example: Mm-Islr-O1
    Alternative design targeting different regions of the same transcript or isoforms
    CDS
    Example: Hs-SLC31A-CDS
    Probe targets the protein-coding sequence only
    EnEmProbe targets exons n and m
    En-EmProbe targets region from exon n to exon m
    Retired Nomenclature
    tvn
    Example: Hs-LEPR-tv1
    Designed to target transcript variant n
    ORF
    Example: Hs-ACVRL1-ORF
    Probe targets open reading frame
    UTR
    Example: Hs-HTT-UTR-C3
    Probe targets the untranslated region (non-protein-coding region) only
    5UTR
    Example: Hs-GNRHR-5UTR
    Probe targets the 5' untranslated region only
    3UTR
    Example: Rn-Npy1r-3UTR
    Probe targets the 3' untranslated region only
    Pan
    Example: Pool
    A mixture of multiple probe sets targeting multiple genes or transcripts

    Enabling research, drug development (CDx) and diagnostics

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