ReviewPflugers Archiv : European journal of physiology2006
Cellular location of insulin-triggered signals and implications for glucose uptake.
Review in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Effects of quercetin on polycystic ovary syndrome in animal models: a systematic review and meta-analysis.Reproductive biology and endocrinology : RB&E · 2024Pooled it
- 1,25(OH)Molecular and cellular biochemistry · 2018Article
- Ligand Screening Systems for Human Glucose Transporters as Tools in Drug Discovery.Frontiers in chemistry · 2018Review
- An actin filament population defined by the tropomyosin Tpm3.1 regulates glucose uptake.Traffic (Copenhagen, Denmark) · 2015Article
- Role of protein tyrosine phosphatases in the modulation of insulin signaling and their implication in the pathogenesis of obesity-linked insulin resistance.Reviews in endocrine & metabolic disorders · 2014Review
- Endometrial signaling pathways during ovarian stimulation for assisted reproduction technology.Fertility and sterility · 2013Article
- Arp2/3- and cofilin-coordinated actin dynamics is required for insulin-mediated GLUT4 translocation to the surface of muscle cells.Molecular biology of the cell · 2010Article
- Changes in the expression of insulin signaling pathway molecules in endometria from polycystic ovary syndrome women with or without hyperinsulinemia.Molecular medicine (Cambridge, Mass.) · 2010Article
- Impaired microvascular perfusion: a consequence of vascular dysfunction and a potential cause of insulin resistance in muscle.American journal of physiology. Endocrinology and metabolism · 2008 · on this mapReview
- Phosphoinositides in insulin action on GLUT4 dynamics: not just PtdIns(3,4,5)P3.American journal of physiology. Endocrinology and metabolism · 2008Review
- Phosphatidylinositol 3-phosphate [PtdIns3P] is generated at the plasma membrane by an inositol polyphosphate 5-phosphatase: endogenous PtdIns3P can promote GLUT4 translocation to the plasma membrane.Molecular and cellular biology · 2006Article
- Glucose transporter 4: cycling, compartments and controversies.EMBO reports · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin stimulation of glucose uptake into muscle and fat cells requires movement of GLUT4-containing vesicles from intracellular compartments to the plasma membrane. Accordingly, insulin-derived signals must arrive at and be recognized by the appropriate intracellular GLUT4 pools. We describe the insulin signals participating in GLUT4 translocation, and review evidence that they are recruited to intracellular membranes in conjunction with cytoskeletal elements. Such segregation may facilitate the encounter between signals and target vesicles. In most animal and cellular models of insulin resistance, insulin-stimulated GLUT4 translocation to the plasma membrane is reduced. Insulin resistance caused by oxidative stress does not affect early insulin signals, rather their intracellular localization is altered. In this and several other insulin-resistant states, insulin-induced actin remodelling is concomitantly diminished. We summarize evidence suggesting that spatial localization of signals is critical for efficient insulin action, and that the cytoskeleton may act as a scaffold to promote efficient translocation of GLUT4 to the cell surface.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.