ArticleThe Journal of physiology2005
Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Inappropriate Diet Exacerbates Metabolic Dysfunction-Associated Steatotic Liver Disease via Abdominal Obesity.Nutrients · 2024Pooled it
- Copper inhibits P2Y(2)-dependent Ca(2+) signaling through the effects on thapsigargin-sensitive Ca(2+) stores in HTC hepatoma cells.Biochemical and biophysical research communications · 2010Article
- Liver TAG transiently decreases while PL n-3 and n-6 fatty acids are persistently elevated in insulin resistant mice.Lipids · 2008Article
- Evidence for AMPK-dependent regulation of exocytosis of lipoproteins in a model liver cell line.Experimental cell research · 2008Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The initial response of liver cells to insulin is mediated through exocytosis of Cl- channel-containing vesicles and a subsequent opening of plasma membrane Cl- channels. Intracellular accumulation of fatty acids leads to profound defects in metabolism, and is closely associated with insulin resistance. It is not known whether the activity of Cl- channels is altered in insulin resistance and by which mechanisms. We studied the effects of fatty acid accumulation on Cl- channel opening in a model liver cell line. Overnight treatment with amiodarone increased the fat content by approximately 2-fold, and the rates of gluconeogenesis by approximately 5-fold. The ability of insulin to suppress gluconeogenesis was markedly reduced indicating that amiodarone treatment induces insulin resistance. Western blot analysis showed that these cells express the same number of insulin receptors as control cells. However, insulin failed to activate exocytosis and Cl- channel opening. These inhibitory effects were mimicked in control cells by exposures to arachidonic acid (15 microm). Further studies demonstrated that fatty acids stimulate the PKC activity, and inhibition of PKC partially restored exocytosis and Cl- channel opening in insulin-resistant cells. Accordingly, activation of PKC with PMA in control cells potently inhibited the insulin responses. These results suggest that stimulation of PKC activity in insulin resistance contributes to the inhibition of cellular responses to insulin in liver cells.
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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 Socratic graph.