Evidence map›Paper›PMID 17053032›Full record

ArticleThe Journal of physiology2007

High-fat diet-induced hepatic steatosis reduces glucagon receptor content in rat hepatocytes: potential interaction with acute exercise.

Alexandre Charbonneau, Cecilia G Unson, Jean-Marc Lavoie

Abstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Article
  2. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Autophagy mediates hepatic GRK2 degradation to facilitate glucagon-induced metabolic adaptation to fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  11. Article
  12. Glucagon Receptor Signaling and Glucagon Resistance.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Review
  15. Article
  16. β(2)-Adrenoreceptor blockade improves early posttrauma hyperglycemia and pulmonary injury in obese rats.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  17. Article
  18. Article
  19. Article
  20. Autophagy in pancreatic cancer pathogenesis and treatment.American journal of cancer research · 2012
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Alexandre CharbonneauDepartment of Kinésiologie, Université de Montréal, Montréal, Québec, Canada. alexandre.charbonneau@crchul.ulaval.ca
Cecilia G Unson
Jean-Marc Lavoie

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have revealed that high-fat (HF) diets promote hyperglycaemia, whole-body insulin resistance and non-alcoholic fatty liver disease (NAFLD). Recently, hepatic glucagon resistance has been shown to occur in rats fed a HF diet. More precisely, diet-induced obesity (DIO) reduces the number of hepatic plasma membrane glucagon receptors (GR), which results in a diminished response to glucagon during a hyperglucagonaemic clamp. The present study was undertaken to test the hypothesis that a HF-DIO is associated with a desensitization and destruction of the hepatic GR. We also hypothesized that a single bout of endurance exercise would modify the GR cellular distribution under our DIO model. Male rats were either fed a standard (SD) or a HF diet for two weeks. Each group was subdivided into a non-exercised (Rest) and an acute exercised (EX) group. The HF diet resulted in a reduction of total hepatic GR (55%) and hepatic plasma membrane GR protein content (20%). These changes were accompanied by a significant increase in endosomal and lysosomal GR content with the feeding of a HF diet. The reduction of GR plasma membrane as well as the increase in endosomal GR was strongly correlated with an increase of PKC-alpha, suggesting a role of PKC-alpha in GR desensitization. EX increased significantly PKC-alpha protein content in both diets, suggesting a role of PKC-alpha in EX-induced GR desensitization. The present results suggest that liver lipid infiltration plays a role in reducing glucagon action in the liver through a reduction in total cellular and plasma membrane GR content. Furthermore, the GR desensitization observed in our in vivo model of HF diet-induced hepatic steatosis and in EX individuals may be regulated by PKC-alpha.

Indexed as

Animalsbeta-Adrenergic Receptor KinasesCell MembraneDietary FatsEndosomesFatty LiverGlycogenG-Protein-Coupled Receptor Kinase 2HepatocytesHyperglycemiaLysosomesMaleObesityPhysical ExertionProtein Kinase C-alphaRatsbeta-Adrenergic Receptor KinasesDietary FatsGlycogenG-Protein-Coupled Receptor Kinase 2Grk2 protein, ratProtein Kinase C-alphaReceptors, GlucagonTriglycerides

Identifiers

PMID17053032
PMCPMC2075374

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.