Evidence map›Paper›PMID 19492426›Full record

ArticleHepatology (Baltimore, Md.)2009

Lipopolysaccharide inhibition of glucose production through the Toll-like receptor-4, myeloid differentiation factor 88, and nuclear factor kappa b pathway.

Carl F Raetzsch, Natasha L Brooks, J McKee Alderman, Kelli S Moore, Peter A Hosick, Simon Klebanov, Shizuo Akira, James E Bear, Albert S Baldwin, Nigel Mackman and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

41 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Sex-specific effect of P2YFrontiers in endocrinology · 2023
    Article
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  7. Article
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  9. Article
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  11. Journal of clinical medicine · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Accuracy of the point-of-care glucose meter for use in calves.The Journal of veterinary medical science · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Protective Effect of CasperomeFrontiers in pharmacology · 2018
    Article
  20. Lipopolysaccharide Potentiates Insulin-Driven Hypoglycemic Shock.Journal of immunology (Baltimore, Md. : 1950) · 2017
    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

11 authors at 3 institutions in 2 countries.

Carl F RaetzschSchool of Medicine, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC 27599-7461, USA.
Natasha L Brooks
J McKee Alderman
Kelli S Moore
Peter A Hosick
Simon Klebanov
Shizuo Akira
James E Bear
Albert S Baldwin
Nigel Mackman
Terry P Combs
University of North Carolina at Chapel Hill · USColumbia University · USOsaka University · JP

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SUSAN M. SMITH · 1999 to 2026
$31.6M
The effects of adiponectin on liver insulin resistanceK01DK075573 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COMBS, TERRY P. · 2006 to 2008
$344k
NIDDK NIH HHS DK056350NIDDK NIH HHS DK075573NIDDK NIH HHS K01 DK075573
6 · The paper itself

Abstract

unlabelledAcute exposure to lipopolysaccharide (LPS) can cause hypoglycemia and insulin resistance; the underlying mechanisms, however, are unclear. We set out to determine whether insulin resistance is linked to hypoglycemia through Toll-like receptor-4 (TLR4), myeloid differentiation factor 88 (MyD88), and nuclear factor kappaB (NFkappaB), a cell signaling pathway that mediates LPS induction of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha). LPS induction of hypoglycemia was blocked in TLR4(-/-) and MyD88(-/-) mice but not in TNFalpha(-/-) mice. Both glucose production and glucose utilization were decreased during hypoglycemia. Hypoglycemia was associated with the activation of NFkappaB in the liver. LPS inhibition of glucose production was blocked in hepatocytes isolated from TLR4(-/-) and MyD88(-/-) mice and hepatoma cells expressing an inhibitor of NFkappaB (IkappaB) mutant that interferes with NFkappaB activation. Thus, LPS-induced hypoglycemia was mediated by the inhibition of glucose production from the liver through the TLR4, MyD88, and NFkappaB pathway, independent of LPS-induced TNFalpha. LPS suppression of glucose production was not blocked by pharmacologic inhibition of the insulin signaling intermediate phosphatidylinositol 3-kinase in hepatoma cells. Insulin injection caused a similar reduction of circulating glucose in TLR4(-/-) and TLR4(+/+) mice. These two results suggest that LPS and insulin inhibit glucose production by separate pathways. Recovery from LPS-induced hypoglycemia was linked to glucose intolerance and hyperinsulinemia in TLR4(+/+) mice, but not in TLR4(-/-) mice.

conclusionInsulin resistance is linked to the inhibition of glucose production by the TLR4, MyD88, and NFkappaB pathway.

Indexed as

Insulin ResistanceAnimalsBlood GlucoseCell Line, TumorHypoglycemiaLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88NF-kappa BRatsToll-Like Receptor 4Blood GlucoseLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID19492426
PMCPMC2822400
OpenAlexW2104084845

What OpenQuestion holds

Textmetadata
LicenceTDM
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.