Evidence map›Paper›PMID 28804981›Full record

ArticleJournal of diabetes investigation2017

Lipopolysaccharide inhibits hepatic gluconeogenesis in rats: The role of immune cells.

Hiroshi Tanaka, Yoshikazu Nishikawa, Toru Fukushima, Ataru Taniguchi, Yoshihito Fujita, Kinsuke Tsuda, Nobuya Inagaki, Masaya Hosokawa

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Deletion of complement factor 5 amplifies glucose intolerance in obese male but not female mice.American journal of physiology. Endocrinology and metabolism · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Anti-Inflammatory and Antioxidant Properties of Black Mulberry (Oxidative medicine and cellular longevity · 2018
    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

8 authors at 5 institutions in 1 country.

Hiroshi TanakaFaculty of Human Sciences, Tezukayama Gakuin University, Osaka, Japan.
Yoshikazu NishikawaDepartment of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, Osaka, Japan.
Toru FukushimaDepartment of Endocrinology, Metabolism and Diabetes, Hirakata Kohsai Hospital, Osaka, Japan.
Ataru TaniguchiDivision of Diabetes and Endocrinology, Kyoto Preventive Medical Center, Kyoto, Japan.
Yoshihito FujitaDepartment of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kinsuke TsudaFaculty of Human Sciences, Tezukayama Gakuin University, Osaka, Japan.
Nobuya InagakiDepartment of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID http://orcid.org/0000-0001-8261-2593
Masaya HosokawaFaculty of Human Sciences, Tezukayama Gakuin University, Osaka, Japan.ORCID http://orcid.org/0000-0002-2336-9113
Tezukayama Gakuin University · JPKyoto University · JPKyoto Medical Center · JPMunicipal Hirakata City Hospital · JPOsaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AIMS/

introductionBacterial septicemia has diverse clinical symptoms including severe hypoglycemia. However, sepsis-induced hypoglycemia has not yet been examined in detail. The aim of the present study was to investigate the mechanisms underlying hypoglycemia in sepsis. MATERIALS AND

methodsWe induced endotoxin shock in rats using lipopolysaccharide (LPS). After an intraperitoneal injection of LPS, we measured gluconeogenesis using the pyruvate tolerance test. The effects of LPS on glucose metabolism were investigated in perfused livers and isolated hepatocytes. Furthermore, its effects on the production of inflammatory cytokines were examined in isolated splenocytes. The interaction between splenocytes and hepatocytes in response to LPS was investigated in vitro using a co-culture of splenocytes and hepatocytes.

resultsIn the pyruvate tolerance test, the pretreatment with LPS decreased gluconeogenesis. The in vivo pretreatment of rats with LPS did not inhibit glucose production in perfused livers. The in vitro treatment of isolated hepatocytes with LPS did not decrease hepatic gluconeogenesis. Although LPS increased the production of inflammatory cytokines (tumor necrosis factor-α, interferon-γ, interleukin-1β, interleukin-6 and interleukin-10) and nitric oxide in isolated splenocytes, only nitric oxide significantly inhibited gluconeogenesis in isolated hepatocytes. When splenocytes and hepatocytes were co-cultured in medium containing LPS, the messenger ribonucleic acid expression of glucose-6-phosphatase in hepatocytes was suppressed.

conclusionsLPS reduced hepatic gluconeogenesis, at least in part, by stimulating the production of nitric oxide in splenocytes. This effect could contribute to the mechanisms responsible for septicemia-induced hypoglycemia.

Indexed as

LipopolysaccharideLiverSpleen

Identifiers

PMID28804981
PMCPMC5934270
OpenAlexW2748648904

What OpenQuestion holds

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LicenceCC BY-NC
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.