Evidence map›Paper›PMID 29802679›Full record

Trial reportJournal of diabetes investigation2019

Soluble CD163 correlates with lipid metabolic adaptations in type 1 diabetes patients during ketoacidosis.

Mads Svart, Nikolaj Rittig, Niels Møller, Holger J Møller, Henning Gronbaek

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Journal of diabetes investigation, 2019. 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
0.9field-weighted citation impact, top 22% 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, 11 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Targeting of CD163International journal of molecular sciences · 2020
    Review
  7. Review
  8. 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

5 authors at 2 institutions in 1 country.

Mads SvartDepartment of Internal Medicine and Endocrinology (MEA) and Medical Research Laboratory, Aarhus University Hospital, Aarhus C, Denmark.ORCID http://orcid.org/0000-0002-9574-0612
Nikolaj RittigDepartment of Internal Medicine and Endocrinology (MEA) and Medical Research Laboratory, Aarhus University Hospital, Aarhus C, Denmark.
Niels MøllerDepartment of Internal Medicine and Endocrinology (MEA) and Medical Research Laboratory, Aarhus University Hospital, Aarhus C, Denmark.
Holger J MøllerDepartment of Clinical Biochemistry, Aarhus University Hospital, Aarhus N, Denmark.
Henning GronbaekDepartment of Hepatology and Gastroenterology, Aarhus University, Aarhus C, Denmark.
Aarhus University Hospital · DKAarhus University · DK

Funding

Danish Council for Strategic Research Funding 0603-00479BDanish Council for Strategic Research Funding 092797Danish Council for Strategic Research Funding 10-092797NOVO Nordisk FoundationSavvaerksejer Jeppe Juhl og hustru Ovita Juhls mindelegat
6 · The paper itself

Abstract

introductionDiabetic ketoacidosis (DKA) is associated with inflammation and increased lipolysis. The macrophage activation marker, soluble CD163 (sCD163), is associated with obesity, non-alcoholic fatty liver disease and type 2 diabetes. We aimed to investigate whether sCD163 correlates with key elements of lipolysis in type 1 diabetes patients during mild DKA. MATERIALS AND

methodsWe investigated nine patients with type 1 diabetes twice during: (i) euglycemic control conditions and a bolus of saline; and (ii) hyperglycemic ketotic conditions induced by lipopolysaccharide administration combined with insulin deprivation. Blood samples, indirect calorimetry, palmitate tracer and adipose tissue biopsies were used to investigate lipid metabolism.

resultsWe observed a significant increase in plasma sCD163 levels after lipopolysaccharide exposure (P < 0.001). Concentrations of sCD163 were positively correlated with plasma concentrations of free fatty acids, palmitate rate of appearance and lipid oxidation rates, and negatively correlated to the expression of G0/G1 switch 2 gene messenger ribonucleic acid content in adipose tissue (P < 0.01 for all). Furthermore, sCD163 levels correlated positively with plasma peak concentrations of cortisol, glucagon, tumor necrosis factor-α, interleukin-6 and interleukin-10 (P < 0.01 for all). Data on lipolysis and inflammation have previously been published.

conclusionsMacrophage activation assessed by sCD163 might play an important role in DKA, as it correlates strongly with important components of lipid metabolism including free fatty acids, palmitate, lipid oxidation, G0/G1 switch 2 gene and pro-inflammatory cytokines during initial steps of DKA. These results are novel and add important knowledge to the field of DKA.

Indexed as

Lipid MetabolismAdultAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenDiabetes Mellitus, Type 1Diabetic KetoacidosisHumansInflammationInflammation MediatorsLipopolysaccharidesMaleReceptors, Cell SurfaceYoung AdultAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenInflammation MediatorsLipopolysaccharidesReceptors, Cell SurfaceG0/G1 switch 2 geneKetoacidosisSoluble CD163

Identifiers

PMID29802679
PMCPMC6319477
OpenAlexW2804808186

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Registered trials

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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.