Evidence map›Paper›PMID 24407290›Full record

ArticleThe Journal of biological chemistry2014

The metabolic origins of mannose in glycoproteins.

Mie Ichikawa, David A Scott, Marie-Estelle Losfeld, Hudson H Freeze

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

49 citing papers in PubMed, 80 citations in OpenAlex.

  1. Oral D-galactose supplementation in PGM1-CDG.Genetics in medicine : official journal of the American College of Medical Genetics · 2017
    Trial
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  9. Review
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  11. Establishing the link between D-mannose and juvenile grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024
    Article
  12. Article
  13. Frontiers in pharmacology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. D-Mannose prevents bone loss under weightlessness.Journal of translational medicine · 2023
    Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Mie IchikawaHuman Genetics Program, Sanford-Burnham Medical Research Institute, La Jolla, California 92037.
David A ScottCancer Research Center, Sanford-Burnham Medical Research Institute, La Jolla, California 92037.
Marie-Estelle LosfeldHuman Genetics Program, Sanford-Burnham Medical Research Institute, La Jolla, California 92037.
Hudson H FreezeHuman Genetics Program, Sanford-Burnham Medical Research Institute, La Jolla, California 92037. Electronic address: hudson@sanfordburnham.org.
Sanford Burnham Prebys Medical Discovery Institute · US

Funding

Carbohydrate Deficient Glycoprotein Syndromes: Models and TherapyR01DK055615 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FREEZE, HUDSON H. · 1999 to 2013
$4.4M
NIDDK NIH HHS R01 DK055615NIDDK NIH HHS R01DK55615
6 · The paper itself

Abstract

Mannose in N-glycans is derived from glucose through phosphomannose isomerase (MPI, Fru-6-P ↔ Man-6-P) whose deficiency causes a congenital disorder of glycosylation (CDG)-Ib (MPI-CDG). Mannose supplements improve patients' symptoms because exogenous mannose can also directly contribute to N-glycan synthesis through Man-6-P. However, the quantitative contributions of these and other potential pathways to glycosylation are still unknown. We developed a sensitive GC-MS-based method using [1,2-(13)C]glucose and [4-(13)C]mannose to measure their contribution to N-glycans synthesized under physiological conditions (5 mm glucose and 50 μm mannose). Mannose directly provides ∼10-45% of the mannose found in N-glycans, showing up to a 100-fold preference for mannose over exogenous glucose based on their exogenous concentrations. Normal human fibroblasts normally derive 25-30% of their mannose directly from exogenous mannose, whereas MPI-deficient CDG fibroblasts with reduced glucose flux secure 80% of their mannose directly. Thus, both MPI activity and exogenous mannose concentration determine the metabolic flux into the N-glycosylation pathway. Using various stable isotopes, we found that gluconeogenesis, glycogen, and mannose salvaged from glycoprotein degradation do not contribute mannose to N-glycans in fibroblasts under physiological conditions. This quantitative assessment of mannose contribution and its metabolic fate provides information that can help bolster therapeutic strategies for treating glycosylation disorders with exogenous mannose.

Indexed as

Cells, CulturedFibroblastsGas Chromatography-Mass SpectrometryGluconeogenesisGlucoseGlycogenGlycoproteinsGlycosylationHumansMannoseProteolysisGlucoseGlycogenGlycoproteinsMannoseGC-MSGenetic DiseasesGlucose MetabolismGlycoconjugateMetabolic Tracers

Identifiers

PMID24407290
PMCPMC3945336
OpenAlexW2137596099

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.