Evidence map›Paper›PMID 20236939›Full record

ArticleThe Journal of biological chemistry2010

Insulin-dependent diabetes mellitus in mice does not alter liver heparan sulfate.

Joseph R Bishop, Erin Foley, Roger Lawrence, Jeffrey D Esko

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. The heparan sulfate proteoglycan grip on hyperlipidemia and atherosclerosis.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Reduced sulfation of chondroitin sulfate but not heparan sulfate in kidneys of diabetic db/db mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013
    Article
  9. The regulation of ApoB metabolism by insulin.Trends in endocrinology and metabolism: TEM · 2013
    Review
  10. Article
  11. Diabetic nephropathy and extracellular matrix.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012
    Review
  12. Article
  13. Article
  14. Review
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.

Joseph R BishopDepartment of Cellular and Molecular Medicine, Glycobiology Research and Training Center, University of California, San Diego, La Jolla, California 92093, USA.
Erin Foley
Roger Lawrence
Jeffrey D Esko
University of California, San Diego · US

Funding

GENETIC CONTROL OF PROTEOGLYCAN METABOLISMR37GM033063 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D · 2000 to 2010
$3.9M
LIPID METABOLISM IN ANIMAL CELLSR01GM033063 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D · 1985 to 2019
$3.4M
NIGMS NIH HHS GM33063NIGMS NIH HHS R01 GM033063NIGMS NIH HHS R37 GM033063
6 · The paper itself

Abstract

Diabetes -associated hyperlipidemia is generally attributed to reduced clearance of plasma lipoproteins, especially remnant lipoproteins enriched in cholesterol and triglycerides. Hepatic clearance of remnants occurs via low density lipoprotein receptors and the heparan sulfate proteoglycan, syndecan-1. Previous studies have suggested alterations in heparan sulfate proteoglycan metabolism in rat and mouse diabetic models, consistent with the idea that diabetic dyslipidemia might be caused by alterations in proteoglycan expression in the liver. In this study we analyzed the content and composition of liver heparan sulfate in streptozotocin-induced insulin-deficient diabetic mice that displayed fasting hypertriglyceridemia and delayed clearance of dietary triglyceride-rich lipoproteins. No differences between normal and diabetic littermates in liver heparan sulfate content, sulfation, syndecan-1 protein levels, or affinity for heparin-binding ligands, such as apolipoprotein E or fibroblast growth factor-2, were noted. Decreased incorporation of [(35)S]sulfate in insulin-deficient mice in vivo was observed, but the decrease was due to increased plasma inorganic sulfate, which reduced the efficiency of labeling of liver heparan sulfate. These results show that hyperlipidemia in insulin-deficient mice is not due to changes in hepatic heparan sulfate composition.

Indexed as

AnimalsAntibiotics, AntineoplasticApolipoproteins EBlood GlucoseDiabetes Mellitus, Type 1Fibroblast Growth Factor 2Heparan SulfateHypertriglyceridemiaLiverMaleMiceMice, Inbred C57BLMice, KnockoutSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationStreptozocinSulfotransferasesAntibiotics, AntineoplasticApolipoproteins EBlood GlucoseFibroblast Growth Factor 2Heparan Sulfateheparitin sulfotransferaseStreptozocinSulfotransferasesSyndecan-1

Identifiers

PMID20236939
PMCPMC2863227
OpenAlexW2041550495

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.