Evidence map›Paper›PMID 23571713›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

Excessive fructose intake causes 1,25-(OH)(2)D(3)-dependent inhibition of intestinal and renal calcium transport in growing rats.

Veronique Douard, Yves Sabbagh, Jacklyn Lee, Chirag Patel, Francis W Kemp, John D Bogden, Sheldon Lin, Ronaldo P Ferraris

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Secondary Osteoporosis and Metabolic Bone Diseases.Journal of clinical medicine · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Idiopathic Osteoporosis and Nephrolithiasis: Two Sides of the Same Coin?International journal of molecular sciences · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Intestinal Absorption of Fructose.Annual review of nutrition · 2018
    Review
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Veronique DouardDepartment of Pharmacology and Physiology, University of Medicine and Dentistry of New Jersey - New Jersey Medical School, Newark, New Jersey;
Yves Sabbagh
Jacklyn Lee
Chirag Patel
Francis W Kemp
John D Bogden
Sheldon Lin
Ronaldo P Ferraris
Rutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

Protection against radiation-induced damage to intestinal nutrient transportRC1AI078518 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI HOWELL, ROGER W. · 2007 to 2009
$1.1M
NIAID NIH HHS RC1-AI-078518
6 · The paper itself

Abstract

We recently discovered that chronic high fructose intake by lactating rats prevented adaptive increases in rates of active intestinal Ca(2+) transport and in levels of 1,25-(OH)2D3, the active form of vitamin D. Since sufficient Ca(2+) absorption is essential for skeletal growth, our discovery may explain findings that excessive consumption of sweeteners compromises bone integrity in children. We tested the hypothesis that 1,25-(OH)2D3 mediates the inhibitory effect of excessive fructose intake on active Ca(2+) transport. First, compared with those fed glucose or starch, growing rats fed fructose for 4 wk had a marked reduction in intestinal Ca(2+) transport rate as well as in expression of intestinal and renal Ca(2+) transporters that was tightly associated with decreases in circulating levels of 1,25-(OH)2D3, bone length, and total bone ash weight but not with serum parathyroid hormone (PTH). Dietary fructose increased the expression of 24-hydroxylase (CYP24A1) and decreased that of 1α-hydroxylase (CYP27B1), suggesting that fructose might enhance the renal catabolism and impair the synthesis, respectively, of 1,25-(OH)2D3. Serum FGF23, which is secreted by osteocytes and inhibits CYP27B1 expression, was upregulated, suggesting a potential role of bone in mediating the fructose effects on 1,25-(OH)2D3 synthesis. Second, 1,25-(OH)2D3 treatment rescued the fructose effect and normalized intestinal and renal Ca(2+) transporter expression. The mechanism underlying the deleterious effect of excessive fructose intake on intestinal and renal Ca(2+) transporters is a reduction in serum levels of 1,25-(OH)2D3. This finding is significant because of the large amounts of fructose now consumed by Americans increasingly vulnerable to Ca(2+) and vitamin D deficiency.

Indexed as

25-Hydroxyvitamin D3 1-alpha-HydroxylaseAge FactorsAnimalsBone and BonesBone DevelopmentCalcitriolCalciumFructoseGene Expression Regulation, EnzymologicGlucaric AcidIntestinal AbsorptionIntestinal MucosaIntestinesKidneyMaleRandom Allocation25-Hydroxyvitamin D3 1-alpha-HydroxylaseCalcitriolCalciumCyp24a1 protein, ratFructoseGlucaric AcidSteroid HydroxylasesVitamin D3 24-HydroxylaseboneFGF23growthintestinekidneyparathyroid hormonevitamin D

Identifiers

PMID23571713
PMCPMC3680696
OpenAlexW2150863184

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.