Evidence map›Paper›PMID 33294462›Full record

ArticleJournal of diabetes research2020

The Therapeutic Effect of Active Vitamin D Supplementation in Preventing the Progression of Diabetic Nephropathy in a Diabetic Mouse Model.

Nakhoul Nakhoul, Tina Thawko, Evgeny Farber, Inbal Dahan, Hagar Tadmor, Rola Nakhoul, Anaam Hanut, Ghasan Salameh, Ibrahim Shagrawy, Farid Nakhoul

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Vitamin D and Diabetic Kidney Disease.International journal of molecular sciences · 2023
    Review
  7. Article
  8. The Role of Vitamin D in Diabetic Nephropathy: A Translational Approach.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
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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

10 authors at 3 institutions in 2 countries.

Nakhoul NakhoulThe Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.ORCID https://orcid.org/0000-0002-1163-3968
Tina ThawkoThe Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Evgeny FarberNephrology & Hypertension Division, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Inbal DahanThe Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Hagar TadmorThe Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Rola NakhoulSzeged Faculty of Medicine, Szeged, Hungary.
Anaam HanutNephrology & Hypertension Division, Bar-Ilan University, Ramat Gan, Israel.
Ghasan SalamehThe Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Ibrahim ShagrawyPathology Division, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Farid NakhoulThe Diabetes & Metabolism Lab, Baruch Padeh Poriya Medical Center, Lower Galilee, Israel.
Poriya Medical Center · ILBar-Ilan University · ILUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is one of the most common microvascular complications of diabetes and is the leading cause of end-stage renal disease (ESRD) and replacement therapy worldwide. Vitamin D levels in DN patients are very low due to the decrease in the synthesis and activity of 1-

methodsDiabetes mellitus (DM) was induced in 94 8-week-old DBA/2J mice by intraperitoneal injection of streptozotocin (STZ). DM mice were randomly divided into receiving vehicle or treatment with paricalcitol, the active vitamin D analog, 1 week after DM induction or paricalcitol treatment 3 weeks after DM induction. An additional control group of healthy wild-type mice was not treated. Urine albumin, blood urea nitrogen, and creatinine levels were measured before and at the end of the paricalcitol treatment. Periodic acid-Schiff, immunohistochemistry staining, and western blot of the renal tissues of vitamin D receptor, villin, nephrin, and podocin expressions, were analyzed.

resultsParicalcitol treatment restored villin, nephrin, and podocin protein levels that were downregulated upon DM induction, and reduced fibronectin protein level. Vitamin D receptor activation by paricalcitol may reduce proteinuria of DN in mice and alleviate high-glucose-induced injury of kidney podocytes by regulating the key molecules such nephrin-podocin.

conclusionsParicalcitol treatment was associated with improved structural changes in type 1 diabetic mice including upregulation of vitamin D receptor expression, and decreased fibrosis markers such as fibronectin. These effects may contribute to the consistent benefit of vitamin D analog to slow the deterioration in glomerular function and reduce the risk of ESRD in patients with type 1 and 2 diabetes mellitus. Our results suggest that additional use of paricalcitol may be beneficial in treating patients with diabetes under standard therapeutic strategies.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease ProgressionErgocalciferolsFibronectinsFibrosisKidneyMice, Inbred DBAProteinuriaReceptors, CalcitriolStreptozocinErgocalciferolsFibronectinsparicalcitolReceptors, CalcitriolStreptozocinVdr protein, mouse

Identifiers

PMID33294462
PMCPMC7714593
OpenAlexW3110253192

What OpenQuestion holds

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LicenceCC BY
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.