Evidence map›Paper›PMID 36634865›Full record

ReviewLife sciences2023

Does maternal low-dose cadmium exposure increase the risk of offspring to develop metabolic syndrome and/or type 2 diabetes?

Saman Saedi, Sara E Watson, Jamie L Young, Yi Tan, Kupper A Wintergerst, Lu Cai

Open access · greenAbstract readReview
In one paragraph

Review in Life sciences, 2023. 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
5.2field-weighted citation impact, top 4% 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, 34 citations in OpenAlex.

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  14. Heavy metal toxicity in poultry: a comprehensive review.Frontiers in veterinary science · 2023
    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

6 authors at 4 institutions in 2 countries.

Saman SaediDepartment of Animal Science, College of Agriculture, Shiraz University, Shiraz, Iran.
Sara E WatsonPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA; Wendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; Division of Endocrinology, Department of Pediatrics, University of Louisville, Norton Children's Hospital, Louisville, KY, USA.
Jamie L YoungDepartment of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA; The Center for Integrative Environmental Health Sciences, University of Louisville School of Medicine, Louisville, KY, USA.
Yi TanPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA; Wendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Kupper A WintergerstPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA; Wendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; Division of Endocrinology, Department of Pediatrics, University of Louisville, Norton Children's Hospital, Louisville, KY, USA; The Center for Integrative Environmental Health Sciences, University of Louisville School of Medicine, Louisville, KY, USA.
Lu CaiPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA; Wendy Novak Diabetes Institute, Norton Children's Hospital, Louisville, KY, USA; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA; The Center for Integrative Environmental Health Sciences, University of Louisville School of Medicine, Louisville, KY, USA; Department of Radiation Oncology, University of Louisville School of Medicine, Louisville, KY 40202, USA. Electronic address: lu.cai@louisville.edu.
Kosair Children's Hospital · USUniversity of Louisville · USNorton Healthcare · USShiraz University · IR

Funding

University of Louisville Center for Integrative Environmental Health SciencesP30ES030283 · NIEHS · UNIVERSITY OF LOUISVILLE · PI Amanda Jo LeBlanc · 2020 to 2026
$10.0M
UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Fibroblast Growth Factor 1 Prevents Hyperlipidemia and atherosclerosisR01HL160927 · NHLBI · UNIVERSITY OF LOUISVILLE · PI Yi Tan · 2022 to 2026
$2.7M
A novel mechanism of stromal cell-derived factor 1 protection against diabetic cardiomyopathyR01HL125877 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TAN, YI · 2017 to 2021
$1.9M
NHLBI NIH HHS R01 HL125877NHLBI NIH HHS R01 HL160927NIEHS NIH HHS P30 ES030283NIEHS NIH HHS T32 ES011564
6 · The paper itself

Abstract

Cadmium is a hazardous metal with multiple organ toxicity that causes great harm to human health. Cadmium enters the human body through occupational exposure, diet, drinking water, breathing, and smoking. Cadmium accumulation in the human body is associated with increased risk of developing obesity, cardiovascular disease, diabetes, and metabolic syndrome (MetS). Cadmium uptake is enhanced during pregnancy and can cross the placenta affecting placental development and function. Subsequently, cadmium can pass to fetus, gathering in multiple organs such as the liver and pancreas. Early-life cadmium exposure can induce hepatic oxidative stress and pancreatic β-cell dysfunction, resulting in insulin resistance and glucose metabolic dyshomeostasis in the offspring. Prenatal exposure to cadmium is also associated with increasing epigenetic effects on the offspring's multi-organ functions. However, whether and how maternal exposure to low-dose cadmium impacts the risks of developing type 2 diabetes (T2D) in the young and/or adult offspring remains unclear. This review collected available data to address the current evidence for the potential role of cadmium exposure, leading to insulin resistance and the development of T2D in offspring. However, this review reveals that underlying mechanisms linking prenatal cadmium exposure during pregnancy with T2D in offspring remain to be adequately investigated.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceMetabolic SyndromePrenatal Exposure Delayed EffectsAdultCadmiumFemaleHumansMaternal ExposurePlacentaPregnancyCadmiumCadmiumInsulin resistanceMaternal exposureMetabolic syndromeOffspringType 2 diabetes

Identifiers

PMID36634865
PMCPMC9912173
OpenAlexW4313893404

What OpenQuestion holds

Textmetadata
LicenceTDM
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.