Evidence map›Paper›PMID 32366959›Full record

ArticleInternational journal of obesity (2005)2020

Nonnutritive sweetener consumption during pregnancy, adiposity, and adipocyte differentiation in offspring: evidence from humans, mice, and cells.

Meghan B Azad, Alyssa Archibald, Mateusz M Tomczyk, Alanna Head, Kyle G Cheung, Russell J de Souza, Allan B Becker, Piushkumar J Mandhane, Stuart E Turvey, Theo J Moraes and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 3 pooled it
3.5field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 3 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. From Fetus to Eight: the CHILD Cohort Study.American journal of epidemiology · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  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

13 authors at 6 institutions in 1 country.

Meghan B AzadDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada. meghan.azad@umanitoba.ca.ORCID http://orcid.org/0000-0002-5942-4444
Alyssa ArchibaldDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada.
Mateusz M TomczykDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada.
Alanna HeadDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada.
Kyle G CheungDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada.
Russell J de SouzaDepartment of Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, ON, Canada.
Allan B BeckerDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada.
Piushkumar J MandhaneDepartment of Pediatrics, University of Alberta, Edmonton, AB, Canada.
Stuart E TurveyDepartment of Pediatrics, BC Children's Hospital, University of British Columbia, Vancouver, BC, Canada.
Theo J MoraesDepartment of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.
Malcolm R SearsDepartment of Medicine, McMaster University, Hamilton, ON, Canada.
Padmaja SubbaraoDepartment of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, ON, Canada.
Vernon W DolinskyDevelopmental Origins of Chronic Diseases in Children Network (DEVOTION) and the Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme of the Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada. vdolinsky@chrim.ca.
Children's Hospital Research Institute of Manitoba · CAUniversity of Toronto · CAMcMaster University · CASt. Michael's Hospital · CAUniversity of Alberta · CAUniversity of British Columbia · CA

Funding

CIHR 144626CIHR 151540
6 · The paper itself

Abstract

backgroundObesity often originates in early life, and is linked to excess sugar intake. Nonnutritive sweeteners (NNS) are widely consumed as "healthier" alternatives to sugar, yet recent evidence suggests NNS may adversely influence weight gain and metabolic health. The impact of NNS during critical periods of early development has rarely been studied. We investigated the effect of prenatal NNS exposure on postnatal adiposity and adipocyte development.

methodsIn the CHILD birth cohort (N = 2298), we assessed maternal NNS beverage intake during pregnancy and child body composition at 3 years, controlling for maternal BMI and other potential confounders. To investigate causal mechanisms, we fed NNS to pregnant C57BL6J mice at doses relevant to human consumption (42 mg/kg/day aspartame or 6.3 mg/kg/day sucralose), and assessed offspring until 12 weeks of age for: body weight, adiposity, adipose tissue morphology and gene expression, glucose and insulin tolerance. We also studied the effect of sucralose on lipid accumulation and gene expression in cultured 3T3-L1 pre-adipocyte cells.

resultsIn the CHILD cohort, children born to mothers who regularly consumed NNS beverages had elevated body mass index (mean z-score difference +0.23, 95% CI 0.05-0.42 for daily vs. no consumption, adjusted for maternal BMI). In mice, maternal NNS caused elevated body weight, adiposity, and insulin resistance in offspring, especially in males (e.g., 47% and 15% increase in body fat for aspartame and sucralose vs. controls, p < 0.001). In cultured adipocytes, sucralose exposure at early stages of differentiation caused increased lipid accumulation and expression of adipocyte differentiation genes (e.g., C/EBP-α, FABP4, and FASN). These genes were also upregulated in adipose tissue of male mouse offspring born to sucralose-fed dams.

conclusionBy triangulating evidence from humans, mice, and cultured adipocytes, this study provides new evidence that maternal NNS consumption during pregnancy may program obesity risk in offspring through effects on adiposity and adipocyte differentiation.

Indexed as

Prenatal Exposure Delayed Effects3T3-L1 CellsAdipocytesAdiposityAnimalsArtificially Sweetened BeveragesAspartameBody CompositionBody Mass IndexCanadaCell DifferentiationChild, PreschoolFemaleHumansLongitudinal StudiesMaleAspartameNon-Nutritive SweetenersSucrosetrichlorosucrose

Identifiers

PMID32366959
OpenAlexW3022593374

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.