Evidence map›Paper›PMID 34568906›Full record

ArticleG3 (Bethesda, Md.)2021

Genome-wide analysis in Drosophila reveals diet-by-gene interactions and uncovers diet-responsive genes.

Deanne Francis, Shila Ghazanfar, Essi Havula, James R Krycer, Dario Strbenac, Alistair Senior, Annabel Y Minard, Thomas Geddes, Marin E Nelson, Fiona Weiss and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in G3 (Bethesda, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 48% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Biomolecules · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Metabolic Syndrome: Lessons from Rodent andBioMed research international · 2022
    Review
  7. 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 1 institution in 1 country.

Deanne FrancisCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.ORCID 0000-0002-4158-1521
Shila GhazanfarCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Essi HavulaCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
James R KrycerCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Dario StrbenacCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Alistair SeniorCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Annabel Y MinardCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Thomas GeddesCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Marin E NelsonCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Fiona WeissCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Jacqueline StöckliCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
Jean Y H YangCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
David E JamesCharles Perkins Centre, The University of Sydney, Sydney, NSW 2006, Australia.
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic and environmental factors play a major role in metabolic health. However, they do not act in isolation, as a change in an environmental factor such as diet may exert different effects based on an individual's genotype. Here, we sought to understand how such gene-diet interactions influenced nutrient storage and utilization, a major determinant of metabolic disease. We subjected 178 inbred strains from the Drosophila genetic reference panel (DGRP) to diets varying in sugar, fat, and protein. We assessed starvation resistance, a holistic phenotype of nutrient storage and utilization that can be robustly measured. Diet influenced the starvation resistance of most strains, but the effect varied markedly between strains such that some displayed better survival on a high carbohydrate diet (HCD) compared to a high-fat diet while others had opposing responses, illustrating a considerable gene × diet interaction. This demonstrates that genetics plays a major role in diet responses. Furthermore, heritability analysis revealed that the greatest genetic variability arose from diets either high in sugar or high in protein. To uncover the genetic variants that contribute to the heterogeneity in starvation resistance, we mapped 566 diet-responsive SNPs in 293 genes, 174 of which have human orthologs. Using whole-body knockdown, we identified two genes that were required for glucose tolerance, storage, and utilization. Strikingly, flies in which the expression of one of these genes, CG4607 a putative homolog of a mammalian glucose transporter, was reduced at the whole-body level, displayed lethality on a HCD. This study provides evidence that there is a strong interplay between diet and genetics in governing survival in response to starvation, a surrogate measure of nutrient storage efficiency and obesity. It is likely that a similar principle applies to higher organisms thus supporting the case for nutrigenomics as an important health strategy.

Indexed as

DrosophilaDrosophila ProteinsAnimalsDiet, High-FatDrosophila melanogasterGenotypeHumansPhenotypeDrosophila ProteinsDGRPdiet–gene interactionsglucose transportmultivariate analysisstarvation

Identifiers

PMID34568906
PMCPMC8496270
OpenAlexW3171111122

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.