# Altered Expression of the MEG3, FTO, ATF4, and Lipogenic Genes in PBMCs from Children with Obesity and Its Associations with Added Sugar Intake

**Authors:** Adrián Hernández-DíazCouder, Pablo J. Paz-González, Maryori Valdez-Garcia, Claudia I. Ramírez-Silva, Karol Iliana Avila-Soto, Araceli Pérez-Bautista, Miguel Vazquez-Moreno, Ana Nava-Cabrera, Rodrigo Romero-Nava, Fengyang Huang, Miguel Cruz

PMC · DOI: 10.3390/nu17152546 · Nutrients · 2025-08-02

## TL;DR

This study found that certain genes linked to obesity and fat production are less active in children with obesity, and this is connected to added sugar intake and insulin resistance.

## Contribution

The study reveals sex- and insulin resistance-related differences in gene expression linked to obesity in children.

## Key findings

- Genes like MEG3, FTO, and ATF4 are less active in children with obesity.
- Added sugar intake is negatively linked to the expression of lipogenic genes.
- Sex-related differences in gene expression were observed in both normal and obese children.

## Abstract

Background: Obesity and its complications have increased in both adults and children, with pediatric populations developing metabolic disorders at earlier ages. Long non-coding RNAs, particularly MEG3, are involved in obesity through regulation of lipogenic genes including ATF4, FTO, SREBP1, FASN, and ACACA. However, data on MEG3 expression in pediatric obesity are limited. This study evaluated MEG3, FTO, and ATF4 expression in PBMCs from children with obesity and their associations with added sugar intake and lipid metabolism genes. Methods: In this cross-sectional study 71 children within the age range of 6 to 12 years were included (28 normal weight and 43 with obesity). Anthropometrical and clinical parameters and dietary added sugar consumption were analyzed. Real-time PCR was performed to assess MEG3, FTO, ATF4, SREBP1, FASN, and ACACA gene expression in peripheral blood mononuclear cells. Results: The expression of MEG3, ATF4, FTO, SREBP1, FASN, and ACACA was decreased in children with obesity. MEG3 and FTO showed sex-dependent expression in children without obesity, while additional sex-related differences were observed for SREBP1, FASN, ACACA, FTO, and MEG3 in children with obesity. MEG3 was associated with the expression of SREBP1, FASN, ACACA, FTO, and ATF4. In insulin-resistant (IR) children, MEG3, ATF4, FTO, ACACA, and SREBP1 were reduced, while FASN was increased. Added sugar intake negatively correlated with FTO, SREBP1, and ACACA. Conclusions: The MEG3, FTO, and ATF4 expression was altered in children with obesity, showing sex- and IR-related differences. Added sugar intake correlated negatively with lipogenic gene expression.

## Linked entities

- **Genes:** MEG3 (maternally expressed 3) [NCBI Gene 55384], FTO (FTO alpha-ketoglutarate dependent dioxygenase) [NCBI Gene 79068], ATF4 (activating transcription factor 4) [NCBI Gene 468], SREBF1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 6720], FASN (fatty acid synthase) [NCBI Gene 2194], ACACA (acetyl-CoA carboxylase alpha) [NCBI Gene 31]
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** MEG3 (maternally expressed 3) [NCBI Gene 55384] {aka FP504, GTL2, LINC00023, Lnc-DLK1-35, NCRNA00023, PRO0518}, SREBF1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 6720] {aka HMD, IFAP2, SREBP1, bHLHd1}, FASN (fatty acid synthase) [NCBI Gene 2194] {aka FAS, OA-519, SDR27X1}, FTO (FTO alpha-ketoglutarate dependent dioxygenase) [NCBI Gene 79068] {aka ALKBH9, BMIQ14, GDFD, IFEX9}, ACACA (acetyl-CoA carboxylase alpha) [NCBI Gene 31] {aka ACAC, ACACAD, ACACalpha, ACC, ACC1, ACCA}, ATF4 (activating transcription factor 4) [NCBI Gene 468] {aka CREB-2, CREB2, TAXREB67, TXREB}
- **Diseases:** metabolic disorders (MESH:D008659), IR (MESH:D007333), Obesity (MESH:D009765)
- **Chemicals:** lipid (MESH:D008055), Added Sugar (-)

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12348735/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC12348735/full.md

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Source: https://tomesphere.com/paper/PMC12348735