# A Study of Small Intestinal Epigenomic Changes Induced by Royal Jelly

**Authors:** Genki Kobayashi, Takahiro Ichikawa, Takuro Okamura, Tomoyuki Matsuyama, Masahide Hamaguchi, Hideto Okamoto, Nobuaki Okumura, Michiaki Fukui

PMC · DOI: 10.3390/cells13171419 · 2024-08-25

## TL;DR

Royal jelly induces beneficial epigenomic changes in the small intestine, improving metabolic health and reducing cancer-related gene activity.

## Contribution

This study identifies specific epigenomic modifications in small intestinal cells caused by royal jelly, linking them to metabolic and cancer-related pathways.

## Key findings

- Royal jelly improved insulin sensitivity and lipid metabolism without affecting body weight.
- RJ altered histone modifications, increasing H3K27me3 and decreasing H3K23Ac in genes related to the G2M checkpoint.
- Genes like Smc2, Mcm3, and Ccnd1 were affected, linking to cancer progression and metabolic regulation.

## Abstract

This study explores the impact of royal jelly (RJ) on small intestinal epigenomic changes. RJ, produced by honeybees, is known for its effects on metabolic diseases. The hypothesis is that RJ induces epigenomic modifications in small intestinal epithelial cells, affecting gene expression and contributing to metabolic health. Male db/m and db/db mice were used to examine RJ’s effects through mRNA sequencing and CUT&Tag methods. This study focused on histone modifications and gene expression changes, with statistical significance set at p < 0.05. RJ administration improved insulin sensitivity and lipid metabolism without affecting body weight. GO and KEGG pathway analyses showed significant enrichment in metabolic processes, cellular components, and molecular functions. RJ altered histone modifications, increasing H3K27me3 and decreasing H3K23Ac in genes associated with the G2M checkpoint. These genes, including Smc2, Mcm3, Ccnd1, Rasal2, Mcm6, and Mad2l1, are linked to cancer progression and metabolic regulation. RJ induces beneficial epigenomic changes in small intestinal epithelial cells, improving metabolic health and reducing cancer-associated gene expression. These findings highlight RJ’s potential as a therapeutic agent for metabolic disorders. Further research is needed to fully understand the mechanisms behind these effects and their implications for human health.

## Linked entities

- **Genes:** SMC2 (structural maintenance of chromosomes 2) [NCBI Gene 10592], MCM3 (minichromosome maintenance complex component 3) [NCBI Gene 4172], CCND1 (cyclin D1) [NCBI Gene 595], RASAL2 (RAS protein activator like 2) [NCBI Gene 9462], MCM6 (minichromosome maintenance complex component 6) [NCBI Gene 4175], MAD2L1 (mitotic arrest deficient 2 like 1) [NCBI Gene 4085]
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** MCM6 (minichromosome maintenance complex component 6) [NCBI Gene 4175] {aka MCG40308, Mis5, P105MCM}, CCND1 (cyclin D1) [NCBI Gene 595] {aka BCL1, D11S287E, PRAD1, U21B31}, MAD2L1 (mitotic arrest deficient 2 like 1) [NCBI Gene 4085] {aka HSMAD2, MAD2}, RASAL2 (RAS protein activator like 2) [NCBI Gene 9462] {aka NGAP}, SMC2 (structural maintenance of chromosomes 2) [NCBI Gene 10592] {aka CAP-E, CAPE, SMC-2, SMC2L1}, MCM3 (minichromosome maintenance complex component 3) [NCBI Gene 4172] {aka HCC5, P1-MCM3, P1.h, RLFB}
- **Diseases:** metabolic diseases (MESH:D008659), cancer (MESH:D009369)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Apis mellifera (bee, species) [taxon 7460], Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11393943/full.md

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Source: https://tomesphere.com/paper/PMC11393943