# Bioactive peptides PDBSN improve mitochondrial function and suppression the oxidative stress in human adiposity cells

**Authors:** Huiping Shen, Yong Lei, Wen Xie, Tieliang Ma, Li Bao, Qin Gao, Bingyu Chen, Biao Dai, Dani Qin

PMC · DOI: 10.1080/21623945.2023.2278213 · 2023-11-09

## TL;DR

A bioactive peptide called PDBSN improves mitochondrial function and reduces oxidative stress in human fat cells, which could help treat obesity and related metabolic diseases.

## Contribution

PDBSN's novel ability to enhance mitochondrial function and reduce oxidative stress in adipocytes is demonstrated for the first time.

## Key findings

- PDBSN increased mitochondrial membrane potential and reduced triglyceride and ROS levels in adipocytes.
- PDBSN upregulated genes and proteins related to mitochondrial biogenesis and function.
- PDBSN improved maximum respiratory capacity and altered mitochondrial fusion and fission markers.

## Abstract

Mitochondria are essential for generating cellular energy and are significant in the pathogenesis of obesity. Human visceral and subcutaneous preadipocytes (HPA-v and HPA-s) were cultured into mature adipocytes. Intracellular triglyceride (TG) content was assessed using oil-red O staining and tissue triglyceride determination. Mitochondrial membrane potential (MMP) and reactive
oxygen species (ROS) levels were measured with fluorescent indicators. Gene and protein expression related to mitochondrial biogenesis were analyzed by real-time quantitative PCR and Western blotting. Morphological changes were observed via electron microscopy. Results show that PDBSN significantly increased MMP while decreasing TG and ROS levels. The transcription and protein levels
of PGC1-α and MTFA were upregulated, and mitochondrial fusion and fission markers (MFN1, MFN2, NRF1, DRP1) were elevated. Additionally, PDBSN enhanced maximum
respiratory capacity and reduced ROS. These findings suggest that PDBSN improves mitochondrial function, providing insights for obesity treatment and metabolic disease management.

## Linked entities

- **Genes:** PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891], mtfA (anti-repressor for DgsA) [NCBI Gene 914176], MFN1 (mitofusin 1) [NCBI Gene 55669], MFN2 (mitofusin 2) [NCBI Gene 9927], NRF1 (nuclear respiratory factor 1) [NCBI Gene 4899], CRMP1 (collapsin response mediator protein 1) [NCBI Gene 1400]
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891] {aka LEM6, PGC-1(alpha), PGC-1alpha, PGC-1v, PGC1, PGC1A}, MFN2 (mitofusin 2) [NCBI Gene 9927] {aka CMT2A, CMT2A2, CMT2A2A, CMT2A2B, CPRP1, HMSN6A}, NRF1 (nuclear respiratory factor 1) [NCBI Gene 4899] {aka ALPHA-PAL}, MFN1 (mitofusin 1) [NCBI Gene 55669] {aka hfzo1, hfzo2}, UTRN (utrophin) [NCBI Gene 7402] {aka DMDL, DRP, DRP1}
- **Diseases:** metabolic diseases (MESH:D008659), adiposity (MESH:D018205), obesity (MESH:D009765)
- **Chemicals:** TG (MESH:D014280), PDBSN (-), ROS (MESH:D017382), oil-red O (MESH:C011049)

## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12184117/full.md

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Source: https://tomesphere.com/paper/PMC12184117