# MOTS-c modulates pancreatic islet function in rats and pigs in vitro

**Authors:** Jakub Bień, Ewa Pruszynska-Oszmalek, Pawel Kolodziejski, Natalia Leciejewska, Dawid Szczepankiewicz, Emilia Grzęda, Maciej Sassek

PMC · DOI: 10.1007/s00418-025-02391-4 · Histochemistry and Cell Biology · 2025-06-06

## TL;DR

MOTS-c affects pancreatic islet function in rats and pigs, with species-specific differences that suggest pigs may be a better model for human studies.

## Contribution

The study is the first to investigate MOTS-c's effects on pancreatic islets in both rats and pigs.

## Key findings

- MOTS-c reduces insulin and glucagon secretion in pancreatic islets.
- MOTS-c enhances cell viability and reduces cell death in islets.
- Species-specific differences in MOTS-c effects were observed between rats and pigs.

## Abstract

MOTS-c is a promising regulator of metabolism and energy homeostasis. While its effects have been studied in cell lines, our team aimed to investigate its influence on more complex structures—specifically, isolated pancreatic islets. We used two animal models: the rat, which is commonly studied, and the pig, which shares greater physiological similarities with humans. This study assessed the expression and secretion of insulin and glucagon, the expression of their receptors, cell viability, and cell death following MOTS-c treatment of the islets. Additionally, we examined how MOTS-c secretion is affected by different incubation media, such as the presence of free fatty acids, pancreatic hormones, and different glucose concentrations. The results indicate that MOTS-c impacts pancreatic islet physiology by, for example, reducing insulin and glucagon secretion and enhancing cell viability. Notably, the effects differed between the two species, which may be attributed to anatomical differences in their pancreatic islets or structural variations in rat and pig MOTS-c. These facts may lead to the conclusion that if MOTS-c may be helpful in human medicine, the pig model should be considered another valuable choice.

## Linked entities

- **Proteins:** PIN (insulin precursor), gcg.S (glucagon S homeolog)
- **Species:** Rattus norvegicus (taxon 10116), Sus scrofa (taxon 9823)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 397415], GCG (glucagon) [NCBI Gene 397595] {aka GLP-1}
- **Chemicals:** free fatty acids (MESH:D005230), glucose (MESH:D005947), MOTS-c (-)
- **Species:** Homo sapiens (human, species) [taxon 9606], Sus scrofa (pig, species) [taxon 9823], Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12144051/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12144051/full.md

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Source: https://tomesphere.com/paper/PMC12144051