Effects of growth hormone-releasing hormone agonistic analog MR-409 on insulin-secreting cells under cyclopiazonic acid-induced endoplasmic reticulum stress.
Rodrigues-Dos-Santos. Karina K; Soares. Gabriela M GM; Guimarães. Dimitrius S P S F DSPSF; Araújo. Thiago R TR; Vettorazzi. Jean F JF; Zangerolamo. Lucas L; Marconato-Júnior. Emilio E; Cai. Renzhi R; Sha. Wei W; Schally. Andrew V AV; Boschero. Antônio C AC; Barbosa. Helena C L HCL
Key Findings
- MR‑409 did not prevent endoplasmic reticulum (ER) stress caused by cyclopiazonic acid.
- Cells exposed to MR‑409 had lower levels of oxidative stress under ER stress conditions.
- MR‑409‑treated cells showed higher survival rates compared to untreated cells during ER stress.
Practical Outcomes
- For DIY health enthusiasts, the data suggest that GHRH analogs like sermorelin might offer some cellular protection against oxidative damage, but they don’t appear to fix the underlying ER stress that contributes to beta‑cell failure. Until human studies confirm these effects, there’s no clear protocol or dosage change to recommend based on this paper.
Summary
A lab study looked at a GHRH‑like peptide called MR‑409 (similar to sermorelin) on insulin‑producing cells that were stressed in a way that mimics type‑2 diabetes. The peptide didn’t stop the stress itself, but the cells treated with it showed less oxidative damage and survived better.
Abstract
The endoplasmic reticulum (ER) stress is one of the mechanisms related to decreased insulin secretion and beta cell death, contributing to the progress of type 2 diabetes mellitus (T2D). Thus, investigating agents that can influence this process would help prevent the development of T2D. Recently, the growth-hormone-releasing hormone (GHRH) action has been demonstrated in INS-1E cells, in which it increases cell proliferation and insulin secretion. As the effects of GHRH and its agonists have not been fully elucidated in the beta cell, we proposed to investigate them by evaluating the role of the GHRH agonist, MR-409, in cells under ER stress. Our results show that the agonist was unable to ameliorate or prevent ER stress. However, cells exposed to the agonist showed less oxidative stress and greater survival even under ER stress. The mechanisms by which GHRH agonist, MR-409, leads to these outcomes require further investigation.
Study Information
pubmed
2021
2021-07-09T00:00:00.000Z
10.1016/j.mce.2021.111379
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