Hexarelin · research summary

Growth hormone secretagogues hexarelin and JMV2894 protect skeletal muscle from mitochondrial damages in a rat model of cisplatin-induced cachexia.

Scientific reports · 2017. Summary drawn from the study's full text. Each statement is followed by the exact sentence it comes from. This is a research summary, not medical advice.

Study type

Animal study using a rat model of cisplatin-induced cachexia to evaluate mitochondrial homeostasis and the effects of growth hormone secretagogues.
“By using a rat model of cisplatin-induced cachexia, we here characterized the mitochondrial homeostasis in tibialis anterior cachectic muscle and evaluated the potential beneficial effects of the growth hormone secretagogues (GHS) hexarelin and JMV2894 in this setting.”

Subjects

Adult male rats.
“Adult male rats were purchased from Charles River Laboratories (Italy).”

Sample size

16 rats total, divided into four groups of 4 rats each.
“Each group consisted of 4 rats.”

Duration

5 days, with treatments administered from day 1 through day 5 and sacrifice on day 5.
“On day 5, 2 h after hexarelin or JMV2894 injection, rats were sacrificed.”

Reported findings

Cisplatin treatment caused a decrease in mitochondrial biogenesis, mitochondrial mass, and fusion index, along with changes in autophagy-related genes and enhanced ROS production.
“We found that cisplatin treatment caused a decrease in mitochondrial biogenesis (PGC-1α, NRF-1, TFAM, mtDNA, ND1), mitochondrial mass (Porin and Citrate synthase activity) and fusion index (MFN2, Drp1), together with changes in the expression of autophagy-related genes (AKT/FoxO pathway, Atg1, Beclin1, LC3AII, p62) and enhanced ROS production (PRX III, MnSOD).”
The growth hormone secretagogues JMV2894 and hexarelin were capable of antagonizing the chemotherapy-induced mitochondrial dysfunction.
“Importantly, JMV2894 and hexarelin are capable to antagonize this chemotherapy-induced mitochondrial dysfunction.”
Cisplatin induced a significant decrease in the muscle/body weight ratio, which was completely inhibited by the administration of both GHS.
“Cisplatin caused a significant decrease (about 15%) in the muscle/body weight ratio compared to control rats (Table 1). This change was completely inhibited by the administration of both GHS.”

Limitations stated by the authors

The molecular mechanisms activated by hexarelin and JMV2894 have not been fully characterized.
“The molecular mechanisms activated by hexarelin and JMV2894 have not been fully characterized.”

Source: PubMed 29026190 · DOI 10.1038/s41598-017-13504-y · all study summaries

Study type

Animal study using a rat model of cisplatin-induced cachexia to evaluate mitochondrial homeostasis and the effects of growth hormone secretagogues.

“By using a rat model of cisplatin-induced cachexia, we here characterized the mitochondrial homeostasis in tibialis anterior cachectic muscle and evaluated the potential beneficial effects of the growth hormone secretagogues (GHS) hexarelin and JMV2894 in this setting.”

Reported findings

Cisplatin treatment caused a decrease in mitochondrial biogenesis, mitochondrial mass, and fusion index, along with changes in autophagy-related genes and enhanced ROS production.

“We found that cisplatin treatment caused a decrease in mitochondrial biogenesis (PGC-1α, NRF-1, TFAM, mtDNA, ND1), mitochondrial mass (Porin and Citrate synthase activity) and fusion index (MFN2, Drp1), together with changes in the expression of autophagy-related genes (AKT/FoxO pathway, Atg1, Beclin1, LC3AII, p62) and enhanced ROS production (PRX III, MnSOD).”

The growth hormone secretagogues JMV2894 and hexarelin were capable of antagonizing the chemotherapy-induced mitochondrial dysfunction.

“Importantly, JMV2894 and hexarelin are capable to antagonize this chemotherapy-induced mitochondrial dysfunction.”

Cisplatin induced a significant decrease in the muscle/body weight ratio, which was completely inhibited by the administration of both GHS.

“Cisplatin caused a significant decrease (about 15%) in the muscle/body weight ratio compared to control rats (Table 1). This change was completely inhibited by the administration of both GHS.”