Hexarelin · research summary

Improvement of cardiomyocyte function by in vivo hexarelin treatment in streptozotocin-induced diabetic rats.

Physiological reports · 2018. 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

In vivo animal study using a streptozotocin-induced diabetic rat model to test the effects of hexarelin on cardiomyocytes.
“This experiment aims to test the effect of hexarelin on cardiomyocytes under experimental diabetes.”

Subjects

Male Wistar rats (6-week-old, 150–200 g) divided into control and streptozotocin-induced diabetic groups.
“Male Wistar rats (6‐week‐old), weighing 150–200 g, were used in the study.”

Sample size

48 rats total (24 control, 24 diabetic), with specific cell counts ranging from 9 to 90 cells per group for various measurements.
“Animals were distributed into 2 groups: 24 nontreated control (NC) and 24 nontreated diabetes (ND).”

Duration

Diabetes was induced for 4 weeks, followed by a 2-week treatment period with hexarelin or vehicle.
“Daily hexarelin (100 μg/kg) treatment was performed for 2 weeks after 4‐week STZ‐induced diabetes.”

Reported findings

Hexarelin treatment reversed reduced cell contraction and depressed intracellular calcium transients in diabetic cardiomyocytes.
“Hexarelin reversed the changes in both contraction and [Ca2+]i.”
Hexarelin normalized prolonged action potential duration and increased transient outward potassium current density in diabetic cardiomyocytes.
“Action potential duration and transient outward potassium current (I to) density were dramatically increased in diabetic cardiomyocytes and hexarelin treatment reverse such changes.”
Hexarelin treatment upregulated GHS receptor expression and induced antiapoptotic changes in Bax, Bcl-2, caspase-3, and caspase-9 expression.
“Upregulated GHS receptor (GHS‐R) expression was observed in both control and diabetic groups after hexarelin treatment, which also caused antiapoptotic changes of Bax, Bcl‐2, caspase‐3 and 9 expression.”

Source: PubMed 29446246 · DOI 10.14814/phy2.13612 · all study summaries

Reported findings

Hexarelin treatment reversed reduced cell contraction and depressed intracellular calcium transients in diabetic cardiomyocytes.

“Hexarelin reversed the changes in both contraction and [Ca2+]i.”

Hexarelin normalized prolonged action potential duration and increased transient outward potassium current density in diabetic cardiomyocytes.

“Action potential duration and transient outward potassium current (I to) density were dramatically increased in diabetic cardiomyocytes and hexarelin treatment reverse such changes.”

Hexarelin treatment upregulated GHS receptor expression and induced antiapoptotic changes in Bax, Bcl-2, caspase-3, and caspase-9 expression.

“Upregulated GHS receptor (GHS‐R) expression was observed in both control and diabetic groups after hexarelin treatment, which also caused antiapoptotic changes of Bax, Bcl‐2, caspase‐3 and 9 expression.”