| Synonyms | GHRP-6 Acetate |
| Molecular Formula | C46H56N12O6 |
| Molecular Weight | 873.01 |
| Sequence | His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 |
| Appearance | White Powder |
| Purity | >98%(HPLC) |
| Identity (ESI-MS) | 873.01 ±1.0 |
| Source | Chemical Synthesis |
| Bacterial Endotoxins | < 5EU/mg |
| Test Parameter | Standard |
| Solubility | Soluble in water or 1% acetic acid |
| Storage | Lyophilized GHRP-6 although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution FST should be stored at 4°C between 2-7 days and for future use below -18°C. |
|
Prokinetic effects of a Ghrelin receptor agonist GHRP-6 in diabetic mice
GHRP-6 is a peptide ghrelin receptor agonist, which has previously been reported to increase gastric emptying in normal rats [1]. Ghrelin has been shown to accelerate gastric emptying in animal models of postoperative ileus [2], septic ileus [3], burn-induced slow gastrointestinal transit [4], and diabetes mellitus [5,6]. The prokinetic effect of GHRP-6 was investigated in a mouse model of diabetes mellitus in present research. This study was designed to investigate the effects of a ghrelin receptor agonist GHRP-6 on delayed gastrointestinal transit in alloxan-induced diabetic mice.
Mice were randomized into two groups: normal mice and diabetic mice< treated with GHRP-6 at doses of 0, 20, 50, 100 and 200 μg/kg ip. The gastric emptying (GE), intestinal transit (IT), and colonic transit (CT) were studied in mice after they had a phenol red meal following injection of GHRP-6. Atropine was given at 1mg/kg for 15 min before the GHRP-6 injection for every measurement. After the death of mice, the percentage of GE, IT and CT were calculated.  Compared to normal mice, GE, IT and CT was significantly decreased in diabetic mice. GHRP-6 definitely accelerated gastric emptying in diabetic mice. Despite the lowest dose, all the other doses normalized the rate of GE in diabetic mice. Hence, the 200 μg/kg dose was considered as the most effective dosage which can increase the rate of GE. GHRP-6 also significantly accelerated intestinal transit in diabetic mice. Despite the 20 μg/kg, all of other doses normalized the delayed IT. Therefore, the 200 μg/kg dose was considered most effective in accelerating intestinal transit. However, there is no result can show GHRP-6 has effect on delayed colonic transit. Moreover, the positive effects of 200 μg/kg GHRP-6 on GE and IT were blocked by atropine. This may suggest that the prokinetic effects are mediated via the cholinergic pathway in the enteric nervous system. In conclusion, GHRP-6 accelerates delayed GE and IT, but has no effect on CT in diabetic mice. GHRP-6 may exert its prokinetic effects via the cholinergic pathway in the enteric nervous system, and therefore, may have therapeutic potential for diabetic patients with delayed upper gastrointestinal transit. But the pharmacotherapeutic potential of GHRP-6 deserves to be further explored in diabetic patients suffering from delayed upper gastrointestinal transit. For Research Purpose only, Not for Human Consumption
|
|
