ACTA ENDOCRINOLOGICA (BUC)

The International Journal of Romanian Society of Endocrinology / Registered in 1938

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Year Volume Issue First page
10.4183/aeb.
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  • General Endocrinology

    Hsu H, Huang W

    Anti-R Ghrelin Serum Stimulated the Plasma Acylated-Ghrelin, GH, and IGF-1 via CCK1 Receptor in Female Rats

    Acta Endo (Buc) 2014 10(3): 373-382 doi: 10.4183/aeb.2014.373

    Abstract
    Background. Dyspepsia is a popular complication in many disease, including diarrhea or constipation. This finding of antir- ghrelin serum can be used to improve the discomfort of patients. Objective. To study the effects of anti-r-ghrelin serum on plasma acylatedghrelin, growth hormone (GH) and insulinlike growth factor-1 (IGF-1) concentration, and mechanism of gastrointestinal (GI) motility (e.g. gastric emptying and intestinal transit) in female rats. Subjects and Methods. Female rats (estrus cycle confirmed) were fasted overnight and treated with i.p (intraperitoneal) injection anti-r-ghrelin serum, cholecystokinin 1 (CCK1) receptor antagonist, and ghrelin receptor antagonist (cortistatin-8, CST-8) to examine the GI motility. The concentration of plasma acylated ghrelin, GH, and IGF-1 was analyzed by ELISA assay. Results. Our data showed that (1) treatment with anti-r-ghrelin serum (diluted 1:100) inhibited the gastric emptying (12.12±2.191 %) but increased the concentration of acylated ghrelin (34.54±3.506 pg/ mL), GH (259.2±24.60 ng/mL) and IGF-1 (1033.9±33.66 ng/mL); (2) the CCK1 receptor antagonist, lorglumide (5 and 10 mg/mL/ kg) reversed the inhibition of gastric emptying (31.95±2.425 % and 30.50±3.624 %) and increased the concentration of plasma acylated ghrelin (101.8±9.422 pg/mL) and GH (508.5±44.11 ng/mL); (3) the ghrelin receptor antagonist, CST-8 under the doses of 1, 20, 40, 100 μg/mL/kg, promoted the gastric emptying (25.85±3.197 % to 33.43±2.513 %) in female rats. Conclusion. Anti-r-ghrelin serum both induced the concentration of plasma acylated-ghrelin, GH and IGF-1 as well as inhibited the GI motility by CCK1 receptor in female rats.