title: The paraventricular nucleus modulates thyroidal motilin release and rat gastric motility.
abstract: Motilin, an important endocrine regulator of gastrointestinal motility, was once considered to be produced in the gastrointestinal tract and brain. In recent years, however, motilin has been found in the human thyroid, as well as in that of the guinea pig. The physiological function and central modulation of thyroidal motilin remain poorly understood. To determine the functional role of thyroidal motilin, we observed the concentration of motilin in the plasma and also gastric motility before and after thyroidectomy. Our studies show that both the concentration of plasma motilin and gastric motility were decreased after thyroidectomy. To explore modulation-related nuclei, a c-Fos immune response experiment was carried out. The PVN of the hypothalamus was the main area of reactivity after thyroidectomy. Subsequently, we studied the effects of electrical excitation and PVN lesions on gastric motility and the expression of motilin in the thyroid and plasma. Excitation of the PVN was shown to prompt gastric motility that was partly prevented by the motilin receptor antagonist, GM-109. The effects of PVN excitation on gastric contraction were significantly reduced in thyroidectomised rats. In addition, the expression of motilin in the thyroid was significantly increased after PVN excitation and decreased after PVN lesions. The changes in the concentration of motilin in plasma induced by PVN stimulation were positively correlated with changes of gastric motility. In our in vitro study, the motilin secreted from TT cells (a parafollicular cell line originating from human thyroid medullary carcinoma) gradually increased on day 6 of culture, and motilin and calcitonin (CT) were co-expressed in TT cells. These results demonstrate that motilin from the thyroid could be secreted into the peripheral plasma and affect gastric motility and that PVN was a central nucleus for modulating gastric motility and motilin expression in the thyroid.
authors.affiliation: Department of Pathophysiology, Medical College of Qingdao University, Qingdao, Shandong, China.
authors.forename: F
authors.initials: F
authors.lastname: Guo
authors.forename: L
authors.initials: L
authors.lastname: Xu
authors.forename: X
authors.initials: X
authors.lastname: Sun
authors.forename: S
authors.initials: S
authors.lastname: Gao
authors.forename: H
authors.initials: H
authors.lastname: Zhu
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D005260:Female; D005769:Gastrointestinal Motility / Q000502:physiology*; D006801:Humans; D008297:Male; D009037:Motilin / Q000097:blood / Q000378:metabolism*; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013961:Thyroid Gland / Q000166:cytology / Q000378:metabolism*; D013964:Thyroid Neoplasms / Q000378:metabolism / Q000473:pathology; D013965:Thyroidectomy; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D014284:Triiodothyronine; D009037:Motilin; D013974:Thyroxine