Premium
Gastric motor dysfunction coincides with the onset of obesity in rats fed with high‐fat diet
Author(s) -
Kaya Sabriye Defne,
Sinen Osman,
Bülbül Mehmet
Publication year - 2021
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13448
Subject(s) - endocrinology , medicine , choline acetyltransferase , antrum , bethanechol , vasoactive intestinal peptide , myenteric plexus , sodium nitroprusside , biology , nitric oxide , stomach , immunohistochemistry , acetylcholine , receptor , neuropeptide , muscarinic acetylcholine receptor
Exposure to a high‐fat diet (HFD) has been reported to impair central autonomic and enteric neurocircuitries, however, the relevant mechanisms and their time course are inadequately clarified. This study aimed to investigate the effects of HFD consumption through the period of adolescence on gastric motor functions in adulthood. Male Sprague‐Dawley rats consumed a regular diet or HFD (60% kcal by fat) from 4 to 12 weeks of age. Body weight and food intake were monitored weekly. In adult rats, gastric emptying (GE) was measured. Additionally, using in‐vitro organ bath, contractile and relaxant responses of antral and fundic strips were assessed with bethanechol and sodium nitroprusside (SNP), respectively. The expressions of choline acetyltransferase (ChAT), neuronal nitric oxide synthase (nNOS) and vasoactive intestinal polypeptide (VIP) were detected by immunofluorescence, whereas, the number of myenteric neurons were evaluated by staining with cuprolinic blue and enteric neuronal marker PGP 9.5. In adulthood, the HFD did not alter food intake, while significantly increasing the body weight. In HFD‐fed adult rats, increased visceral fat mass was accompanied by delayed GE. Moreover, bethanechol‐ and SNP‐induced responses were attenuated in antral and fundic tissues. HFD remarkably decreased the number of myenteric neurons and NOS immunoreactivity both in fundus and antrum. HFD remarkably decreased ChAT expression, while increasing the immunoreactivity for VIP in antrum. In conclusion, consumption of HFD between early adolescence and adulthood results in obesity and impairment of gastric motor functions. Particularly, HFD‐induced gastric dysmotility appears to be predominantly dependent on the modifications in the non‐adrenergic non‐cholinergic inhibitory neurotransmission.