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High-fat Diet Enhances Gastric Contractility, but Abolishes Nesfatin-1-induced Inhibition of Gastric Emptying

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dc.contributor.authorYEGEN, BERRAK
dc.contributor.authorsOzdemir-Kumral, Zarife N.; Koyuncuoglu, Turkan; Arabaci-Tamer, Sevil; Cilingir-Kaya, Ozlem T.; Koroglu, Ayca K.; Yuksel, Meral; Yegen, Berrak C.
dc.date.accessioned2022-03-14T09:54:59Z
dc.date.available2022-03-14T09:54:59Z
dc.date.issued2021-04-30
dc.description.abstractNeither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND- and HFD-rats, but only lucigenin-chemiluminescence was Background/Aims Gastrointestinal motility changes contribute to development and maintenance of obesity. Nesfatin-1 (NES-1) is involved in central appetite control. The aim is to elucidate effects of NES-1 and high-fat diet (HFD) on gastrointestinal motility and to explore myenteric neuron expressions of tyrosine hydroxylase (TH), vasoactive intestinal peptide (VIP), and neuronal nitric oxide synthase (nNOS) in HFDinduced oxidative injury. Methods Sprague-Dawley rats were fed with normal diet (ND) or HFD. Gastric emptying rate was measured following NES-1 (5 pmol/rat, intracerebroventricular) preceded by subcutaneous injections of glucagon-like peptide 1 (GLP-1), cholecystokinin 1 (CCK-1), and gastrin/CCK-2 receptor antagonists. In carbachol-contracted gastric and ileal strips, contractile changes were recorded by adding NES1 (0.3 nmol/L), GLP-1, CCK-1, and gastrin/CCK-2 antagonists. Results Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND-and HFD-rats, but only lucigenin-chemiluminescence was increased in HFD-rats. Vasoactive intestinal peptide (VIP) and TH immunoreactivities were depressed and nNOS immunoreactivity was increased in gastric tissues of HFD-rats, while VIP and TH were enhanced, but nNOS was reduced in their intestines. Conclusions HFD caused mild systemic inflammation, disrupted enteric innervation, enhanced gastric contractility, inhibited ileal contractility, and eliminated inhibitory effect of NES-1 on gastric motility. (J Neurogastroenterol Motil 2021;27:265-278)
dc.identifier.doi10.5056/jnm20206
dc.identifier.eissn2093-0887
dc.identifier.issn2093-0879
dc.identifier.pubmed33795544
dc.identifier.urihttps://hdl.handle.net/11424/243638
dc.identifier.wosWOS:000640313500001
dc.language.isoeng
dc.publisherKOREAN SOC NEUROGASTROENTEROLOGY & MOTILITY
dc.relation.ispartofJOURNAL OF NEUROGASTROENTEROLOGY AND MOTILITY
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCholecystokinin
dc.subjectGastric emptying
dc.subjectNesfatin-1
dc.subjectNitric oxide synthase type I
dc.subjectVasoactive intestinal peptide
dc.subjectDISTENSION-SENSITIVE NEURONS
dc.subjectGLUCAGON-LIKE PEPTIDE-1
dc.subjectCHOLECYSTOKININ
dc.subjectINFLAMMATION
dc.subjectSECRETION
dc.subjectRECEPTOR
dc.subjectMOTILITY
dc.subjectSATIETY
dc.subjectOBESITY
dc.subjectRAT
dc.titleHigh-fat Diet Enhances Gastric Contractility, but Abolishes Nesfatin-1-induced Inhibition of Gastric Emptying
dc.typearticle
dspace.entity.typePublication
local.avesis.ida9f6a1ed-e39c-46f4-b864-14029ebf6d99
local.import.packageSS16
local.indexed.atWOS
local.indexed.atPUBMED
local.journal.numberofpages14
oaire.citation.endPage278
oaire.citation.issue2
oaire.citation.startPage265
oaire.citation.titleJOURNAL OF NEUROGASTROENTEROLOGY AND MOTILITY
oaire.citation.volume27
relation.isAuthorOfPublicatione4eaf9ac-f8dc-4e2b-b940-895cc906790d
relation.isAuthorOfPublication.latestForDiscoverye4eaf9ac-f8dc-4e2b-b940-895cc906790d

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