title: Abundance of mRNA of growth hormone receptor and insulin-like growth factors-1 and -2 in duodenal and colonic biopsies of dogs with chronic enteropathies*.
abstract: Repair processes of the inflamed intestine are very important for dissolution of chronic enteropathies (CE). Therefore, we examined the mRNA abundance of growth hormone receptor (GHR), insulin-like growth factors (IGF)-1 and -2 in duodenal and colonic biopsies of dogs with CE such as food-responsive diarrhoea (FRD) and inflammatory bowel disease (IBD) before and after treatment as compared with each other and healthy dogs. A clinical score (Canine IBD Activity Index = CIBDAI) was applied to judge the severity of CE. Biopsies of duodenum and colon from client-owned dogs with CE were sampled before (FRD(bef), n = 5; IBD(bef), n = 5) and after treatment (FRD(aft), n = 5; IBD(aft), n = 5). Intestinal control samples were available from a homogenous control population (n = 15; C). Intestinal samples were homogenized, total RNA was extracted, reverse transcribed and analysed by real-time polymerase chain reaction to measure mRNA levels of GHR, IGF-1 and IGF-2. Results were normalized with glyceraldehyde phosphate dehydrogenase as housekeeping gene. The CIBDAI decreased during the treatment period in FRD and IBD (P < 0.01). In duodenum, GHR mRNA levels were higher in all groups than in C (P < 0.001). Duodenal IGF-1 mRNA levels in FRD(aft) and IBD(aft) tended to be higher than in C (P < 0.1). The IGF-2 mRNA abundance in FRD(aft) was higher than in C (P < 0.05) in duodenum. In colon, mRNA levels of IGF-1 in IBD(aft) were higher than in FRD(aft) (P < 0.05) and levels differed between IBD(aft) and C (P < 0.05). In conclusion, mRNA levels of GHR, IGF-1 and IGF-2 in the gastrointestinal tract were increased during CE when compared with gastrointestinally healthy dogs. The data suggest that GHR, IGF-1 and IGF-2 are involved in gastrointestinal repair processes.
authors.affiliation: Division of Nutrition and Physiology, Institute of Animal Genetics, Nutrition and Housing, University of Bern, Bremgartenstrasse 109A, CH-3012 Bern, Switzerland.
authors.forename: A C
authors.initials: AC
authors.lastname: Spichiger
authors.forename: K
authors.initials: K
authors.lastname: Allenspach
authors.forename: E
authors.initials: E
authors.lastname: Ontsouka
authors.forename: F
authors.initials: F
authors.lastname: Gaschen
authors.forename: C
authors.initials: C
authors.lastname: Morel
authors.forename: J W
authors.initials: JW
authors.lastname: Blum
authors.forename: S N
authors.initials: SN
authors.lastname: Sauter
mesh_terms: D000818:Animals; D001706:Biopsy / Q000662:veterinary; D003106:Colon / Q000737:chemistry* / Q000378:metabolism / Q000473:pathology; D004283:Dog Diseases / Q000378:metabolism* / Q000473:pathology; D004285:Dogs; D004386:Duodenum / Q000737:chemistry* / Q000378:metabolism / Q000473:pathology; D005260:Female; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D007335:Insulin-Like Growth Factor II / Q000235:genetics / Q000378:metabolism; D007410:Intestinal Diseases / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D008297:Male; D016133:Polymerase Chain Reaction / Q000662:veterinary; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D011986:Receptors, Somatotropin / Q000235:genetics / Q000378:metabolism*; D012189:Retrospective Studies; D013002:Somatomedins / Q000235:genetics / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D013002:Somatomedins; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II