title: Metabolic effects of subchronic peripheral oxytocin administration in lean and obese zucker rats.
abstract: Increasing evidence indicates a role of oxytocin in controlling energy metabolism. The aim of his study was to investigate oxytocin effects on obese phenotype in leptin-resistant Zucker fatty rats, focusing on glucose and lipid metabolism. Zucker fatty rats and their lean controls were treated with oxytocin (3.6 μg/100g body weight/day) by osmotic minipumps implanted subcutaneously for 2 weeks. Two-hours intraperitoneal glucose tolerance test was performed in fasting rats. Oxytocin decreased food intake in both phenotypes while body weight gain reduced only in obese animals. In obese rats oxytocin impaired hepatic insulin extraction and enhanced liver triglyceride accumulation. Moreover, in the skeletal muscle of lean rats oxytocin treatment downregulated insulin signal transduction by decreasing of insulin receptor substrate 1 protein level and stimulating of its serine phosphorylation. Concurrently, the gene expression of insulin receptor substrate 1 in the skeletal muscle and adipose tissue was downregulated by oxytocin. In obese rats, oxytocin reduced adipocyte size and normalised mRNA levels of both fatty acid binding protein 4 and fatty acid synthase but attenuated gene expression of glucose transporter 4. The present study in Zucker fatty rats demonstrated ambivalent effects of oxytocin treatment with predominantly negative impact on skeletal muscle insulin pathway in lean animals.
authors: Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia. balazova.luc@gmail.com.
authors: L
authors: L
authors: Balazova
authors: Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.|Institute for Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
authors: K
authors: K
authors: Krskova
authors: Chair of Pharmacology, Jagiellonian University Medical College, Cracow, Poland.
authors: M
authors: M
authors: Suski
authors: Institute of Pathological Anatomy, Faculty of Medicine, Comenius University, University Hospital, Bratislava, Slovakia.
authors: V
authors: V
authors: Sisovsky
authors: Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
authors: N
authors: N
authors: Hlavacova
authors: Chair of Pharmacology, Jagiellonian University Medical College, Cracow, Poland.
authors: R
authors: R
authors: Olszanecki
authors: Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
authors: D
authors: D
authors: Jezova
authors: Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
authors: S
authors: S
authors: Zorad
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D002096:C-Peptide / Q000097:blood; D004435:Eating / Q000187:drug effects; D054890:Fatty Acid Synthase, Type I / Q000235:genetics; D050556:Fatty Acid-Binding Proteins / Q000235:genetics; D005951:Glucose Tolerance Test; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D010121:Oxytocin / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D011924:Rats, Zucker; D018045:Receptors, Oxytocin / Q000235:genetics; D014280:Triglycerides / Q000378:metabolism
chemical_list: D002096:C-Peptide; C524662:FABP4 protein, rat; D050556:Fatty Acid-Binding Proteins; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D018045:Receptors, Oxytocin; D014280:Triglycerides; C588222:oxytocin receptor, rat; D010121:Oxytocin; D054890:Fatty Acid Synthase, Type I