title: Sex-dependent effects of high-fat-diet feeding on rat pancreas oxidative stress.
abstract: OBJECTIVE
  The objective of the study was to investigate whether sex differences in oxidative stress-associated insulin resistance previously reported in rats could be attributed to a possible sex dimorphism in pancreas redox status.
  
  
  METHODS
  Fifteen-month-old male and female Wistar rats were fed a control diet or a high-fat diet for 14 weeks. Serum glucose, lipids, and hormone levels were measured. Insulin immunohistochemistry and morphometric analysis of islets were performed. Pancreas triglyceride content, oxidative damage, and antioxidant enzymatic activities were determined. Lipoprotein lipase, hormone-sensitive lipase, and uncoupling protein 2 (UCP2) levels were also measured.
  
  
  RESULTS
  Male rats showed a more marked insulin resistance profile than females. In control female rats, pancreas Mn-superoxide dismutase activity and UCP2 levels were higher, and oxidative damage was lower compared with males. High-fat-diet feeding decreased pancreas triglyceride content in female rats and UCP2 levels in male rats. High-fat-diet female rats showed larger islets than both their control and sex counterparts.
  
  
  CONCLUSIONS
  These results confirm the existence of a sex dimorphism in pancreas oxidative status in both control and high-fat-diet feeding situations, with female rats showing higher protection against oxidative stress, thus maintaining pancreatic function and contributing to a lower risk of insulin resistance.
authors.affiliation: Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Institut Universitari d'Investigació en Ciències de la Salut, Universitat de les Illes Balears, Palma de Mallorca, Spain. yolanda.gomez@uib.es
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Gómez-Pérez
authors.forename: Magdalena
authors.initials: M
authors.lastname: Gianotti
authors.forename: Isabel
authors.initials: I
authors.lastname: Lladó
authors.forename: Ana M
authors.initials: AM
authors.lastname: Proenza
mesh_terms: D050154:Adiposity; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects*; D005260:Female; D006728:Hormones / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D007473:Ion Channels / Q000378:metabolism; D007515:Islets of Langerhans / Q000033:anatomy & histology; D008055:Lipids / Q000097:blood; D008297:Male; D024101:Mitochondrial Proteins / Q000378:metabolism; D009929:Organ Size; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012727:Sex Characteristics; D002787:Sterol Esterase / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism; D000071246:Uncoupling Protein 2
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D006728:Hormones; D007328:Insulin; D007473:Ion Channels; D008055:Lipids; D024101:Mitochondrial Proteins; D014280:Triglycerides; C000604391:Ucp2 protein, rat; D000071246:Uncoupling Protein 2; D013482:Superoxide Dismutase; D002787:Sterol Esterase