title: High-fat diet with stress impaired islets' insulin secretion by reducing plasma estradiol and pancreatic GLUT2 protein levels in rats' proestrus phase.
abstract: This study was conducted to determine whether two estrus phases (proestrus and diestrus) in female rats may influence the metabolic response to a high-fat diet and/or stress, focusing on pancreatic insulin secretion and content. Animals were divided into high-fat and normal diet groups, then each group was subdivided into stress and non-stress groups, and finally, each one of these was divided into proestrus and diestrus subgroups. At the end of high-fat diet treatment, foot-shock stress was applied to the animals. Then, blood samples were taken to measure plasma factors. Finally, the pancreas was removed for determination of glucose transporter 2 (GLUT2) protein levels and assessment of insulin content and secretion of the isolated islets. In the normal and high-fat diet groups, stress increased plasma corticosterone concentration in both phases. In both study phases, high-fat diet consumption decreased estradiol and increased leptin plasma levels. In the high-fat diet group in response to high glucose concentration, a reduction in insulin secretion was observed in the proestrus phase compared with the same phase in the normal diet group in the presence and absence of stress. Also, high-fat diet decreased the insulin content of islets in the proestrus phase compared with the normal diet. High-fat diet and/or stress caused a reduction in islet GLUT2 protein levels in both phases. In conclusion, it seems possible that high-fat diet alone or combined with foot-shock, predispose female rats to impaired insulin secretion, at least in part, by interfering with estradiol levels in the proestrus phase and decreasing pancreatic GLUT2 protein levels.
authors.affiliation: Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: M
authors.initials: M
authors.lastname: Salimi
authors.affiliation: Neurophysiology Research Center and Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. homeira_zardooz@yahoo.com, homeira_zardooz@sbmu.ac.ir.|Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: H
authors.initials: H
authors.lastname: Zardooz
authors.affiliation: NeuroBiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.|Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: F
authors.initials: F
authors.lastname: Khodagholi
authors.affiliation: Department of Biology, College of Basic Sciences, Yadegar-e-Imam Khomeini (RAH) Branch, Islamic Azad University, Tehran, Iran.
authors.forename: F
authors.initials: F
authors.lastname: Rostamkhani
authors.affiliation: Department of Physiology, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
authors.forename: F
authors.initials: F
authors.lastname: Shaerzadeh
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003345:Corticosterone / Q000097:blood; D004031:Diestrus / Q000097:blood / Q000378:metabolism; D059305:Diet, High-Fat; D004558:Electric Stimulation; D004958:Estradiol / Q000097:blood*; D005260:Female; D005528:Foot; D051273:Glucose Transporter Type 2 / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism; D010179:Pancreas / Q000378:metabolism*; D011359:Proestrus / Q000097:blood / Q000378:metabolism*; D017208:Rats, Wistar; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000097:blood / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D051273:Glucose Transporter Type 2; D007328:Insulin; C495683:Slc2a2 protein, rat; D004958:Estradiol; D003345:Corticosterone