A single early postnatal estradiol injection affects morphology and gene expression of the ovary and parametrial adipose tissue in adult female rats.
Events during early life can affect reproductive and metabolic functions in adulthood. We evaluated the programming effects of a single early postnatal estradiol injection (within 3h after birth) in female rats. We assessed ovarian and parametrial adipose tissue morphology, evaluated gene expression related to follicular development and adipose tissue metabolism, and developed a non-invasive volumetric estimation of parametrial adipose tissue by magnetic resonance imaging. Estradiol reduced ovarian weight, increased antral follicle size and number of atretic antral follicles, and decreased theca interna thickness in atretic antral follicles. Adult estradiol-injected rats also had malformed vaginal openings and lacked corpora lutea, confirming anovulation. Estradiol markedly reduced parametrial adipose tissue mass. Adipocyte size was unchanged, suggesting reduced adipocyte number. Parametrial adipose tissue lipoprotein lipase activity was increased. In ovaries, estradiol increased mRNA expression of adiponectin, complement component 3, estrogen receptor α, and glucose transporter 3 and 4; in parametrial adipose tissue, expression of complement component 3 was increased, expression of estrogen receptor α was decreased, and expression of leptin, lipoprotein lipase, and hormone-sensitive lipase was unaffected. These findings suggest that early postnatal estradiol exposure of female rats result in long-lasting effects on the ovary and parametrial adipose tissue at adult age.
Institute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden. camilla.alexanderson@wlab.gu.se
Camilla
C
Alexanderson
Elisabet
E
Stener-Victorin
Joel
J
Kullberg
Staffan
S
Nilsson
Max
M
Levin
Stefan
S
Cajander
Lars
L
Lönn
Malin
M
Lönn
Agneta
A
Holmäng
D015502:Absorptiometry, Photon; D017667:Adipocytes / Q000166:cytology / Q000648:ultrastructure; D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D003176:Complement C3 / Q000235:genetics / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology*; D047628:Estrogen Receptor alpha / Q000235:genetics / Q000378:metabolism; D005260:Female; D051274:Glucose Transporter Type 3 / Q000235:genetics / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D006651:Histocytochemistry; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000235:genetics / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D010053:Ovary / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D012313:RNA / Q000737:chemistry / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D002787:Sterol Esterase / Q000235:genetics / Q000378:metabolism
D052242:Adiponectin; D003176:Complement C3; D047628:Estrogen Receptor alpha; D051274:Glucose Transporter Type 3; D051275:Glucose Transporter Type 4; D020738:Leptin; D004958:Estradiol; D012313:RNA; D002787:Sterol Esterase; D008071:Lipoprotein Lipase