title: Reduced urea flux across the blood-testis barrier and early maturation in the male reproductive system in UT-B-null mice.
abstract: A urea-selective urine-concentrating defect was found in transgenic mice deficient in urea transporter (UT)-B. To determine the role of facilitated urea transport in extrarenal organs expressing UT-B, we studied the kinetics of [(14)C]urea distribution in UT-B-null mice versus wild-type mice. After renal blood flow was disrupted, [(14)C]urea distribution was selectively reduced in testis in UT-B-null mice. Under basal conditions, total testis urea content was 335.4 +/- 43.8 microg in UT-B-null mice versus 196.3 +/- 18.2 microg in wild-type mice (P < 0.01). Testis weight in UT-B-null mice (6.6 +/- 0.8 mg/g body wt) was significantly greater than in wild-type mice (4.2 +/- 0.8 mg/g body wt). Elongated spermatids were observed earlier in UT-B-null mice compared with wild type mice on day 24 versus day 32, respectively. First breeding ages in UT-B knockout males (48 +/- 3 days) were also significantly earlier than that in wild-type males (56 +/- 2 days). In competing mating tests with wild-type males and UT-B-null males, all pups carried UT-B-targeted genes, which indicates that all pups were produced from breeding of UT-B-null males. Experiments of the expression of follicle-stimulating hormone receptor (FSHR) and androgen binding protein (ABP) indicated that the development of Sertoli cells was also earlier in UT-B-null mice than that in wild-type mice. These results suggest that UT-B plays an important role in eliminating urea produced by Sertoli cells and that UT-B deletion causes both urea accumulation in the testis and early maturation of the male reproductive system. The UT-B knockout mouse may be a useful experimental model to define the molecular mechanisms of early puberty.
authors.affiliation: Dept. of Reproductive Pathophysiology, School of Basic Medicine, Jilin University, Changchun, 130021, Jilin province, China.
authors.forename: Lirong
authors.initials: L
authors.lastname: Guo
authors.forename: Dan
authors.initials: D
authors.lastname: Zhao
authors.forename: Yuanlin
authors.initials: Y
authors.lastname: Song
authors.forename: Yan
authors.initials: Y
authors.lastname: Meng
authors.forename: Huashan
authors.initials: H
authors.lastname: Zhao
authors.forename: Xuejian
authors.initials: X
authors.lastname: Zhao
authors.forename: Baoxue
authors.initials: B
authors.lastname: Yang
mesh_terms: D000727:Androgen-Binding Protein / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001814:Blood-Testis Barrier / Q000254:growth & development / Q000378:metabolism*; D002199:Capillary Permeability; D005298:Fertility / Q000235:genetics; D018507:Gene Expression Regulation, Developmental; D008297:Male; D026901:Membrane Transport Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D009929:Organ Size; D012333:RNA, Messenger / Q000378:metabolism; D011962:Receptors, FSH / Q000235:genetics / Q000378:metabolism; D012708:Sertoli Cells / Q000378:metabolism / Q000473:pathology; D012726:Sexual Behavior, Animal; D012741:Sexual Maturation / Q000235:genetics; D013087:Spermatids / Q000378:metabolism / Q000473:pathology; D013091:Spermatogenesis / Q000235:genetics; D013737:Testis / Q000254:growth & development / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D014508:Urea / Q000097:blood / Q000378:metabolism*
chemical_list: D000727:Androgen-Binding Protein; D026901:Membrane Transport Proteins; D012333:RNA, Messenger; D011962:Receptors, FSH; C452857:urea transporter B, mouse; D014508:Urea