title: Reduction of glucose availability suppresses pulsatile luteinizing hormone release in female and male rats.
abstract: Glucose availability controls reproductive activity through modulation of LH secretion. The aim of the present study was to determine whether the glucoprivic suppression is potentiated by gonadal steroids and if glucoprivic suppression of pulsatile LH release is sexually differentiated. Pulsatile LH secretion was examined in rats after peripheral (jugular) administration of the competitive inhibitor of glycolysis, 2-deoxyglucose (2DG). Fourteen days after gonadectomy, blood samples were collected every 6 min for 3 h. One hour after the onset of sampling, 2DG was administered peripherally (200, 400, or 800 mg/kg BW, iv), and food intake was determined after 2DG injection in gonadectomized males and females in the presence or absence of sex steroids (testosterone or estradiol). To test the ability of the pituitary to produce LH under glucoprivic conditions, LHRH was injected every 30 min for 2.5 h in ovariectomized (OVX) rats 30 min after treatment with 400 mg/kg 2DG. At all peripheral doses of 2DG in females and at the middle and high doses of 2DG in males, mean plasma LH and LH pulse frequency decreased (P < 0.05) in the presence of steroids. However, in the absence of sex steroids, the lowest dose in females and the middle dose in males were not effective. Pituitary function appeared normal, because increases in mean plasma LH in response to the exogenous LHRH occurred in OVX rats treated with the middle dose of 2DG. Food intake significantly (P < 0.05) increased after 2DG injection in all groups except estrogen-treated OVX females at the low and high doses of 2DG. These findings suggest that glucoprivic suppression of LH pulses is potentiated by gonadal steroids in both sexes. Moreover, the hypothalamo-hypophyseal axis of the female rat seems to be more sensitive to the decreased glucose availability induced by 2DG than that of the male.
authors.affiliation: School of Agricultural Sciences, Nagoya University, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Nagatani
authors.forename: D C
authors.initials: DC
authors.lastname: Bucholtz
authors.forename: K
authors.initials: K
authors.lastname: Murahashi
authors.forename: M A
authors.initials: MA
authors.lastname: Estacio
authors.forename: H
authors.initials: H
authors.lastname: Tsukamura
authors.forename: D L
authors.initials: DL
authors.lastname: Foster
authors.forename: K I
authors.initials: KI
authors.lastname: Maeda
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001682:Biological Availability; D002369:Castration; D003847:Deoxyglucose / Q000494:pharmacology; D004435:Eating / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000493:pharmacokinetics*; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D008297:Male; D009994:Osmolar Concentration; D011673:Pulsatile Flow; D051381:Rats; D017208:Rats, Wistar; D012737:Sex Factors
chemical_list: D004958:Estradiol; D007986:Luteinizing Hormone; D003847:Deoxyglucose; D005947:Glucose