title: Effect of transient hypothyroidism during infancy on the postnatal ontogeny of luteinising hormone release in the agonadal male rhesus monkey (Macaca mulatta): implications for the timing of puberty in higher primates.
abstract: The present study examined whether a transient thyroid hormone (T(4)) deficit during infancy in male monkeys would compromise the arrest of luteinising hormone (LH) secretion during the infant-juvenile transition, and/or interfere with the pubertal resurgence of LH. Animals were orchidectomized and thyroidectomized (n = 3; Tx) or sham Tx (n = 3) within 5 days of birth. T(4) replacement was initiated in two Tx monkeys at age 19 weeks to reestablish a euthyroid condition. Blood samples were drawn weekly for hormone assay. Body weight, crown-rump length, and bone age were assessed throughout the study. Within a week of Tx, plasma T(4) declined to undetectable levels and, by 6-8 weeks of age, signs of hypothyroidism were evident. Transient hypothyroidism during infancy failed to prevent either arrest of LH secretion during the infant-juvenile transition or the pubertal resurgence of LH secretion, both of which occurred at similar ages to sham Tx animals. Although body weight exhibited complete catch-up with T(4) replacement, crown-rump length and bone age did not. Thus, bone age at the time of the pubertal LH resurgence in Tx animals was less advanced than that in shams. Although Tx did not influence qualitatively the pattern of gonadotrophin secretion, LH levels during infancy and after pubertal LH resurgence were elevated in Tx monkeys. This was not associated with changes in LH pulse frequency and amplitude, but half-life (53 versus 65 min) of the slow second phase of LH clearance was greater in Tx animals. These results indicate that hypothalamic mechanisms dictating the pattern of gonadotrophin-releasing hormone release from birth to puberty are not dependent on T(4) action during infancy, and fail to support the notion that onset of puberty is causally coupled to skeletal maturation. They also indicate that LH renal clearance mechanisms may be programmed in a T(4) dependent manner during infancy.
authors.affiliation: Department of Cell Biology and Physiology, Magee-Womens' Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
authors.forename: T M
authors.initials: TM
authors.lastname: Plant
authors.forename: S
authors.initials: S
authors.lastname: Ramaswamy
authors.forename: G K
authors.initials: GK
authors.lastname: Bhat
authors.forename: C D
authors.initials: CD
authors.lastname: Stah
authors.forename: C R
authors.initials: CR
authors.lastname: Pohl
authors.forename: D R
authors.initials: DR
authors.lastname: Mann
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D007987:Gonadotropin-Releasing Hormone / Q000097:blood; D006801:Humans; D007037:Hypothyroidism; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008253:Macaca mulatta / Q000502:physiology*; D008297:Male; D009919:Orchiectomy; D011627:Puberty / Q000502:physiology*; D012741:Sexual Maturation / Q000502:physiology*; D013965:Thyroidectomy; D013974:Thyroxine / Q000008:administration & dosage / Q000172:deficiency
chemical_list: D007987:Gonadotropin-Releasing Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013974:Thyroxine; D002118:Calcium