Reproductive workers insufficiently signal their reproductive ability in a paper wasp

Why workers forfeit direct reproduction is a crucial question in eusocial evolution. Worker reproduction provides an excellent opportunity to understand the mechanism of kin conflict resolution between the queen and workers. We evaluated behavioral and physiological differences among females in the paper wasp Polistes chinensis antennalis to examine why some workers reproduce under queenright conditions. Reproductive workers were old and foraged less early in the season; their cuticular hydrocarbon (CHC) profiles overlapped with those of queens but were significantly different. The distinct CHC profile of the eggs of the queen likely represented a cue for policing against those by workers. Juvenile hormone (JH) and dopamine seemed to be associated with gonadotropic function, and the JH level of reproductive workers was similar to that of the queen. The high JH level of reproductive workers likely facilitated their reproduction even under queenright conditions. Gene expression levels of the queen and reproductive workers differed only in vitellogenin. These results suggest that worker reproduction is facilitated by an increase in JH level; however, CHC is not a fertility-linked signal, but a queen-linked signal; consequently, reproductive workers without a queen-linked signal might be allowed to stay within the colony.

The state of steroidogenesis in the adrenal glands and gonads in patients with polycystic ovary with inhibition of gonadotropic function

Relationships between secretion of pituitary gonadotropic hormones, adrenal glucocorticoid and androgenic function, and ovarian steroid production were studied in 14 patients with the polycystic ovaries syndrome (POS) under conditions of suppressed endogenous gonadotropic secretion, which was induced by tonic administration of busereline, a GnRH agonist. The bRH/iRH ratio is not changed in POS patients under conditions of suppressed gonadotropic secretion. Inhibition of gonadotropic secretion leads to decrease of estrogen secretion in the ovaries and does not affect the adrenal glucocorticoid function. Activation of adrenal androgen production by the delta-5 pathway was observed in 57% patients under conditions of gonadotroph inhibition. Three months after busereline was discontinued, adrenal steroidogenesis normalized. The results permit a conclusion that prolonged inhibition of gonadotropic secretion with GnRH agonist does not change the bLH/iLH ratio but can lead to activation of adrenal androgen production in part of patients with POS.

PREDICTORS OF THE DEVELOPMENT OF SYNDROME OF THE HYPER-INHIBITION OF GONADOTROPIC FUNCTION OF THE HYPOPHYSIS FOLLOWING LONG-TERM INTAKE OF COMBINED ORAL CONTRACEPTIVES

The review presents information on the syndrome of hyper-inhibition of gonadotropic function of the pituitary gland (HIGHFG) developing in patients against the background of a long (from a year or more) intake of combined oral contraceptives. This syndrome is presented in the form of secondary amenorrhea after drug withdrawal. Depending on the severity, moderate and full forms of the syndrome are separated. The pathogenesis of the development of HIGHFG, diagnostic criteria, clinical and laboratory predictors of the development, and preventive measures are considered.

Reproductive system of women with acromegaly

192 patients with acromegaly were examined. Their reproductive disorders were found to be a result of the suppressed synthesis of gonadotropin hormones due to the tumor compression of the adenohypophysis, due to blocking effect of hyperprolactinemia on the gonadotropic function or as a result of the direct impact of insulin-like growth factor-I stimulating hyperplastic processes in target organs, such as ovaries, the glandular epithelium of the breast and myometrium. The structure of reproductive disorders in patients with acromegaly includes menstrual disturbances, infertility, early menopause and hyperplastic processes. Close management of the reproductive system, early detection of neoplasia and correction of the existing disorders are highly required during therapy for acromegaly.

Acute inflammation reduces kisspeptin immunoreactivity at the arcuate nucleus and decreases responsiveness to kisspeptin independently of its anorectic effects

Severe inflammatory challenges are frequently coupled to decreased food intake and disruption of reproductive function, the latter via deregulation of different signaling pathways that impinge onto GnRH neurons. Recently, the hypothalamic Kiss1 system, a major gatekeeper of GnRH function, was suggested as potential target for transmitting immune-mediated repression of the gonadotropic axis during acute inflammation, and yet key facets of such a phenomenon remain ill defined. Using lipopolysaccharide S (LPS)-treated male rats as model of inflammation, we document herein the pattern of hypothalamic kisspeptin immunoreactivity (IR) and hormonal responses to kisspeptin during the acute inflammatory phase. LPS injections induced a dramatic but transient drop of serum LH and testosterone levels. Suppression of gonadotropic function was associated with a significant decrease in kisspeptin-IR in the arcuate nucleus (ARC) that was not observed under conditions of metabolic stress induced by 48-h fasting. In addition, absolute responses to kisspeptin-10 (Kp-10), in terms of LH and testosterone secretion, were significantly attenuated in LPS-treated males that also displayed a decrease in food intake and body weight. Yet pair-fed males did not show similar alterations in LH and testosterone secretory responses to Kp-10, whose magnitude was preserved, if not augmented, during food restriction. In summary, our data document the impact of acute inflammation on kisspeptin content at the ARC as key center for the neuroendocrine control of reproduction. Our results also suggest that suppressed gonadotropic function following inflammatory challenges might involve a reduction in absolute responsiveness to kisspeptin that is independent of the anorectic effects of inflammation.