Influence of streptozotocin-induced diabetes and insulin treatment on the pituitarv-testicular axis during sexual maturation in rats

Abstract

Effects of streptozotocin (STZ) diabetes and insulin treatment on the functioning of pituitary-testicular axis during sex ual maturation was studied. Prepubertal (30 days old) and pubertal (50 days old) male Wistar rats were made diabetic by a single injec tion of STZ. A group of diabetic rats was given insulin (3U/100 g b.wt./day in 2 equally divided doses), 3 days after STZ treatment. Prepubertal and pubertal rats of all groups were killed on postnatal days 51 and 71, respectively. STZ-diabetes caused marked reduction in serum EH, ESH, prolactin, testosterone and testicular interstitial tluid testosterone as well as the activities of Leydig cellular ster oidogenic enzymes (3[i-and 17P-hydroxysteroid dehydrogenases). Insulin treatment to diabetic rats maintained these changes at con trol range except FSH and prolactin in prepubertal rats. The results indicate that (i) diabetes-induced steroidogenic lesions in l.eydig cells represent a direct consequence of dysfunctioning of pituitarytesticular axis, (ii) the adverse effects of diabetes on pituitarytesticular functions are influenced by age of its induction and (iii) optimum insulin level is essential for the acquisition of Eeydig cellular steroidogenic efficacy during sexual development.

Antidiabetic therapies and male reproductive function: where do we stand?

“…Insulin was observed to restore serum LH and testosterone levels in both groups, highlighting the regulatory role of insulin in gonadotrophin secretion and on Leydig cell steroidogenic ability acquisition during sexual maturation. Nonetheless, FSH and prolactin levels were not restored by insulin on prepubertal rats, suggesting that the initiation of diabetes before puberty impairs the functional maturation of the pituitary-testicular axis in a different fashion and that insulin regulates the pituitary differently, depending on the stage of development (Sudha et al 2000).…”

“…In fact, this degenerative disease was described to affect not only sperm quality and function R S Tavares and others R14 (Bartak et al 1975, Padron et al 1984, Handelsman et al 1985, Vignon et al 1991, Baccetti et al 2002, Soudamani et al 2005, Amaral et al 2006, Scarano et al 2006, Agbaje et al 2007, Delfino et al 2007, Shrilatha & Muralidhara 2007a, Rama Raju et al 2012, Roessner et al 2012, Schoeller et al 2012a, Mangoli et al 2013 but also the hypothalamus-pituitary-gonadal axis (HPG) (Benitez & Perez Diaz 1985, Seethalakshmi et al 1987, Sudha et al 2000, Baccetti et al 2002, Lopez-Alvarenga et al 2002, Ballester et al 2004, Kim & Moley 2008, Schoeller et al 2012b, the testicular function and spermatogenesis (Cameron et al 1985, Gondos & Bevier 1995, Sanguinetti et al 1995, Sainio-Pollanen et al 1997, Ballester et al 2004, Arikawe et al 2006, Amaral et al 2009, Kianifard et al 2012, Schoeller et al 2012b, Wankeu-Nya et al 2013, Kyathanahalli et al 2014, Tavares et al 2016, the accessory organs (epididymis, prostate and seminal vesicles) (Murray et al 1981, Fukumoto et al 1993, Ikeda et al 2000, Saito et ...…”

“…There is a wide disparity regarding the effects of insulin treatment on gonadotrophin levels in diabetic individuals with reports ranging from a total recovery of both LH and FSH (Seethalakshmi et al 1987), to the recovery of just one (Perez Diaz et al 1982, Hutson et al 1983, Benitez & Perez Diaz 1985, Sudha et al 2000 or even the absence of effects (Steger & Kienast 1990), suggesting that testicular function regulation is the result of a complex process in which several players are involved. Other studies have explored these aspects in more detail, and insulin treatment was observed to totally reverse all parameters of pulsatile LH secretion, which were reduced in diabetic rats and, at least partially, due to a decreased responsiveness of the pituitary to GnRH (Dong et al 1991).…”

“…Furthermore, central insulin infusion was observed to increase LH pulse frequency, although in a lower extension than the peripheral one, suggesting that central insulin has also a role in pulsatile GnRH secretion regulation (Tanaka et al 2000). Aiming to clarify if the insulin action is dependent on the sexual maturation phase in which diabetes is detected, a study was conducted in both prepubertal and pubertal diabetic rats (Sudha et al 2000). Insulin was observed to restore serum LH and testosterone levels in both groups, highlighting the regulatory role of insulin in gonadotrophin secretion and on Leydig cell steroidogenic ability acquisition during sexual maturation.…”

Protective effects of <i>Lycium barbarum</i> polysaccharide on male sexual dysfunction and fertility impairments by activating hypothalamic pituitary gonadal axis in streptozotocin-induced type-1 diabetic male mice

“…The failure of the hypothalamic pituitary gonadal axis maintaining proportionate levels of these endogenous hormones may result in disruption of spermatogenic and sexual function; and ultimately leads to infertility [18]. Systemic metabolic imbalance in long-standing severe hyperglycaemia affects the hypothalamic pituitary testis axis function, disturbs the jurisdiction function of the endocrine system, and influences steroidogenic capacity of Leydig cells [19][20][21]. Studies have suggested that STZ induced diabetes caused 2 major changes in Leydig cells: 1) a decrease in total Leydig cells number, and 2) an impairment in cells function [21].…”