Abstract:The effects of 4-6 days of food deprivation on the pituitary-testicular function of adult male rats were studied. Fasting decreased body weights on average by 23% (P less than 0.01) and those of seminal vesicles by 55% (P less than 0.01) in 4 days. No consistent changes were found in testicular and ventral prostate weights. The pituitary levels of gonadotrophin-releasing hormone (GnRH) receptors decreased by 50% (P less than 0.01). Serum and pituitary levels of LH, FSH and prolactin decreased by 25-50% (P less… Show more
“…We also showed that starvation induced decreases in mRNAs encoding the LHβ-, FSHβ-and common α-subunit precursor molecules in the Japanese quail. In the rat, it was reported that starvation had a suppressive effect on the levels of FSHβ and common α mRNAs and no effect on the level of LHβ mRNA in the pituitary gland (Bergendahl et al, 1989 andBergendahl and Huhtaniemi, 1993). In the sheep, it was reported that long-term food restriction had no effect on the levels of gonadotropin subunit mRNA while it decreased levels of plasma gonadotropins (Thomas et al, 1990).…”
Section: Discussionmentioning
confidence: 99%
“…A series of papers with such approach has been published for the rat (Bergendahl et al ., 1989 andBergendahl and Huhtaniemi, 1993), with a similar paper also on the sheep (Thomas et al ., 1990).…”
“…We also showed that starvation induced decreases in mRNAs encoding the LHβ-, FSHβ-and common α-subunit precursor molecules in the Japanese quail. In the rat, it was reported that starvation had a suppressive effect on the levels of FSHβ and common α mRNAs and no effect on the level of LHβ mRNA in the pituitary gland (Bergendahl et al, 1989 andBergendahl and Huhtaniemi, 1993). In the sheep, it was reported that long-term food restriction had no effect on the levels of gonadotropin subunit mRNA while it decreased levels of plasma gonadotropins (Thomas et al, 1990).…”
Section: Discussionmentioning
confidence: 99%
“…A series of papers with such approach has been published for the rat (Bergendahl et al ., 1989 andBergendahl and Huhtaniemi, 1993), with a similar paper also on the sheep (Thomas et al ., 1990).…”
“…CR-induced suppression of the pulsatile release of GnRH from the hypothalamus is considered to be the central mechanism by which this reproductive perturbation occurs (Veldhuis et al, 1993;Cameron et al, 1991). It has been shown that GnRH receptor content (which is controlled by GnRH levels in the hypophyseal portal system) in the pituitary is sensitive to CR and fasting (Bergendahl et al, 1989;Greuenwald and Matusmoto, 1993). The resultant effects of short-term fasting, i.e.…”
Reduced energy intake, or caloric restriction (CR), is known to extend life span and to retard agerelated health decline in a number of different species, including worms, flies, fish, mice and rats. CR has been shown to reduce oxidative stress, improve insulin sensitivity, and alter neuroendocrine responses and central nervous system (CNS) function in animals. CR has particularly profound and complex actions upon reproductive health. At the reductionist level the most crucial physiological function of any organism is its capacity to reproduce. For a successful species to thrive, the balance between available energy (food) and the energy expenditure required for reproduction must be tightly linked. An ability to coordinate energy balance and fecundity involves complex interactions of hormones from both the periphery and the CNS and primarily centers upon the master endocrine gland, the anterior pituitary. In this review article we review the effects of CR on pituitary gonadotrope function and on the male and female reproductive axes. A better understanding of how dietary energy intake affects reproductive axis function and endocrine pulsatility could provide novel strategies for the prevention and management of reproductive dysfunction and its associated comorbidities.
“…Reduced food intake is known to be associated with reproductive dysfunction in humans (1,2), and rats (3)(4)(5). Several kinds of endogenous sugar acids found in rat blood have been reported to be involved in control of food intake (6,7).…”
Section: Introductionmentioning
confidence: 99%
“…There are some reports (3)(4)(5) that fasting impairs the pulsatile secretion of LH and that the specific opioid antagonist, naloxone or naltrexone, reverses this impairment (12,13). Therefore, EOPs may be involved in the 2-B4O-induced decrement in LH secretion.…”
Objective: To clarify the mechanism of the suppressive effect of 2-buten-4-olide (2-B4O), an endogenous feeding suppressant, on the pulsatile secretion of luteinizing hormone (LH), by studying whether endogenous opioid peptides are involved in this suppressive effect. Methods: Using ovariectomized (ovx) rats, blood samples were taken every 6 min for 2 h after administration of 2-B4O or saline into the third cerebroventricle (3V) and sequential i.v. injection of naloxone (0.5 mg/kg per h) or saline. Rats were divided into three experimental groups: group 1: 3V saline þ i.v. saline (control); group 2: 3V 2-B4O þ i.v. saline; group 3: 3V 2-B4O+i.v. naloxone. Serum LH concentrations were determined by double-antibody RIA. To determine whether 2-B4O affected the biosynthetic activity of the opioidergic neurons within the ovx rat arcuate nucleus, we measured the concentrations of pro-opiomelanocortin (POMC) mRNA, a precursor of b-endorphin, in the rostral arcuate nucleus using non-radioactive in situ hybridization and a computerized image-analysis system. Results: 2-B4O significantly suppressed the pulse frequency of LH (group 2: 1.5 Ϯ 0.33 pulses/2 h, group 1: 2.43 Ϯ 0.2 pulses/2 h; P < 0.05), but naloxone blocked its suppressive effect and restored the pulse frequency (group 3: 3.29 Ϯ 0.36 pulses/2 h, group 2: 1.5 Ϯ 0.33 pulses/2 h; P < 0.01). There were no significant changes in the mean LH concentrations and amplitude. Furthermore, 2-B4O significantly stimulated the expression of POMC mRNA in the rostral arcuate nucleus. Conclusion: These results suggest that 2-B4O may impair the pulsatile secretion of LH by activating the opioid pathway within the hypothalamus.
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