• Development and Reproduction
• /
• v.5 no.2
• /
• pp.175-180
• /
• 2001

The ectopic expression of gonadotropin releasing hormone(GnRH and luteinizing hormone(LH) in several tissues is a quite intriguing phenomenon. Recently, the presence of GnRH and its receptor has been clearly demonstrated in rodents and human mammary gland. In this context, one can postulate that the presence of local circuit composed of GnRH and LH in the gland. The present study was undertaken to elucidate whether there is a correlation between the LH expression in rat mammary gland and physiological status during the process of mammary differentiation. LH contents in mammary gland from cycling to weaning rats were measured by radioimmunoassay(RIA). In cycling rats, changes of the LH level in both serum and mammary gland showed similar pattern as the highest level in proestrus and the lowest level in diestrus II stage. While the serum LH levels were fluctuated from pregnant through involution stage, a sharp decline of mammary LH contents was observed in the lactating rats. This decrement was recovered in involuting rats to the level of proestrus stage. Reverse transcription-polymerase chain reaction (RT-PCR) and Southern blot analyses demonstrated that the transcriptional activities of the mammary LH and GnRH were increased from diestrus I stage to estrus stage, and the increased levels were maintained in pregnant, lactation and involution stages. To test the hypothesis that the alteration in mammary LH expression might be steroid-dependant, ovariectomy(OVX) and steroid supplement model was employed. As expected, supplement of estradiol(E$_2$) after OVX remarkably decreased serum LH level compared to that in serum from vehicle-only treated rats. Likewise, administration of E$_2$ significantly reduced the mammary LH content. The present study demonstrated that (i) the LH expression in mammary gland could be altered by some physiological parameters such as estrous cycle, pregnancy, lactation and involution, and (ii) ovarian steroid especially estrogen seems to be one of major endocrine factors which are responsible for regulation of mammary LH expression.

• Asian-Australasian Journal of Animal Sciences
• /
• v.29 no.1
• /
• pp.36-42
• /
• 2016

Milk-related traits (milk yield, fat and protein) have been crucial to selection of Holstein. It is essential to find the current selection trends of Holstein. Despite this, uncovering the current trends of selection have been ignored in previous studies. We suggest a new formula to detect the current selection trends based on single nucleotide polymorphisms (SNP). This suggestion is based on the best linear unbiased prediction (BLUP) and the Fisher's fundamental theorem of natural selection both of which are trait-dependent. Fisher's theorem links the additive genetic variance to the selection coefficient. For Holstein milk production traits, we estimated the additive genetic variance using SNP effect from BLUP and selection coefficients based on genetic variance to search highly selective SNPs. Through these processes, we identified significantly selective SNPs. The number of genes containing highly selective SNPs with p-value <0.01 (nearly top 1% SNPs) in all traits and p-value <0.001 (nearly top 0.1%) in any traits was 14. They are phosphodiesterase 4B (PDE4B), serine/threonine kinase 40 (STK40), collagen, type XI, alpha 1 (COL11A1), ephrin-A1 (EFNA1), netrin 4 (NTN4), neuron specific gene family member 1 (NSG1), estrogen receptor 1 (ESR1), neurexin 3 (NRXN3), spectrin, beta, non-erythrocytic 1 (SPTBN1), ADP-ribosylation factor interacting protein 1 (ARFIP1), mutL homolog 1 (MLH1), transmembrane channel-like 7 (TMC7), carboxypeptidase X, member 2 (CPXM2) and ADAM metallopeptidase domain 12 (ADAM12). These genes may be important for future artificial selection trends. Also, we found that the SNP effect predicted from BLUP was the key factor to determine the expected current selection coefficient of SNP. Under Hardy-Weinberg equilibrium of SNP markers in current generation, the selection coefficient is equivalent to $2^*SNP$ effect.

• Development and Reproduction
• /
• v.12 no.3
• /
• pp.251-259
• /
• 2008

The plasticizer di(2-ethylhexyl)phthalate(DEHP) is one of the most well known endocrine disrupting chemicals (EDCs) because of its strong anti-androgenic effects on the reproductive and developmental process in male rodents and human. The present study was performed to examine whether prepubertal exposure to DEHP can make any alteration during the maturation of accessory sex organs in male rats. As a result, there was no significant change in body weights, serum T levels and tissue weights except of seminal vesicle and ventral prostate in DEHP-treated animals compared to vehicle-treated ones. The seminal vesicle weights in high-dose group (200 mg/kg) were significantly lower than those from the control group (p<0.05), and ventral prostate weights were significantly lower than those from the control group (p<0.05) in both low-dose (20 mg/kg) and high-dose group. Histological studies revealed that the seminal vesicles from DEHP-treated groups showed reduced areas of mucosal folds. Pseudostratified columnar epithelia were observed in the ventral prostates of DEHP-treated samples while cuboidal epithelia were found in the control group. The transcriptional activities of ER-$\alpha$ in seminal vesicle from high-dose group (p<0.05) were significantly higher than those from the control group, and ER-$\beta$ expression was significantly decreased in low-dose group (p<0.05) compared to the control. In ventral prostate, ER-$\beta$ mRNA levels from low-dose group (p<0.05) were significantly lower than those from the control group, and significantly increased in high-dose group (p<0.01). AR expressions, however, were not significantly different in all experimental groups of both seminal vesicle and ventral prostate. In conclusion, the present study demonstrated that (i) adverse effect (s) of DEHP on sexual maturation during prepubertal period could be limited, (ii) seminal vesicle and prostate gland were sensitive targets to DEHP in prepubertal rats and (iii) the deleterious effects of DEHP might be mediated through ER-associated mechanism.