An experiment was conducted to study the effects of feeding regimens on reproductive performance, plasma hormone and metabolite levels, and hepatic lipid metabolism of Cobb 500 broiler breeder hens from 26 to 38 wk of age. Seventy-two birds were used in a completely randomized design with 3 treatments, each replicated 4 times. Treatments were as follows: 1) once a day feeding, in which birds were fed once a day at 0615 h (control), 2) twice a day feeding, in which daily allocated feed was fed in 2 equal meals at 0615 and 1215 h, and 3) thrice a day feeding in which daily allocated feed was offered in 3 equal meals at 0615, 1215, and 1815 h. Through 38 wk of age, total hen-day egg production in the hens fed twice and thrice a day was greater (67.1 and 67.2 vs. 62.2 eggs/hen, P < 0.01). Similarly, egg weight was higher (P < 0.01) in birds fed more than once a day. Multi-meal-fed birds had significantly lower plasma triiodothyronine and glucose at 32 wk and also lower glucose and cholesterol, and higher 17β-estradiol levels at 38 wk than those fed once a day (P ≤ 0.05). Hepatic expression of malic enzyme, fatty acid synthase, acetyl-CoA carboxylase, and ATP citrate lyase relative to β-actin decreased (P < 0.05) in birds fed twice and thrice a day compared with birds fed once a day at peak egg production (32 wk). In contrast, feeding regimens did not affect the hepatic gene expression of lipogenic enzymes after peak egg production at 38 wk. Stearoyl-CoA desaturase 1 (SCD1) gene expression was constant over dietary regimens. There was no difference in malic enzyme activity in multi-meal-fed birds at 38 wk. In summary, feeding broiler breeder hens 2 or 3 meals per day improved the reproductive performance during the early lay cycle. Implementing twice or thrice a day feeding regimens altered hepatic lipogenic gene expression in broiler breeder hens only at peak egg production, which indicated a short-term effect of increasing feeding frequency on hepatic lipid metabolism.

Background and purpose The human X chromosome is enriched with testis-specific genes that may be crucial for male fertility. Mutations in USP26 gene have been proposed to be associated with male infertility. Moreover, the importance of the ubiquitin pathway during different stages of mammalian fertilization and even embryo development has been addressed. Some mutations and haplotypes on this gene have been proposed to be associated with male infertility. In this study, five different mutations on USP26 were investigated: 1737 G>A, 1090 C >T, 370-371ins ACA, 494 T>C and 1423 C>T. Methods The study included 166 infertile men with nonobstructive azoospermia, 72 male partners of couples who had previously experienced ≥3 clinical first trimester spontaneous abortions and 60 fertile men. Besides family history of reproduction, hormonal evaluation and semen analysis were performed. DNA was extracted from blood samples. PCR-SSCP, PCR-RFLP and PCR Product Cloning methods were used and resumed by sequencing to insure about the mutations. Moreover, USP26 gene expression was studied by Real-Time PCR after RNA extraction followed by cDNA synthesis from 24 testis biopsies in obstructive and non-obstructive azoospermia patients.Results The results indicate that there is a haplotype between three observed mutations in Iranian population include: 370-371insACA, 1423C>T and 494 T>C. This haplotype was seen in control group as well. Surprisingly, total frequency of mutations in men with history of idiopathic RPL and azoospermic cases were significantly higher than that of in control groups (p<0.05). Serum testosterone concentrations and testicular volume did not differ in the mutation positive group compared with the non-mutation group. About the USP26 gene expression, there is a significant difference between the expression levels of obstructive azoospermia, complete maturation arrest samples and SCO samples (P<0.05). Conclusions According to our results, the USP26 gene may play an important role in male reproduction. The alterations of this gene may be involved in male infertility and RPL in Iranian population and may negatively affect testicular function. Keywords Polymorphism . Male infertility . USP26Capsule In recent years, a lot of attention has been paid to genetic causes of male infertility. Moreover altered gene expression in spermatogenesis has been showed. Studies are mainly focusing on genes with a testis-specific expression pattern. Such genes which located on the sex chromosomes seem to be more important as men are hemizygous for these chromosomes. We analyzed the Ubiquitin Specific Protease 26 (USP26) gene for the presence of mutations in men with severe fertility problems.

No abstract