Background Global consumption of protein per capita is rising, while rates of infertility are increasing. However, a clear relationship between protein intake and reproductive health has not been demonstrated. The activation of the quiescent primordial follicles is the first step of folliculogenesis, and their activation must be tightly controlled to prevent premature exhaustion of the ovarian follicular reserve. Methods The primordial follicle reserve of wild-type or liver-specific ablation of fibroblast growth factor 21 (FGF21) in mice, subjected to limited or excessive protein diets or oral gavage test, were detected in vivo. Mouse ovary organ cultures were used to examine the direct role of metabolites or metabolic hormones on primordial follicle activation. Findings Mouse primordial follicle activation, was reduced by restricted protein intake and was accelerated by excessive protein intake, in an ovarian mTORC1 signaling-dependent manner. Furthermore, restricted or excessive protein intake resulted in an augmentation or decline of oocyte number and fertility at older age, respectively. Liver-specific ablation of FGF21, which resulted in a reduction of 87% in circulating FGF21, abrogated the preserving effect of low-protein intake on primordial follicle pool. Interestingly, FGF21 had no direct effect on the activation of primordial follicles, but instead required an adipokine adiponectin. Moreover, AdipoRon, an oral adiponectin receptor agonist, prevented the over-activation effect of excessive protein intake on primordial follicle activation. Interpretation Dietary protein consumption controlled ovarian primordial follicle reserve and fertility, which required coordination between FGF21 and adiponectin. Fund (Grant 31772616).

Both ovarian E2 and hepatic fibroblast growth factor 21 (FGF21) are critical for energy homeostasis and white adipose tissue browning. Estrogen receptor α (ERα) is abundantly expressed in liver. However, whether FGF21 has a role in E2-induced white adipose tissue browning remains uncertain. In this study, we showed that hepatic Fgf21 expression and secretion during estrus cycle changed with the tetradian oscillatory secretion of circulation E2 in adult, female mice, with their peak expressions and secretions at the proestrus. In addition, exogenous E2 robustly stimulated liver Fgf21 expression and elevated serum FGF21 concentrations, which induced browning gene expression and reduced the tissue weight in subcutaneous white adipose in mice with ovariectomies. The inhibitor of mammalian target of rapamycin (mTOR) and of ERα blocked the induction effect of E2 on the expression of Fgf21 in primary hepatocytes, which revealed that E2 might stimulate FGF21 expression via the ERα-mTOR pathway. Furthermore, FGF21 liver-specific deficiency abolished E2-induced white adipose browning in mice with ovariectomies. This study indicates that ovarian E2 increased liver FGF21 expression directly, which in turn, functioned as an endocrine signal to influence inguinal white adipose tissue browning.-Hua, L., Zhuo, Y., Jiang, D., Li, J., Huang, X., Zhu, Y., Li, Z., Yan, L., Jin, C., Jiang, X., Che, L., Fang, Z., Lin, Y., Xu, S., Li, J., Feng, B., Wu, D. Identification of hepatic fibroblast growth factor 21 as a mediator in 17β-estradiol-induced white adipose tissue browning.

The objective of this study was to investigate the effects of dietary supplementation with various fat sources (3.8-3.9% of diet) during late pregnancy and lactation on the reproductive performance, fatty acids profile in colostrum, milk and serum of sow progeny. A total of 80 multiparous sows were randomly fed a control (adding no oil), palm oil (PO), fish oil (FO) or soybean oil (SO) supplemented diet from 90 days of pregnancy to weaning. Supplementation of FO increased litter size of weak piglets, compared with the control-fed sows (P < 0.05). Dietary FO and SO supplementation, enhanced the weaning survival rate, litter weaning weight, litter weight gain and fat content in milk (P < 0.05). The highest immunoglobulin (Ig)G and IgM levels in colostrum and milk were observed in the FO group (P < 0.05). Meanwhile, the highest concentration of C22:5 (n-3) and C22:6 (n-3) in colostrum, milk and piglet serum was observed in the FO group (P < 0.05). Taken together, dietary inclusion of FO or SO improved growth performance of nursing piglets by increasing milk fat output, and FO consumption by sows might benefit the piglets via increasing n-3 polyunsaturated fatty acid availability and immunoglobulins (IgG and IgM) secretion.

BACKGROUND: Limited studies have examined links between maternal methyl donor (MET) supplementation and the growth-development characteristics of offspring, and possible underlying mechanisms for such links. This study investigated the effect of maternal or post-weaning MET-supplementation on growth performance, carcass characteristics, and meat quality of the finishing (d 180) offspring. Twenty-four sows were placed on a control (C) or MET-supplemented diet during pregnancy and lactation. Forty-eight female offspring were fed the control or MET-supplemented diet from weaning to 6 months of age, resulting in four study groups (six litters per group): C/C, C/MET, MET/C, and MET/MET. RESULTS: Maternal MET-supplementation increased average daily gain (ADG), body weight (BW), lean percentage and longissimus dorsi (LD) of the offspring at day 180 (P < 0.05), and upregulated the myosin heavy chain IIx, myogenic differentiation and muscle regulatory factor 4 mRNA levels in the LD muscle (P < 0.05). Meanwhile, offspring from maternal MET-supplementation exhibited a higher pH 24h post mortem and superoxide dismutase activity, a lower L * 45min , glycolytic potential, malonaldehyde content in the LD muscle, and plasma homocysteine concentration (P < 0.05). CONCLUSION: Maternal MET-supplementation has a remarkable effect on growth performance, carcass traits, and meat quality of the offspring, which is associated with increased expression levels of myogenic genes and anti-oxidant capacity.

No abstract