It is known that maternal nutrition during pregnancy could have impacts on the reproductive success of the offspring.
Our experiment was designed to determine if maternal consumption of differing levels of energy and selenium (Se) impacts fetal ovarian development.
We determined that the numbers of follicles and proliferation of different cell types in the fetal ovary are impacted by maternal diet. Therefore, future studies in which ewe lambs are allowed to grow and are mated may have different success in attaining pregnancy.
It has been clearly demonstrated that environmental factors, including nutrition can affect growth, development and physiology in the fetal and postnatal life of mammals. Both, undernutrition and overnutrition of pregnant ewes negatively affect fetal growth and development. In fact, cellular proliferation in fetal ovaries is regulated by numerous fetal and maternal factors including factors originating from maternal diet. It is interesting to think that the reproductive success of the offspring may be preset in the womb, prior to birth. We believe that the uterine environment may impact the female fetus so that she may be more reproductively capable later in life.
We hypothesized that undernutrition and level of Se in maternal diet will affect cellular proliferation in fetal ovaries.
Therefore, the objective of this experiment was to determine:
1) if maternal dietary restriction and differing levels of Se in diet impacts cellular proliferation in fetal ovarian follicles, stromal tissue and blood vessels, and
2) incidence of apoptosis and blood vessel distribution in fetal ovaries obtained from sheep in late pregnancy.
Animals and Treatments
The Institutional Animal Care and Use Committee at NDSU approved all animal procedures in this study. Following breeding, ewes were assigned randomly to either an adequate (ASe) or high (HSe) dietary Se treatment. Ewes were pen-fed a basal diet (2.04 kg/ewe/day) that contained (dry matter basis) 47% alfalfa hay, 20% corn, 20% sugarbeet pulp pellets, 8% malt barley straw, and 5% concentrated separator byproduct. In addition to the basal diet, ewes assigned to the ASe treatment were fed 100 g/day of a control pellet that was balanced to contain 0.30 ppm Se (6 μg/kg body weight), whereas HSe ewes were fed 100 g/day (80 μg/kg body weight) of a high-Se pellet balanced to contain 47.5 ppm Se, provided as Se-enriched yeast (Sel-Plex, Alltech, Nicholasville, KY). The control (ASe) and HSe pellets were formulated using similar ingredients to maintain similar concentrations of metabolizable energy (ME), crude protein, acid detergent fiber, neutral detergent fiber, Ca, and P. Selenium-enriched yeast replaced soybean meal and partially replaced ground corn relative to the control pellet. The approach by which dietary Se was supplemented to pregnant, primigravid ewes has been used previously by our laboratory.
On day 50 of gestation, ewes within each Se treatment were stratified by average breeding date and assigned to 1 of 2 distinct planes of nutrition treatments. Ewes were offered diets that were balanced to meet either 100% [maintenance (M)] or 60% [restricted (R)] of predicted metabolizable energy (ME) requirements of pregnant ewe lambs. The plane of nutrition treatments were applied from day 50 to 135, which resulted in 4 distinct treatment combinations designated by the following; M ASe (n=8 ewes), M HSe (n=8), R ASe (n=10) and R HSe (n=6). Ewes (n=32) with female singleton fetuses from which fetal ovaries were collected were included to this study.
Tissue Collection and Immunohistochemistry
On day 135 of the pregnancy, fetal weight was recorded, and fetal ovaries were collected and weighed. One ovary was fixed in Carnoy’s solution and the other ovary in 10% formalin solution, and after dehydration, ovaries were embedded in paraffin. Ovaries (n=6-10/treatment) were sectioned (one section/ovary along the longitudinal axis) at 5 μm and mounted onto a glass slide.
Detection of proliferating cell nuclear antigen (PCNA; a marker of proliferating cells) and factor VIII (a marker of endothelial cells and thus vascularization) was performed as previously described in Carnoy’s fixed tissues. Briefly, ovarian tissue sections were deparaffinized, rehydrated, and incubated with 3% H2O2 in methanol to eliminate endogenous peroxidase activity. Then, sections were rinsed several times in PBS containing Triton-X100 (0.3%, vol/vol) and treated for 20 min with PBS containing normal horse serum (3%, vol/vol; ABC kit, Vector Laboratories, Burlingame, CA) to block nonspecific binding of antibodies. Sections were incubated overnight at 4ºC in PBS containing a primary monoclonal mouse antibody against PCNA (1:500 dilution; MAB24R, Chemicon International, Temecula, CA) or rabbit polyclonal antibody against factor VIII (1:100 dilution; Sigma, St. Louis, MO). Primary PCNA or factor VIII antibodies were detected by using biotin-labeled secondary anti-mouse or anti-rabbit antibodies (Vector Laboratories), respectively, and the ABC method. For color development, SG substrate was used as described. For controls, the primary antibody was replaced with normal mouse IgG (4 µg/mL) or rabbit serum. After immunostaining of PCNA, tissue sections were counterstained with nuclear fast red to visualize nuclei.
To localize apoptotic cells in fetal ovarian sections fixed in formalin, TdT-FragELTM , DNA fragmentation detection kit was used according to the manufacturer’s protocol (Oncogene Research Products, San Diego, CA). As a positive control, tissues sections from the corpora lutea undergoing luteolysis were used as described before.
For all ovaries, the images of stained sections (0.025 mm2 per field) were taken for each of the four types of follicles (e.g., primordial, primary, secondary and antral), for stromal tissue not containing follicles and for all visible blood vessels (2-12 images/ovary). The primordial follicle was considered as proliferating when at least one granulosa cell was PCNA-positive. For secondary and antral follicles, labeling index (LI) was determined for granulosa and theca layers separately. Labeling index was calculated as a percentage of proliferating cells out of the total cells per marked area of follicle, stromal tissue or blood vessel. The total number of primary, secondary and antral follicle analyzed was 320, 446 and 324, respectively. The LI for thecal cells included all labeled cells, and no attempt was made to distinguish between thecal cell types within thecal layer. For blood vessels (>20 μm diameter), both endothelium and smooth muscle cell layers were analyzed together. The images were then used for quantitative image analysis using the Image Pro-plus software (Media Cybernetics Inc., Silver Spring, MD) to determine the proportion (%) of proliferating primordial follicle of the total number of primordial follicles in the area, and LI for granulosa and theca cells of the primary, secondary and antral follicles, stromal tissues and blood vessels for the four types of treatment groups.
Data are expressed as mean ± SEM. Data were analyzed as a completely randomized design with a 2 x 2 factorial arrangement of treatments using PROC GLM (SAS Inst. Inc. Cary, NC, 2005). The model contained effects for nutrition (M and R), level of Se (ASe and HSe), and the nutrition X Se interactions. When the F-test was significant (P < 0.05), differences among means were evaluated by using the least square means procedure. Means were considered different when P < 0.05 unless otherwise stated.
Fetal weight tended (P < 0.1) to be less in groups fed R diet (3,427 ± 192 g) than those fed M diet (3,860 ± 165 g). However, levels of Se in diet did not affect fetal weight, and there were no interactions between plane of nutrition and Se levels in diet. Dietary restriction in maternal diet affected fetal ovarian weight, which was less (P < 0.01) for groups fed R diet (66 ± 4 mg) than for those fed M diet (93 ± 9 mg). However, levels of Se in diet did not affect fetal ovarian weight, and there were no interactions between plane of nutrition and Se levels in diet. Fetal ovarian weight in groups fed R diet with ASe or HSe was less (P < 0.03) than in group fed M diet with HSe but similar to group fed M diet with ASe (Table 2).
All fetal ovaries contained primordial, primary, and secondary follicles. Presence of antral follicles was detected in 72% ovaries (23 out of 32 ovaries analyzed). Maternal diet did not have any effect on incidence of antral follicles in fetal ovaries. Proliferating cells were detected in primordial, primary, secondary, and antral follicles, in stromal tissues and blood vessel of fetal ovaries.
The effects of dietary restriction (P < 0.08) and Se (P < 0.07) levels but no interaction between plane of nutrition and Se in diet on proportion of proliferating primordial follicles were observed. In addition, the effects of dietary restrictions (P < 0.08) but not Se or interactions between plane of nutrition and Se in diet on LI of primordial follicles were observed. The proportion of proliferating primordial follicles was less (P < 0.08) in groups fed R diet than groups fed M diet (7.4 ± 1.2 vs.11.3 ± 1.7%), and was less (P < 0.07) in groups fed HSe than ASe (7.0 ± 1.0 vs.10.9 ± 1.6). The proportion of proliferating primordial follicles was greater (P < 0.05) in the group fed M diet with ASe than in other treatment group. Labeling index of primordial follicles tended (P<0.08) to be less in groups fed R than M diet (2.9 ± 0.4 vs. 4.9 ± 094). Labeling index tended (P=0.1) to be greater in group fed M diet with ASe that in any other group.
Overall, LI was greatest (P < 0.001) in granulosa cells of secondary and antral follicles, less in primary follicles, and least in primordial follicles (19.4 ± 0.6 and 19.5 ± 0.6 vs. 10.4 ± 0.4 vs 4.6 ± 0.5%). Labeling index in granulosa and theca cells of secondary (granulosa, 21.1 ± 0.8% vs. theca, 17.8 ± 0.7%) and antral (granulosa, 19.4 ± 0.8% vs. theca, 19.7 ± 1%) follicles was similar. Therefore, data for granulosa and theca were combined and analyzed together within secondary and antral follicles.
For primary follicles, interactions (P < 0.02) between plane of nutrition and Se levels in diet on LI was observed. Labeling index in granulosa layer of primary follicles was less (P < 0.04) in group fed R diet with HSe than in groups fed M diet with HSe or R diet with ASe. For secondary follicles, the interactions (P < 0.09) between plane of nutrition and Se levels in diet, and the effects of level of Se in diet (P < 0.005) on LI in were observed. Labeling index was less (P < 0.005) in groups fed diet with HSe than with ASe (17.3 ± 0.8 vs. 21.0 ± 0.8%). Labeling index was less (P < 0.03) in the group fed M diet with HSe than in the groups fed M diet with ASe or fed R diet with ASe, but it was similar to group fed R diet with HSe. For antral follicles, LI was affected by level of Se in diet, which was less (P < 0.01) in groups fed with HSe than with ASe (17.3 ± 0.9 vs. 20.9 ± 0.8%). Labeling index was less (P < 0.002) in group fed M diet with HSe that in any other treatment group. For stromal tissues, interactions (P < 0.09) between plane of nutrition and Se levels and the effects of Se level in diet (P < 0.03) on LI were observed. Labeling index was less (P < 0.03) in groups fed diet with HSe than with ASe (3.6 ± 0.8 vs. 6.9 ± 1.1 %). Labeling index was greater (P < 0.05) in the group fed M diet with ASe than in any other treatment group. For blood vessels, the effects of plane of nutrition (P < 0.09) and Se level (P < 0.01) in diet on LI were observed. Labeling index tended (P < 0.09) to be less in groups fed R than M diet (7.9 ± 2.2 vs. 11.6 ± 2.7 %), and LI was less (P < 0.01) in groups fed diet with HSe than with ASe (6.2 ± 1.5 vs. 13.7 ± 0.7 %). Labeling index in blood vessels was greater (P < 0.04) in the group fed M diet with ASe than any other treatment group. In the majority of fetal ovarian tissue sections apoptotic cells were not detected. Only in a few tissues sections (5 out of 32), apoptotic cells were present occasionally in a granulosa layer or stromal tissues in fetal ovaries. Apoptotic cells were also detected in ovine luteal tissues serving as a control. Appearance of apoptotic cells in fetal ovaries was not affected by nutritional treatment. Blood vessels marked by factor VIII staining were detected in fetal ovaries. Smaller size (≤ 30 μm) blood vessels were present in the areas containing primordial to antral follicles, and larger (> 30 μm) and small blood vessels were detected in ovarian medulla and hilus. For antral follicles, a network of blood vessels was detected in the theca layer. However, areas containing primordial follicles were rather poorly vascularized. Distribution of blood vessels in the ovaries seemed to not be affected by nutritional treatment.
The results of this experiment show that both maternal dietary restrictions and level of Se in the diet differentially affected cell proliferation depending on fetal ovarian tissue compartment. This indicates that plane of nutrition and Se in the maternal diet are involved in the regulation of early folliculogenesis and ovarian tissue growth. In fact, dietary restriction tended to suppress cellular proliferation in primordial follicles and blood vessels but high Se levels suppressed cellular proliferations in primordial, secondary and antral follicles, stromal tissues and blood vessels. These observations are novel, since very limited information is available concerning maternal diet on cellular processes within specific compartments of fetal ovaries including developing follicles and supporting tissues such as stroma and blood vessels. In addition, these data emphasize importance of maternal diet for fetal tissue and organ growth, which is a central concept of fetal/developmental programming (Nathanielsz, 2006; Barker, 2007).
Dietary restrictions, but not Se, in the maternal diet tended to affect fetal weight of the female lambs in our study. However, inconsistent results of the effects of nutrient restrictions on total fetal weight (i.e. difference due to fetal sex were not reported) at the end of pregnancy in sheep were reported, showing decrease or no effects on fetal weight (Osgerby et al. 2002; Rae et al. 2001; Redmer et al. 2004; Lea et al. 2006; Luther et al. 2007). Similar to our findings, a lack of effect of the maternal dietary restriction or environmental pollutants on ovine fetal ovarian weight was reported by others (Rae et al. 2001; Osgerby et al. 2002; Murdoch et al. 2003; Fowler et al., 2008). Thus, the effects of maternal diet restriction on fetal growth seem to depend on the level and/or length of restriction, and the time of restriction implementation. In addition, it seems that level of Se in maternal diet composition does not affect fetal ovarian growth.
By the end of pregnancy, fetal ovaries may contain all types of follicles including primordial, primary, secondary and antral follicles, as observed in this and other studies in sheep and cattle (Wandji et al. 1992; Lundy et al. 1999; Bodensteiner et al. 2000; Rae et al. 2001). Growth and development of fetal ovaries is regulated by numerous factors of fetal and maternal origin including FSH, LH, estrogens, activin, c-kit and its ligand stem cell factor, enzymes controlling steroidogenesis, growth differentiation factor 9, epidermal growth factor and many other factors (McNatty et al. 2000; Tanaka et al. 2001; Juengel et al. 2002; Sawyer et al. 2002; Byskov & Westergaard 2004; van der Hurk & Zhao 2005; Pepe et al., 2006). Since we rarely detected apoptotic cells and atretic follicles in fetal ovaries, it seems that by the end of pregnancy, selected ovarian compartments are rather in the growing phase, and the apoptotic process is minimal. In fact, our observations are in agreement with previously published data demonstrating very low apoptosis in ovine fetal ovaries on day 99 of pregnancy, but enhanced apoptosis in the earlier stages (days 58 to 73) of pregnancy (Murdoch et al. 2003; Qi et al. 2008). Although altered expression of genes Bax and Mcl-1 which are associated with apoptosis, in fetal ovaries on day 110 of pregnancy was reported for underfed sheep, it is unclear if changes in gene expression were accompanied with appearance of apoptotic cells/bodies (Lea et al. 2006). Thus, these data indicate that apoptosis in fetal ovaries is negligible during late pregnancy.
In our study, 8-13% of primordial follicles had at least one granulosa cells that stained positively for PCNA. In contrast, Lundy et al. (1999) demonstrated that 98.7% primordial follicles contained at least one proliferating granulosa cell in fetal ovaries on day 135 of gestation in sheep. These differences are likely due to different techniques used to determine proportion of proliferating cells even though both studies used PCNA as a marker of proliferating cells. We used 5 μm histological sections to determine differences in proportion of proliferating primordial follicles in between nutritional treatments. However, Lundy et al. (1999) used a nucleator technique to determine a proportion of proliferating follicles within a follicle type which allowed for determination of the absolute number of granulosa cells in the individual follicle.
The present study demonstrated that the LI was less in primordial than primary follicles, and than in secondary and antral follicles (5% vs 10% vs. 19%). Similar to our study, LI was less in primary follicles than secondary and antral follicles in adult rat ovaries (Gaytan et al. 1996). Since a longer period of time is required for a new growing follicle to reach the preantral stage than for a transition from the preantral stage to antral follicle (Gougeon 2004), we hypothesize that differences in LI in follicle types may reflect the timing of growth from primordial to primary, from primary to secondary follicle stage, or from secondary to antral follicle stage. However, this subject requires additional study, since very little information is available concerning timing of the follicular growth in fetal ovaries.
The proliferation in granulosa and theca cells of antral fetal follicles (17-20%) was within a range of LI (17-22%) reported for small follicles from adult ovine ovaries (Jablonka-Shariff et al. 1994, 1996). This indicates that cellular proliferation within small antral follicles remains at similar level in fetal ovaries and ovaries from adult animals. In addition, the LI in stromal cells (3-9%) and in blood vessels (9-20%) were also very high. These great levels of cellular proliferation clearly demonstrate that growth of ovarian follicles is accompanied by growth of surrounding stromal tissues and angiogenesis in fetal ovaries at the end of pregnancy. In addition to providing the scaffold for growing follicles and blood vessels, stromal tissues are the source of matrix metalloproteinases and tissue inhibitors which likely play a role in fetal gonadal development (Robinson et al. 2001). Stromal tissues also express estrogen, androgen and progesterone receptors, which are likely involved in the regulation of fetal ovarian growth (Juengel et al. 2002). Vasculogenesis and angiogenesis, marked in this study with high proliferation in blood vessels and a dense network of blood vessels in medulla, hilus, and areas containing primordial to antral follicles, are critical for supporting fetal organ growth (Augustin 2000). In addition, vascular endothelial growth factor protein, the potent angiogenic factor, is expressed in ovine fetal ovaries (Grazul-Bilska, unpublished). Although angiogenesis in adult ovaries has been studied extensively (Redmer & Reynolds 1996; Grazul-Bilska et al. 2001; Fraser 2006), little is known about the angiogenic process in fetal ovaries, and therefore, it needs further investigation. Nevertheless, a high density of blood vessels in ovarian medulla and hilus, and high proliferation in blood vessels and stromal tissues observed in this study indicates that fetal ovaries are fast growing and differentiating. In fact, it seems that by the end of pregnancy, fetal ovaries are approaching a very fast growth stage, as ovaries increase more than 10-fold (from ~80 mg to 1 g), while offspring weight increases only 3-fold (from ~3.5 to 10 kg) from day 135 of gestation to day 20 postpartum (Grazul-Bilska, Vonnahme et al., unpublished). Thus, it is reasonable to postulate that high cellular proliferation in stroma and blood vessels observed in this study is critical for ovarian growth support. Moreover, a complex vascular network in the mouse fetal ovaries has been recently described by Bullejos et al. (2002) which emphasize the importance of blood supply to developing organs. Cellular proliferation in stromal tissues and blood vessels in fetal ovaries are likely controlled by growth and other factors. However, very little information is available concerning the expression and function of growth factors in fetal ovaries (McNatty et al., 2000), and mechanism of regulation of fetal ovarian growth remains to be elucidated.
The present results clearly demonstrated that maternal diet affects cellular proliferation in fetal ovaries. The similar pattern of cellular proliferation decrease in primordial, secondary or antral follicles, stromal tissues and blood vessels was observed in groups fed R diet or in groups fed high Se comparing with groups fed M diet with ASe in our study. However, differential effects of maternal diet on cellular proliferation in follicle types (e.g., primary vs. secondary or antral) were observed in this study. These differences are likely due to a specific stage of follicular development regulation by factors controlling ovarian growth and function (McNatty et al. 2000; Erickson, 2001; Sawyer et al. 2002; Byskov & Westergaard 2004; van der Hurk & Zhao 2005). In fact, the diverse effects of maternal diet on ovine fetal ovaries including ovarian weight, delayed ovarian growth and development, and altered ovarian cell proliferation and apoptosis have been reported by others (Borwick et al. 1997; Rae et al. 2001; Da Silva et al. 2002, 2003; Osgerby et al. 2002). In addition, maternal undernutrition has been demonstrated to reduce the number of follicles beyond the primordial stage in sheep (Rae et al. 2001). This may be associated with reduced cellular proliferations in primordial follicles observed in our study, which likely progressed at slower rates to primary and secondary follicle stage in underfed compared to normally fed animals.
In contrast to our observations, Lea et al. (2006) reported enhanced cellular proliferation in granulosa layer of fetal follicles on day 110 of gestation in underfed sheep. In addition, undernutrition did not change cellular proliferation in primordial follicles (Lea et al. 2006). These differences are likely due to different length of nutritional restrictions and different gestational time point for tissue collection.
In our study, high Se in the maternal diet decreased cellular proliferation in primordial, secondary and antral follicles, stromal tissues and blood vessels. Interestingly, high Se in the maternal diet also decreased jejunal proliferation in female and male fetuses in a similar study (Carlson et al. 2008). In fact, it has been demonstrated that Se is involved in the regulation of cell proliferation (Zeng et al. 2002) and angiogenesis inhibition in mammary cancer (Jiang et al. 1999). Furthermore, high Se concentration can decrease cell proliferation through inhibition of DNA synthesis and induction of apoptosis (Salbe et al. 1990; Yeh et al. 2006; Zeng & Combs 2008). Since, we rarely detected apoptotic cells in fetal ovaries in this study, we hypothesize that high Se in the maternal diet suppresses cell proliferation through affecting DNA synthesis and cell cycle events. However, additional studies should be undertaken at the cellular and molecular levels to determine the mechanism of Se regulation of cell proliferation in fetal ovaries.
The role of Se in regulation of ovarian function in the fetus is unclear. However, for adult ovaries in animal models, it has been demonstrated that Se may modulate granulosa cell proliferation and estradiol-17β synthesis in vitro, and Se administration may affect the ovulation process, implantation and the number of live embryos (Parshad 1999; Basini & Tamanini 2000).
We have clearly demonstrated that maternal diet affected fetal ovarian function marked in this study by changes in cellular proliferation. In fact, the effects of maternal diet and other environmental factors on fetal and postnatal organ growth and function have been investigated for several models including humans (Rhind et al. 2003; Redmer et al. 2004; Luther et al. 2005; Barker 2007; Gardner et al., 2008). It has been demonstrated that environmental factors including maternal diet composition affect fetal development through many different mechanisms including alternations of gene expression or changes in organ structure and physiology (Rhind et al. 2003). However, the mechanism of the effects of undernutrition and Se in the maternal diet on fetal ovarian function remains to be elucidated.
In summary, maternal dietary restriction and/or high level of Se in diet decreased cell proliferation in primordial, secondary and/or antral follicles, stromal cells and blood vessels in fetal ovaries. Moreover, the LI was greater in secondary and antral than in primordial and primary follicles, and LI was similar for granulosa and theca cells. Thus, dietary restriction and Se in maternal diet affect fetal ovarian growth at the end of pregnancy. Furthermore, apoptosis was minimal and a dense network of blood vessels is present in fetal ovaries by the end of pregnancy.
Educational & Outreach Activities
Ms. Wendy Arndt completed a seminar project entitled: “Cellular proliferation in fetal ovarian follicles obtained from sheep in late pregnancy fed maintenance or restricted diet with normal or enhanced selenium concentrations”.
Grazul-Bilska, A.T., W.J. Arndt, J.S. Caton, E. Borowczyk, P.P. Borowicz, M.A.Ward, D.A. Redmer, L.P. Reynolds, and K.A. Vonnahme. 2006. Cellular proliferation in fetal ovarian follicles from late pregnant sheep fed maintenance or restricted diets with normal or enhanced selenium concentrations. Proceedings, 32nd Annu. Conf. Internat. Embryo Transfer Soc., Orlando FL, January. Link: http://www.publish.csiro.au/?paper=RDv18n2Ab231
Grazul-Bilska, A. T., J. S. Caton, W. Arndt, K. Burchill, C. Thorson, E. Borowczyk, J. J. Bilski, D. A. Redmer, L. P. Reynolds and K. A. Vonnahme. 2009. Cellular proliferation in ovine fetal ovaries: Effects of energy restrictions and selenium in maternal diet. Reproduction. Accepted to Reproduction on 1/7/09. A final copy of the manuscript will be sent to you upon final remittance.
The results of this study will help to understand the role of maternal dietary restrictions and Se level in diet in regulation of cell proliferation in fetal tissues and how maternal diet may affect growing tissues. In addition, these results emphasize importance of vascularization in folliculogenesis and ovarian growth. Thus, maternal diet may impact fetal and likely postnatal/adult ovarian development and function, emphasizing the importance of maternal diet on reproductive and overall health of the offspring.
On the other hand, it is currently unknown if changes in fetal ovaries at the cellular level induced by maternal factors may affect fertility of the offspring. Since very limited and inconclusive data are available concerning maternal effects on offspring fertility, further investigation is required. The next step is to allow the offspring to be born, and then monitor growth and reproductive success of the offspring.
It is currently unknown what the economic impact from this project could be. However, if we can determine how maternal diet could enhance reproductive performance of our ruminant female offspring, we could have the potential of increasing the longevity of our breeding females, thus needing fewer replacement females. Currently there are over 1.5 million sheep and lambs, and 37.3 million cattle and calves in the North Central Region of the United States [National Agricultural Statistics Service (NASS), 2007]. These animals are produced on more than 312 thousand livestock operations in this region (NASS, 2007), and their quality has been collectively determined by each producer’s reproductive, nutritional and rangeland management practices. Small changes in one of these management practices have the potential to impact the economic success of each livestock enterprise. Even when genetics and nutritional management are constant, cattle and lamb reproductive parameters vary over time. Recent evidence has shown that maternal protein supplementation during the last trimester of pregnancy can greatly impact reproductive performance of the offspring. While this model has been established in the beef animal, this information could be useful to the sheep producer, and potential mechanisms that will be generated from this proposal will assist both sheep and cattle producers. Nothing is more sustainable than development of replacement females that have a greater chance of attaining pregnancy at a younger age and remain in the herd or flock for many parities.
The beneficiaries of this research would be any seed stock or feedlot producer within the North Central Region, and potentially throughout the nation. This work is particularly pertinent to livestock producers in drought stricken areas where forage quantity and quality is not adequate. Future research may further show that there is a certain time point (i.e. a particular stage of gestation) when supplementation needs to occur for production of healthy offspring. Thus, supplementation may only need to be provided during a short, specific time point of gestation, further aiding in the economic benefit.
Not determined at this time.
Areas needing additional study
This was a necessary project to determine if a more lengthy experiment should be conducted. We have shown that maternal diet does impact the reproductive tissues of the female offspring. The next step is to determine if we can alter reproductive performance of the offspring born from dams receiving different nutrients during gestation. In order to do this lengthy project, cooperation of producers and/or extension centers need to be utilized. Moreover, it will take a period of time to conduct the study. However, I believe that if we can enhance reproductive success within our ruminant livestock may see increases in the longevity of our herds or flocks, making this a huge economic advantage to the producer as there would be need for fewer replacement animals.