Maternal nutrition is of critical importance for fetal growth. An unbalanced nutrient supply will result in low birthweight and, subsequently, compromise future growth and development. Apart from short-term outcomes, accumulating evidence from animal and human studies indicates that early life experiences can impact offspring phenotype, a concept known as Developmental Origins of Health and Disease (DOHaD) hypothesis [1]. Variation in the maternal plane of nutrition, and particularly maternal under or over nutrition, appears to be a dominant factor in developmental programming, in both humans and livestock, including metabolic [2], productive ^[3][4][3,4], and reproductive outcomes ^[5][6][5,6]. In addition, maternal nutritional imbalances in terms of both macro and micro nutrients can induce oxidative stress, which may affect fetal growth and development [7]. Recently, the role of colostrum in affecting the critical developmental process, as a conduit of transmission of certain bioactive molecules from mother to offspring, has attracted considerable attention, according to lactocrine signaling hypothesis [8]. The periconceptional period is playing a crucial role in programming effects, since it is characterized by extensive reorganization of cellular phenotype during oocyte maturation, fertilization, and embryonic genome activation [9]. Even in poultry species, the prenatal environment can be divided into pre-lay and egg storage/incubation environments, both of which can affect offspring outcomes. In particular, maternal nutrition is of paramount importance because all nutrients required by the developing embryo are deposited in the egg and therefore exert an effect not only during embryonic but also during posthatch development [10].

Apart from the well-established role of micronutrients in short-term pregnancy outcomes [11], accumulating evidence also supports a role for micronutrients in developmental programming ^[12][13][14][12,13,14]. Trace elements affect the endocrine regulation of energy metabolism and energy homeostasis, as well as oxidative balance, both of which are related to normal growth [15]. In particular, Se possesses antioxidant, chemopreventive, and anti-inflammatory properties and is considered as a trace element of great importance to the health of both mammals and avian species. Its action is related to its presence within at least 25 selenoproteins, i.e., Se-containing proteins products of twenty-five genes. Among them some are well characterized with respect to their function like the glutathione peroxidases (GPX1, GPX2, GPX3, GPX4, and GPX 6), the thioredoxin reductases (TXNRD1, TXNRD2, and TXNRD3), and the iodothyronine deiodinases (DIO1, DIO2, and DIO3). Other selenoproteins include but are not limited to selenophosphate synthetase 2 (SEPHS2), selenoprotein F or selenoprotein 15 (SELENOF), selenoprotein H (SELENOH), selenoprotein I (SELENOI), selenoprotein K (SELENOK), selenoprotein M (SELENOM), selenoprotein N (SELENON), selenoprotein O (SELENOO), selenoprotein P (SELENOP), selenoprotein S (SELENOS), selenoprotein T (SELENOT), selenoprotein V (SELENOV), and selenoprotein W (SELENOW) ^[16][17][16,17]. Selenoprotein P is the major Se transporting protein [18], and is considered the only known protein that contains multiple selenocysteine residues per protein molecule [19].

Selenomethionine and selenocysteine are identical to methionine and cysteine, respectively, except that the sulphur atom is replaced by Se. Plants synthesize selenomethionine and a variety of methylated amino acids. Plants absorb Se from the soil in the form of selenite or selenate and synthesize selenomethionine ^[20][21][20,21]. In feed ingredients, Se can be found in form of selenomethionine. In addition, to the amount of Se received from feed ingredients, feeds of farm animals are widely supplemented. Selenium is generally supplemented in the form of inorganic Se or in organic form, and the most widely used sources include sodium selenite, sodium selenate, controlled-release sodium selenite bolus, SeMet, zinc L-selenomethionine complex, hydroxy-analogue of selenomethionine, Se-yeast, elemental Se at nano size, soybean Se proteinate, Se-enriched malt, chlorella algae, cabbage, and garlic ^{[22][23][24][25]}[22,23,24,25]. Selenium efficiency depends on the level of supplementation and form of Se in the diet, and organic sources proven to be effective sources of Se for poultry and animal production ^[26][27][26,27]. In EU, the maximum supplementation with organic Se is 0.2 mg Se per kg of complete feed, while the maximum content of Se (total Se) is 0.5 mg/kg of complete feed [28]. Similarly, the Food and Drug Administration (FDA) regulations limit the amount of dietary Se supplementation, to 0.3 mg/kg (as fed) [29]. Given the FDA limits, any concentration that exceeds 0.3 mg/kg and is below the maximum tolerable level can be considered as supranutritional.

Recently, the role of Se in maternal nutrition and its impact on the Se status of offspring has received considerable attention. In mammals, Se is transferred both via the placenta, the colostrum, and milk to the fetus and the neonate [30]. In avian species, laying hen transfers Se to the egg and in turn to the developing embryo and newly hatched chick ^[10][31][32][10,31,32]. Selenium affects non-enzymatic and enzymatic antioxidant defense mechanisms, helping build a strong antioxidant defense for both mother and the developing embryo. Recent studies in humans have also revealed an association between maternal Se status and specific early childhood outcomes. Both low and high levels of cord serum Se have adverse effects on an infant’s neurobehavioral development [33]. More interestingly, a positive effect of maternal selenium status on children’s development at 1.5 years of age has been reported, related to language and psychomotor development improvement [34]. These findings have been supported by data from human cohort studies. In particular, in a Polish cohort study involving 410 mother-child pairs, a significant positive association was detected between Se levels in the blood collected during the first trimester of pregnancy and child motor skills at 1 and 2 years of age and cognitive development at 2 years of age [35].

2. Combined Effects of Maternal Plane of Nutrition and Selenium Status on Progeny

Numerous studies have investigated the interaction between maternal plane of nutrition and Se status on a number of physiological parameters in the offspring. In particular, inconsistent results of the effects of maternal supranutritional Se supplementation regarding birth weight or weight at weaning have been reported in sheep ranging from no effect [36] to an increase in birth weight and weight at weaning, regardless of global maternal nutrient intakes ^[37][38][37,38]. On the other hand, supranutritional Se supplementation to nutritionally restricted dams (60% of their needs) resulted in improved fetal growth, implicating a sparing effect of Se and long-term developmental consequences ^[37][38][37,38]. In pigs, maternal supplementation with SeMet significantly increases litter weight at weaning and body mass of piglets [39], whereas in chickens, inclusion of Se in the maternal diet could positively affect embryo viability, hatchability, and growth of the progeny ^[10][31][32][10,31,32]. In the same species, dietary inclusion of organic Se (zinc L-selenomethionine complex) promoted heavier hatchling weight until egg production peak, (33 week), without affecting hatchling quality [40]. Moreover, supplementation of the breeder’s diet with organo-Se appears to enhance the DHA concentration of the chick brain [10], in good agreement with the well accepted role of Se in protecting polyunsaturated fatty acids (PUFA) oxidation [41]. In large animals, the majority of the studies examining the role of Se in modifying the effects of nutrition are mostly limited to the late gestation fetus, and only a few examine later outcomes. Six-months old lambs, derived from ewes supplemented with supranutritional Se and artificially reared to avoid confounding effects with colostral Se, showed greater small intestinal weight, which, however, was not accompanied by an increase in jejunal cell proliferation [42]. As is pointed out by authors, this increase could be translated to increased crypt cell proliferation and altered villi number, leading probably to more efficient nutrient absorption. It has been well documented that maternal nutritional status impacts mammary gland development and, subsequently, colostrum and milk yield ^[36][43][36,43]. However, data from primiparous ewes indicate that supranutritional supplementation from conception to term may be a more potent factor in driving milk production [43]. Interestingly, Se supplementation in ewes at approximately 10 times above current recommendations was reported to increase mammary gland capillary area density and vascularity, a finding explaining the increase in milk production, possibly by enhancing the nutrient availability to the mammary gland [44]. Recently, the role of Se in metabolic programming has gained interest [45]. This micronutrient, through the activity of selenoproteins, such as glutathione peroxidase and selenoprotein P, has been reported to play a role in the regulation of enzymes in the insulin signaling cascade, the expression of lipogenic enzymes, and carbohydrate metabolism in the liver ^[46][47][48][46,47,48]. In this respect, studies in sheep revealed an interaction between nutritional and Se maternal status on insulin sensitivity in offspring. Lambs born to high-Se but restricted-diet mothers exhibit an elevated insulin release following intravenous glucose tolerance test [37]. Moreover, the same offspring were characterized by greater total visceral adiposity, attributed mainly to an increase in visceral rather than omental fat [37]. The involvement of Se and its selenoproteins, glutathione peroxidase and selenoprotein P, in insulin regulation has been confirmed from a number of studies, indicating a role in insulin signaling cascade ^[48][49][48,49]. However, recent evidence indicates that effects are related to the level of supplementation. Adequate concentrations exert a key role in insulin function, but an excess is associated with insulin resistance [50]. The underlying mechanism probably involves formation of antioxidant selenoproteins and thus reduced concentrations of reactive oxygen species, which are required for insulin signaling ^[51][52][51,52]. Therefore, the exact impact of maternal Se and especially the level of supplementation in insulin-glucose axis regulation in the offspring is not yet clear and needs further elucidation. A summary of selected animal studies reporting combined effects of maternal plane of nutrition and Se status on progeny is presented in Table 1.