Maternal backfat depth in gestating sows has a greater influence on offspring growth and carcass lean yield than maternal feed allocation during gestation.

A commercial pig spends nearly half of its life in utero and its nutrition during this time can influence birth weight and postnatal growth. We hypothesised that postnatal growth is increased in pigs raised by sows with a high backfat depth and high level of energy intake during gestation compared with sows with a low backfat depth and low level of energy intake during gestation. This was tested in a 2 × 3 factorial design experiment with 2 factors for gilt backfat depth (Thin and Fat) and 3 factors for gestation feed allowance (Restricted, Control and High). Between d 25 and d 90 of gestation, Thin gilts (n=68; 12 ± 0.6 mm P2 backfat) and Fat gilts (n=72; 19 ± 0.6 mm P2 backfat) were randomly allocated, as individuals, to a gestation diet (6.19 g/kg lysine, 13.0 MJ DE/kg) at the following feed allowances: 1.8 kg/day (Restricted); 2.5 kg/day (Control) and 3.5 kg/day (High). For the remainder of gestation and during lactation all gilts were treated similarly. At weaning (day 28), 155 piglets were sacrificed and 272 were individually housed and followed through to slaughter (day 158). At day 80 of gestation, fasted Thin Restricted gilts had lower serum IGF-1 concentrations than Thin High or Thin Control fed gilts (P<0.001). Pigs born from Fat gilts had greater backfat depths (P<0.05), a lower lean meat yield (P<0.05) and were heavier (P<0.05) at slaughter than pigs born from Thin gilts. Gilt gestation feed allowance had only transitory effects on average daily gain and feed conversion efficiency and had no effect on pig weight at slaughter (P>0.05) or lean meat yield (P>0.05). In conclusion, gilts with a backfat depth of ~19 mm at insemination produced pigs that were heavier and fatter at ~158 days of age than those born from gilts with ~12 mm backfat depth at insemination. Maternal body condition during gestation had a more predominant influence on growth parameters of the offspring, such as weight at slaughter and backfat depth, than did feed level during gestation.

Feed allowance and maternal backfat levels during gestation influence maternal cortisol levels, milk fat composition and offspring growth.

The fetal and early postnatal environment can have a long-term influence on offspring growth. Using a pig model, we investigated the effects of maternal body condition (thin or fat) and maternal gestation feeding level (restricted, control or high) on maternal stress, milk composition, litter size, piglet birth weight and pre-weaning growth. A total of sixty-eight thin (backfat depth about 8 mm) and seventy-two fat (backfat depth about 12 mm) gilts were selected at about 22 weeks. This backfat difference was then accentuated nutritionally up to service at about 32 weeks. During gestation, individual gilts from within each group were randomly allocated to a gestation diet at the following feed allowances: 1·8 kg/d (restricted); 2·5 kg/d (control) and 3·5 kg/d (high) until day 90 of gestation. During gestation restricted gilts had higher levels of cortisol than high and control fed animals. Piglets born to fat gilts had higher average daily gain during the lactation period and higher weaning weights at day 28 than piglets born to thin gilts. Gilts on a high feed level had heavier piglets than those provided with restricted and control allocations. Fat gilts had less saturated fat in their milk at day 21 of lactation and higher unsaturated fat levels. No differences were found in the n-6:n-3 PUFA ratio in the milk between thin and fat gilts. In conclusion, maternal body condition influenced the daily weight gain of offspring up to weaning (day 28) and milk fat composition. Furthermore, maternal feed level during gestation alters maternal cortisol levels and milk fat composition.

In ovo temperature manipulation differentially influences limb musculoskeletal development in two lines of chick embryos selected for divergent growth rates.

Selective breeding has led to diverging phenotypic evolution in layer and broiler chickens through genomic and epigenetic modifications. Here we show that in ovo environmental manipulation differentially influences embryonic limb muscle phenotype in these two breeds. We demonstrate that raising incubation temperature from 37.5 to 38.5°C between embryonic days (ED) 4 and 7 increased motility and body mass in both layer and broiler embryos. In layers, this was accompanied by gastrocnemius muscle hypertrophy, increased fibre and nuclei numbers and a higher nuclei to fibre ratio (ED18), preceded by increased hindlimb Myf5 (ED5-8), Pax7 (ED5-10), BMP4 (ED6-9) and IGF-I (ED9-10, ED18) mRNAs. In broilers, the same temperature treatment led to reduced gastrocnemius cross-sectional area with fewer fibres and nuclei and an unchanged fibre to nuclei ratio (ED18). This was preceded by a delay in the peak of hindlimb Myf5 expression, increased Pax7 (ED5, ED7-10) and BMP4 (ED6-8) but reduced IGF-I (ED8-10) mRNAs. Rather than promoting myogenesis as in layer embryos, the temperature treatment promoted gastrocnemius intramuscular fat deposition in broilers (ED18) preceded by increased hindlimb PPARγ mRNA (ED7-10). The treatment increased tibia/tarsus bone length as well as femur cross-sectional area in both breeds, but femur length and bone to cartilage ratio in the femur and tibia/tarsus were only increased in treated layers (ED18). We conclude that in ovo temperature manipulation differentially affected the molecular regulation of hindlimb myogenic, adipogenic and growth factor expression in broiler and layer embryos, leading to differential changes in muscle phenotype. The underlying interactive mechanisms between genes and the environment need further investigation.

Muscle specific differences in the regulation of myogenic differentiation in chickens genetically selected for divergent growth rates.

With the human population predicted to reach 9 billion by 2050, increasing food supplies while maintaining adequate standards of animal welfare has become a global priority. In the poultry industry, broilers are genetically selected for greater pectoral but not leg muscularity yield leading to leg disorders and thereby welfare issues. It is known that the pectoralis major of broilers contains more muscle fibres of larger diameters than egg-layers but little is known about the leg gastrocnemius muscle cellular characteristics. As muscle fibre numbers are set by hatch, the molecular regulation of myogenesis was investigated in pectoral (selected) and gastrocnemius (unselected) muscles of chick embryos to help explain diverging post-hatch phenotypes. Results showed that broilers were more active from embryonic day (ED) 8 and heavier from ED12 to 18 than layers. The pectoral muscle of broilers exhibited increased myoblast proliferation on ED15 (raised myonuclei, MyoD and PCNA) followed by increased differentiation from ED16 (raised myogenin, IGF-I) leading to increased muscle fibre hyperplasia and mass by ED18 compared to layers. In the gastrocnemius muscle of broilers, cell proliferation was also raised up to ED15 accompanied by increased PCNA, MyoD and IGF-I mRNAs. However, from ED16, myogenin and IGF-I mRNAs were similar to that of layers and PCNA was reduced leading to similar fibre area, nuclei numbers and muscle mass at ED18. We conclude that genetic selection for enhanced post-hatch pectoral muscle growth has altered the temporal expression of IGF-I and thereby myogenin transcription affecting cellular characteristics and mass by hatch in a muscle specific manner. These observations should help develop intervention strategies aimed at improving leg muscle strength and thereby animal welfare to meet growing consumer demand.

Dietary lecithin source affects growth potential and gene expression in Sparus aurata larvae.

Soybean lecithin (SBL), used as a phospholipid source in larval fish diets, may compromise growth and survival in marine species, and affect gene expression, due to differences in fatty acid composition relative to marine lecithins (ML). The potential of SBL as a phospholipid source in gilthead seabream microdiets as compared to ML was evaluated. Two stocking densities were tested in order to exacerbate possible dietary effects: 5 and 20 larvae L(-1). Larvae reflected dietary fatty acid profiles: linoleic acid was higher, whereas eicosapentaenoic and arachidonic acids were lower in SBL fed groups than in ML fed larvae. Highest stocking density decreased survival, and led to elevated saturates and lower docosahexaenoic acid levels in polar lipid. Muscle histology observations showed hindered growth potential in SBL fed larvae. Despite similar cortisol levels between treatments, higher glucocorticoid receptor (GR), as well as hormone-sensitive lipase (HSL) mRNA levels in SBL fed groups revealed a role for fatty acids in gene regulation. Further analysed genes suggested these effects were independent from the hypothalamus-pituitary-interrenal axis control and the endocannabinoid system. Cyclooxygenase-2 and gluconeogenesis seemed unaffected. For the first time in fish, a link between dietary lecithin nature and HSL gene transcription, perhaps regulated through GR fatty acid-induced activation, is suggested. Enhanced lipolytic activity could partly explain lower growth in marine fish larvae when dietary ML is not provided.

A maternal "junk food" diet in pregnancy and lactation promotes nonalcoholic Fatty liver disease in rat offspring.

With rising obesity rates, nonalcoholic fatty liver disease is predicted to become the main cause of chronic liver disease in the next decades. Rising obesity prevalence is attributed to changes in dietary habits with increased consumption of palatable junk foods, but maternal malnutrition also contributes to obesity in progeny. This study examines whether a maternal junk food diet predisposes offspring to nonalcoholic fatty liver disease. The 144 rat offspring were fed either a balanced chow diet alone or with palatable junk foods rich in energy, fat, sugar, and/or salt during gestation, lactation, and/or after weaning up to the end of adolescence. Offspring fed junk food throughout the study exhibited exacerbated hepatic steatosis, hepatocyte ballooning, and oxidative stress response compared with offspring given free access to junk food after weaning only. These offspring also displayed sex differences in their hepatic molecular metabolic adaptation to diet-induced obesity with increased expression of genes associated with insulin sensitivity, de novo lipogenesis, lipid oxidation, and antiinflammatory properties in males, whereas the gene expression profile in females was indicative of hepatic insulin resistance. Hepatic inflammation and fibrosis were not detected indicating that offspring had not developed severe steatohepatitis by the end of adolescence. Hepatic steatosis and increased oxidative stress response also occurred in offspring born to junk food-fed mothers switched to a balanced chow diet from weaning, highlighting a degree of irreversibility. This study shows that a maternal junk food diet in pregnancy and lactation contributes to the development of nonalcoholic fatty liver disease in offspring.

Potential molecular mechanisms for the prenatal compartmentalisation of muscle and connective tissue in pigs.

Foetal development and growth can be influenced by environmental factors. We have previously demonstrated that the smallest porcine foetus within a litter develops a higher proportion of fat and connective tissue in its muscles than the largest littermate. The present study aims to highlight the molecular mechanisms involved in this variation. Twenty-three pairs of porcine foetuses ranging from 36 to 86 days of gestation were used. The transcription rate of eight genes involved in cell growth and lipid synthesis was measured in the m. semitendinosus of the smallest and largest littermates together with the immunocytochemical localisation of myosin and IGFBP-5. Results showed that the myosin-expressing area was reduced in the smallest littermate supporting an increased proportion of connective tissue growth at the expense of muscle. IGF-1, IGF-1R, IGFBP-5, PPARgamma and myostatin mRNAs were upregulated in the smallest littermate, while IGF-2 was down-regulated and MyoD as well as CTGF were unaffected. The IGF system controls the growth of many cell types including cells of the extracellular matrix and skeletal muscle, but IGFBP-5 protein was predominantly localised in the extracellular matrix with a denser staining in the smallest littermate. In light of this, we propose that IGFBP-5 may play a role in directing an increased IGF-1-stimulated connective tissue growth in the smallest littermate. PPARgamma promotes lipid deposition in both adipocytes and muscle fibres and increased expression in the smallest littermate concurs with our previous findings of increased fat content in this group. Similarly, the upregulation of myostatin, a negative regulator of muscle growth, in the smallest littermate suggests that this factor may be involved in regulating the reduced myosin-expressing area observed. In conclusion, IGFBP-5, PPAR-gamma and myostatin may play a role in regulating the compartmentalisation of muscle versus connective tissue in the intralitter variation model of prenatal nutrition.

Evidence that a maternal "junk food" diet during pregnancy and lactation can reduce muscle force in offspring.

BACKGROUND: Obesity is a multi-factorial condition generally attributed to an unbalanced diet and lack of exercise. Recent evidence suggests that maternal malnutrition during pregnancy and lactation can also contribute to the development of obesity in offspring. We have developed an animal model in rats to examine the effects of maternal overeating on a westernized "junk food" diet using palatable processed foods rich in fat, sugar and salt designed for human consumption. Using this model, we have shown that such a maternal diet can promote overeating and a greater preference for junk food in offspring at the end of adolescence. The maternal junk food diet also promoted adiposity and muscle atrophy at weaning. Impaired muscle development may permanently affect the function of this tissue including its ability to generate force. AIMS: The aim of this study is to determine whether a maternal junk food diet can impair muscle force generation in offspring. METHODS: Twitch and tetanic tensions were measured in offspring fed either chow alone (C) or with a junk food diet (J) during gestation, lactation and/or post-weaning up to the end of adolescence such that three groups of offspring were used, namely the CCC, JJC and JJJ groups. RESULTS: We show that adult offspring from mothers fed the junk food diet in pregnancy and lactation display reduced muscle force (both specific twitch and tetanic tensions) regardless of the post-weaning diet compared with offspring from mothers fed a balanced diet. CONCLUSIONS: Maternal malnutrition can influence muscle force production in offspring which may affect an individual's ability to exercise and thereby combat obesity.

A maternal 'junk food' diet in pregnancy and lactation promotes an exacerbated taste for 'junk food' and a greater propensity for obesity in rat offspring.

Obesity is generally associated with high intake of junk foods rich in energy, fat, sugar and salt combined with a dysfunctional control of appetite and lack of exercise. There is some evidence to suggest that appetite and body mass can be influenced by maternal food intake during the fetal and suckling life of an individual. However, the influence of a maternal junk food diet during pregnancy and lactation on the feeding behaviour and weight gain of the offspring remains largely uncharacterised. In this study, six groups of rats were fed either rodent chow alone or with a junk food diet during gestation, lactation and/or post-weaning. The daily food intakes and body mass were measured in forty-two pregnant and lactating mothers as well as in 216 offspring from weaning up to 10 weeks of age. Results showed that 10 week-old rats born to mothers fed the junk food diet during gestation and lactation developed an exacerbated preference for fatty, sugary and salty foods at the expense of protein-rich foods when compared with offspring fed a balanced chow diet prior to weaning or during lactation alone. Male and female offspring exposed to the junk food diet throughout the study also exhibited increased body weight and BMI compared with all other offspring. This study shows that a maternal junk food diet during pregnancy and lactation may be an important contributing factor in the development of obesity.

In ovo temperature manipulation influences embryonic motility and growth of limb tissues in the chick (Gallus gallus).

The chick embryo, developing in the egg, is an ideal system in which to investigate the effects of incubation environment on the development of the embryo. We show that raising the temperature of the eggs by just one degree, from 37.5 degrees C to 38.5 degrees C, during embryonic days (ED) 4-7 causes profound changes in development. We demonstrate that embryonic movement is significantly increased in the chicks raised at 38.5 degrees C both during the period in which they are at the higher temperature but also 4 days after their return to the control temperature. Concomitant with this increase in embryonic activity, the embryos raised at higher temperature grow to significantly heavier weights and exhibit significantly longer leg bones (tibia and tarsus) than the controls from ED12 onwards, although mineralization occurs normally. Additionally, the number of leg myonuclei is increased from ED12 in the embryos raised at the higher temperature. This is likely to promote greater leg muscle growth later in development, which may provide postural stability to the chicks posthatch. These changes are similar to those seen when drugs are injected to increase embryonic activity. We therefore believe that the increased embryonic activity provides a mechanism that can explain the increased growth of leg muscle and bone seen when the eggs are incubated for 3 days at higher temperature.

A maternal cafeteria diet during gestation and lactation promotes adiposity and impairs skeletal muscle development and metabolism in rat offspring at weaning.

We examined the effects of a maternal cafeteria diet on skeletal muscle and adipose tissue development in the offspring at weaning. Rats born to mothers fed the cafeteria diet either during gestation alone or during both gestation and lactation exhibited a 25% reduction in muscle cross-sectional area with approximately 20% fewer fibres compared with pups fed a balanced chow diet. Maintaining the cafeteria diet during lactation increased intramuscular lipid content and fat pad weights characterized by adipocyte hypertrophy but not hyperplasia. These pups also had elevated muscle IGF-1, IGF-1 receptor, and PPARgamma mRNA levels, which may indicate an attempt to maintain normal insulin sensitivity. The increased adiposity and elevated IGF-1, IGF-1 receptor and PPARgamma mRNAs were not seen in the pups rehabilitated to the balanced diet during lactation. However, these pups exhibited reduced muscle cell proliferation (PCNA) with reduced insulin receptor and a trend towards reduced glucose transporter (GLUT)-4 mRNAs when compared with pups fed a balanced chow diet, indicating possible alterations in glucose uptake by muscle tissue. Therefore, rats born to mothers fed a cafeteria diet during gestation alone or during both gestation and lactation exhibited impaired skeletal muscle development and metabolic disorders normally associated with insulin resistance as early as the weaning stage.

The influence of undernutrition during gestation on skeletal muscle cellularity and on the expression of genes that control muscle growth.

We examined the effects of two levels of gestational undernutrition (50 % and 40 % of ad libitum) on postnatal growth rate, skeletal muscle cellularity and the expression of genes that control muscle growth, in the offspring at weaning. The results showed that the rat pups born to mothers fed the 50 % diet during gestation and a control diet during lactation had an increased postnatal growth rate compared with the pups fed the more restricted diet (40 % of ad libitum). Surprisingly, the growth rate of the control group (ad libitum) was intermediate between the 50 % and 40 % groups. The restricted diets did not alter the number of muscle fibres in the semitendinosus muscle of the offspring but the number of muscle nuclei was reduced by 16 % in the 40 % group compared with the control group. In the 50 % group, the lightest pups at birth (L) had elevated muscle insulin-like growth factor (IGF)-1, IGF binding protein (BP)-5 and proliferating cell nuclear antigen (PCNA) mRNA compared with the L pups from both the control and 40 % groups. The heaviest pups at birth (H) in the 50 % group had increased levels of IGFBP-4, PCNA and M-cadherin mRNA compared with both the control and 40 % groups. Levels of IGF-1 receptor, myostatin and MyoD mRNA did not correlate with postnatal growth. Both H and L pups from the 40 % group had reduced muscle IGF-1 mRNA but all other transcripts examined were similar to control levels. The results suggest that the increased postnatal growth rate, which accompanied milder fetal undernutrition (50 %), may be due to a more active local muscle IGF system and increased muscle-cell proliferation.