Location: Forage and Livestock Production ResearchTitle: Milk leptin in sows and blood leptin and growth of their offspring Author
Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/20/2009
Publication Date: 1/30/2009
Citation: Whitley, N.C., O'Brien, D.J., Quinn, R.W., Keisler, D.H., Walker, E.L., Brown, M.A. 2009. Milk leptin in sows and blood leptin and growth of their offspring. Journal of Animal Science. 87:1659-1663. Interpretive Summary: Though leptin is secreted from other tissues, it is produced primarily by white adipose tissue that also contains the leptin receptor. In the pig, along with adipose tissue, expression for the leptin receptor was also found in the hypothalamus, anterior pituitary, ovary, uterine body, liver, kidney, pancreas, adrenal gland, heart, spleen, lung, intestine, bone marrow and muscle. Therefore, it is possible that leptin can influence a variety of physiological functions. Leptin has also been found in placenta where it passes through to the fetus during its transition to the neonate, so both maternal and fetal levels of leptin are high during pregnancy. Leptin is also produced by the mammary gland, and thus has been found in the milk of several species, including goats, sheep, pigs, horses, cattle, and humans. There has been some evidence suggesting a small protective effect of breastfeeding against later obesity in humans with leptin in breast milk as a possible factor involved, indicating that early ingestion of leptin in milk by the baby might influence later growth and development. However, little research has been conducted to determine the relation of leptin in pigs to preweaning growth. Research was initiated to investigate possible relationships among sow milk and pig serum leptin and subsequent pig growth to weaning. Milk serum leptin was not associated with litter size, parity, pig birth weight, ADG to weaning or weaning weight. Pig serum leptin at birth was also not significantly related to birth weight, weaning weight or ADG to weaning in the present study. Overall, results of this study indicate that leptin is not directly related to early neonatal growth in the pig. However, more in-depth studies are needed to determine possible indirect or long-term effects of early leptin exposure.
Technical Abstract: Twenty-one mixed parity (average 2.4 ± 0.49) crossbred sows and their offspring were used to determine if sow milk leptin at farrowing was related to neonatal serum leptin and pig growth to weaning. During farrowing, pigs were randomly allotted to suckled (n=99) or unsuckled (n = 89) groups with unsuckled pigs placed in a group pen apart from the dam prior to suckling. Both groups had access to heat lamps. Colostrum samples were collected no more than 2 hr after farrrowing the first pig. Blood samples and BW were collected from all pigs approximately 2 h after farrowing was complete and BW were recorded again at weaning. Milk and blood serum were collected by centrifugation and leptin levels were analyzed using RIA. Leptin was detected in colostral milk, as expected, and averaged 46.0 ± 1.1 ng/ml. Pig serum leptin (P < 0.02) was higher for suckled than for unsuckled pigs, averaging 0.69 ± 0.08 and 0.54 ± 0.07 ng/ml, respectively. Suckling status did not influence ADG to weaning or weaning weight of pigs. Though male pigs were heavier (P < 0.01) at birth than female pigs (1507 ± 52 and 1381 ± 43 g, respectively), ADG to weaning and weaning weights were similar for both sexes, averaging 229 ± 14 g and 5829 ± 323 g, respectively for all pigs, and serum leptin levels were not associated with pig sex. Milk serum leptin was not associated with litter size, parity, pig birth weight, ADG to weaning or weaning weight. Pig serum leptin at birth was also not significantly related to birth weight, weaning weight or ADG to weaning in the present study. Overall, results of this study indicate that leptin is not directly related to early neonatal growth in the pig. However, more in depth studies are needed to determine possible indirect or long-term effects of early leptin exposure.