Abstract

Weaning is associated with increased occurrence of infections and diseases in piglets. Recent findings indicate that weaning induces mitochondrial dysfunction and oxidative stress conditions that more severely impact smaller piglets. The objective of this study was to characterize the molecular mechanisms underlying these physiological consequences and the relation with systemic inflammatory status in both normal and low birth weight (NBW and LBW) piglets throughout the peri-weaning period. To conduct the study, 30 sows were inseminated, and specific piglets from their litters were assigned to one of two experimental groups: NBW (n = 60, 1.73 ± 0.01 kg,) and LBW piglets weighing less than 1.2 kg (n = 60, 1.01 ± 0.01 kg). Then, 10 piglets from each group were selected at 14, 21 (weaning), 23, 25, 29 and 35 days of age to collect organ and plasma samples. Specific porcine RT2 Profiler™ PCR Arrays related to mitochondrial function, oxidative stress, inflammation and apoptosis processes were first used to target genes that are modulated after weaning in NBW piglets (d 23 and d 35 vs. d 14). Expression of selected genes was evaluated by quantitative PCR. These analyses revealed that expression of inflammatory genes CXCL10 and CCL19 increased after weaning in intestinal mucosa, while expression of genes encoding subunits of the mitochondrial respiratory chain was downregulated in liver and kidney of both groups. Interestingly, major modulators of mitophagy (BNIP3), cell survival (BCL2A1) and antioxidant defense system (TXNRD2, GPx3, HMOX1) were found to be highly expressed in NBW piglets. The systemic levels of TNF-α and IL1-β significantly increased following weaning and were higher in NBW piglets. These results provide novel information about the molecular origin of mitochondrial dysfunction and oxidative stress observed in weaned piglets and suggest that clearance of dysfunctional mitochondria, antioxidant defenses and inflammatory response are compromised in LBW piglets.

Highlights

  • The separation of piglets from sows at weaning is known to induce many simultaneous stressors resulting in low feed intake, intestinal disturbances, inflammation and increased occurrence of diseases [1]

  • The decision to target the normal birth weight (NBW) piglets and to use the mitochondrial energy metabolism and oxidative stress arrays is based on previous results showing that energy production and antioxidant response are compromised in liver of both low birth weight (LBW) and NBW piglets

  • Our results indicate that the expression of specific subunits of the respiratory complexes of the mitochondrial electron transport chain (ETC) tended to decrease two days after weaning in comparison with the lactation period in liver samples

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Summary

Introduction

The separation of piglets from sows at weaning is known to induce many simultaneous stressors resulting in low feed intake, intestinal disturbances, inflammation and increased occurrence of diseases [1]. The post-weaning period is characterized by higher morbidity and mortality rates that cause substantial economic losses for producers This is true for low birth weight (LBW) piglets, which have become common in modern swine production with the advent of genetic selection for sows producing large litters [2, 3]. These LBW piglets are recognized to have a lower feed intake than their normal birth weight (NBW) counterparts and to suffer from an incomplete development of both digestive and immune systems [4, 5] These conditions result in an increase vulnerability of LBW piglets to bacterial infections and various pathologies known to be associated with the post-weaning period. Alternatives to these products commonly used to promote health and growth of weaned piglets need to be developed

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