Abstract
Simple SummaryLow birth-weight piglets normally have a higher growth retardation and are more prone to disease such as diarrhea compared to NBW piglets, which are strongly associated with intestinal health, body redox status and mitochondrial morphology and function. The present study showed that low birth-weight piglets exhibited abnormal intestinal development and impaired intestinal barrier function and redox status when compared to normal- birth-weight piglets. Furthermore, we found that the impaired mitochondrial structure and functions may be one of the main causes of intestinal dysfunction in low birth-weight piglets. These results provided insights for the mechanisms of intestinal dysfunction in low birth-weight piglets.Low birth-weight (LBW) neonates exhibit a lower growth rate and impaired intestinal development. However, the reasons for abnormal development of small intestine in LBW piglets have not been widely studied. The present study focused on the redox status and mitochondrial morphology and functions of the small intestine in LBW newborn piglets. Ten newborn normal birth-weight (NBW) piglets and LBW piglets from 10 primiparous sows with the same parturition day were selected and sampled immediately without sucking colostrum. The small intestine tissues were collected and measured. Compared with NBW newborn piglets, LBW newborn piglets had a significantly decreased length and weight of the small intestine (p < 0.05) as well as the villus height/crypt depth (V/C) index in the jejunum (p < 0.05). Furthermore, LBW piglets had a lower gene expression of tight junction protein zonula occluden-1 (ZO1), claudin 1, antioxidant enzyme catalase (CAT), glutathione peroxidase (GPX) and heme oxygenase-1 (HO-1) in jejunum (p < 0.05). Meanwhile, LBW induced mitochondrial vacuolation and significantly decreased the mRNA expression of PPARγ coactivator-1α (PGC-1α) (p < 0.05) and tended to decrease the expression of cytochrome coxidase IV (Ccox IV) (p = 0.07) and cytochrome C (Cytc) (p = 0.08). In conclusion, LBW newborn piglets showed an abnormal development of the small intestine and disturbed redox status, and this may be caused by impaired morphology and the functions of mitochondria in the jejunum.
Highlights
In the past decade, the average litter size of pigs had been increased gradually by genetic selection associated with the reduction of the mean piglets’ birth weight and the rise in the proportion of small piglets [1]
The present study showed that the mitochondria of the jejunum in LBW piglets were subjected to oxidative stress, and the disturbed mitochondrial morphology and structure may be the main cause of oxidative stress in the jejunum of LBW piglets
Wang et al found that neonates with intrauterine growth restriction (IUGR) had higher tight-junction permeability and significantly reduced occludin expression [11], suggesting that the intestinal barrier was impaired in LBW piglets
Summary
The average litter size of pigs had been increased gradually by genetic selection associated with the reduction of the mean piglets’ birth weight and the rise in the proportion of small piglets [1]. Previous studies reported that the poor growth of LBW piglets was partly due to the impairment of digestive and absorptive functions in the small intestine [7,8]. Studies indicated that the dysfunction of small intestine of LBW piglets is associated with a longer and thinner intestine [9], lower villi height, thinner mucosa and muscle layers [10], as well as higher intestinal permeability in the small intestine at birth [11]. Recent research demonstrated that altered proteomes with increased abundances of protein associated with oxidative stress and apoptosis, as well as decreased protein associated with cell structure and absorption of nutrients, might be the major reason responsible for the dysfunctional intestine in LBW piglets [12]. LBW piglets had a dysfunction of the intestine with underdeveloped morphology, higher permeability, free radicals and lower antioxidant capacity. The underlying mechanisms of intestinal dysfunction in LBW piglets remain unclear
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