Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Jan 3:8:783688.
doi: 10.3389/fnut.2021.783688. eCollection 2021.

Early-Life Nutrition Interventions Improved Growth Performance and Intestinal Health via the Gut Microbiota in Piglets

Chengzeng Luo  1   2 , Bing Xia  1   3 , Ruqing Zhong  1 , Dan Shen  1 , Jiaheng Li  1 , Liang Chen  1 , Hongfu Zhang  1
Affiliations
Free PMC article

Early-Life Nutrition Interventions Improved Growth Performance and Intestinal Health via the Gut Microbiota in Piglets

Chengzeng Luo et al. Front Nutr. .
Free PMC article

Abstract

Intestinal infections in piglets are the main causes of morbidity before and after weaning. Studies have not explored approaches for combining pre-weaning and post-weaning nutritional strategies to sustain optimal gut health. The current study thus sought to explore the effects of early-life nutrition interventions through administration of synthetic milk on growth performance and gut health in piglets from 3 to 30 days of age. Twelve sows were randomly allocated to control group (CON) and early-life nutrition interventions group (ENI). Piglets were fed with the same creep diet from 7 days of age ad libitum. Piglets in the ENI group were provided with additional synthetic milk from Day 3 to Day 30. The results showed that early-life nutrition interventions improved growth performance, liver weight, spleen weight, and reduced diarrhea rate of piglets after weaning (P < 0.05). Early-life nutrition interventions significantly upregulated expression of ZO-1, Occludin, Claudin4, GALNT1, B3GNT6, and MUC2 in colonic mucosa at mRNA level (P < 0.05). Early-life nutrition interventions reduced activity of alkaline phosphatase (AKP) in serum and the content of lipopolysaccharides (LPS) in plasma (P < 0.05). The number of goblet cells and crypt depth of colon of piglets was significantly higher in piglets in the ENI group relative to that of piglets in the CON group (P < 0.05). The relative mRNA expression levels of MCP-1, TNF-α, IL-1β, and IL-8, and the protein expression levels of TNF-α, IL-6, and IL-8 in colonic mucosa of piglets in the ENI group were lower compared with those of piglets in the CON group (P < 0.05). Relative abundance of Lactobacillus in colonic chyme and mucosa of piglets in the ENI group was significantly higher relative to that of piglets in the CON group (P < 0.05). Correlation analysis indicated that abundance of Lactobacillus was positively correlated with the relative mRNA expression levels of ZO-1, Claudin4, and GALNT1, and it was negatively correlated with the level of MCP-1 in colonic chyme and mucosa. In summary, the findings of this study showed that early-life nutrition interventions improved growth performance, colonic barrier, and reduced inflammation in the colon by modulating composition of gut microbiota in piglets. Early-life nutrition intervention through supplemental synthetic milk is a feasible measure to improve the health and reduce the number of deaths of piglets.

Keywords: early-life nutrition interventions; growth performance; gut microbiota; inflammatory cytokines; intestinal barrier; short-chain fatty acids (SCFAs).

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Effects of early-life nutrition interventions on growth performance and visceral organs in piglets. CON, control group, ENI, early-life nutrition interventions group. (A) The feeding mode diagram. (B) The weight changes of piglets at 3, 21, and 30 days of age in each group. (C) The diarrhea rate of pre-weaning and post-weaning of piglets. (D) The liver weight of piglets in each group. (E) The spleen weight of piglets in each group. (F) The relative weights of liver to living body weight. (G) The relative weights of spleen to living body weight. (H) The length of colon in each group. (I) The length of whole intestine. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 2
Figure 2
Effects of early-life nutrition interventions on the intestinal barrier of the colon in piglets. CON, control group, ENI, early-life nutrition interventions group. (A) The content of LPS in plasma. (B) The activity of AKP in serum. (C) The mRNA expression levels of ZO-1, Occludin, and Claudin4 in the colon. (D) The mRNA expression levels of GALNT1, B3GNT6, and MUC2 in the colon. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 3
Figure 3
Effects of early-life nutrition interventions on the morphology of the colon and the number of goblet cells. CON, control group, ENI, early-life nutrition interventions group. (A). HE and PAS staining of colon tissue. (B) The crypt depth of the colon. (C) The number of goblet cells of the colon. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 4
Figure 4
Effects of early-life nutrition interventions on inflammation in the piglet colon. CON, control group, ENI, early-life nutrition interventions group. (A) The mRNA expression levels of MCP-1, TNF-α, IL-1β, and IL-8 in colon. (B) The protein expression levels of TNF-α, IL-6, and IL-8 in piglets. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 5
Figure 5
Effects of early-life nutrition interventions on concentrations of SCFAs in the colonic mucosa and colonic chyme. CON, control group, ENI, early-life nutrition interventions group. (A) Acetate acid. (B) Propionic acid. (C) Isobutyric acid. (D) Butyric acid. (E) Isovaleric acid. (F) Valeric acid. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 6
Figure 6
The analysis of gut microbiota diversity in the colonic chyme and colonic mucosa of piglets. CON, control group, ENI, early-life nutrition interventions group. (A) The Chao index of microbiota in colonic chyme. (B) The Shannon index of microbiota in colonic chyme. (C) The Chao index of microbiota in colonic mucosa. (D) The Shannon index of microbiota in colonic mucosa. (E) PCoA analysis of microbiota in colonic chyme at the phylum level. (F) PCoA analysis of microbiota in colonic chyme at the genus level. (G) PCoA analysis of microbiota in colonic mucosa at the phylum level. (H) PCoA analysis of microbiota in colonic mucosa at the genus level. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 7
Figure 7
Gut microbiota community composition in the colonic chyme and colonic mucosa of piglets. CON, control group, ENI, early-life nutrition interventions group. (A) The relative abundances of microbiota in colonic chyme at the phylum level. (B) The relative abundances of microbiota in colonic chyme at the genus level. (C) The top 6 bacteria in colonic chyme at the phylum level statistical comparison of the relative abundances. (D) The top 10 bacteria in colonic chyme at the genus level statistical comparison of the relative abundances. (E) The relative abundances of microbiota in colonic mucosa at the phylum level. (F) The relative abundances of microbiota in colonic mucosa at the genus level. (G) The top 6 bacteria in colonic mucosa at the phylum level statistical comparison of the relative abundances. (H) The top 10 bacteria in colonic mucosa at the genus level statistical comparison of the relative abundances. Data are expressed as mean ± SEM (n = 4). The independent-samples t-test was used to compare data between two groups. *P < 0.05.
Figure 8
Figure 8
The differentially abundant taxa among the two groups by LEfSe analysis. CON: control group, ENI: early-life nutrition interventions group. (A) LEfSe analysis of microbiota in colonic chyme. (B) LEfSe analysis of microbiota in colonic mucosa.
Figure 9
Figure 9
The correlation of intestinal microbiota, intestinal barrier, and immune-related indexes. (A) The correlation of intestinal microbiota, intestinal barrier, and immune-related indexes in colonic chyme. (B) The correlation of intestinal microbiota, intestinal barrier, and immune-related indexes in colonic mucosa. *P < 0.05.
Figure 10
Figure 10
Early-life nutrition interventions improved growth performance and intestinal health via the gut microbiota in piglets: a possible mechanism.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Syrovnev GI, Mykytyuk VV, Khmeleva EV. The presence of a potential patient of Colibacterisis in the population of pigs of local selection of ukrainian meat breed. J Anim Breed Genet. (2020) 59:115–23. 10.31073/abg.59.13 - DOI
    1. Campbell JM, Crenshaw JD, Polo J. The biological stress of early weaned piglets. J Anim Sci Biotechnol. (2013) 4:19. 10.1186/2049-1891-4-19 - DOI - PMC - PubMed
    1. Huting AMS, Middelkoop A, Guan X, Molist F. Using nutritional strategies to shape the gastro-intestinal tracts of suckling and weaned piglets. Animals. (2021) 11:402. 10.3390/ani11020402 - DOI - PMC - PubMed
    1. Vente-Spreeuwenberg M, Verdonk J, Bakker G, Beynen AC, Verstegen M. Effect of dietary protein source on feed intake and small intestinal morphology in newly weaned piglets. Livest Prod Sci. (2004) 86:169–77. 10.1016/S0301-6226(03)00166-0 - DOI - PubMed
    1. Croxen MA, Finlay B. Molecular mechanisms of Escherichia coli pathogenicity. Nat Rev Microbiol. (2010) 8:26–38. 10.1038/nrmicro2265 - DOI - PubMed