Abstract
Fasting-induced autophagy in the intestine is beneficial for body health. This study was designed to explore the relationship between the host metabolism and intestinal autophagy. Broilers were randomly assigned into 48 cages. At 0 (CT), 12 (FH12), 24 (FH24), 36 (FH36), 48(FH48), and 72 h (FH72) before 09:00 a.m. on day 25, eight cages of birds were randomly allotted to each fasting time point using completely random design, and their food was removed. At 09:00 a.m. on day 25, the blood and jejunum were sampled for serum metabolome and autophagy gene analyses, respectively. The results showed that the autophagy gene Atg7 has a good quadratic fit with fasting duration (R2 = 0.432, p < 0.001). Serum phosphatidylethanolamine (PE) and lyso-PE were decreased in the birds that were fasted for 24 h or longer. Conversely, the serum phosphatidylcholine (PC) and lyso-PC were increased in the birds that were fasted for 36 h or longer. Metabolism pathway analysis showed that the serum glycerophospholipid, phenylalanine, and GnRH signaling pathways were downregulated with the extended fasting duration. The serum metabolites involved in glycosylphosphatidylinositol anchor biosynthesis, autophagy, and ferroptosis were upregulated in all of the fasted groups. Correlation analysis showed that serum PE (18:3(9Z,12Z,15Z)/P-18:0) was a potential biomarker for intestinal autophagy. Our findings provide a potential biomarker related to intestinal autophagy.
Highlights
This study showed that the mRNA level of Atg 7 was significantly (p < 0.05) upregulated at every fasting time point, except for 12 h of fasting (Figure 2)
The Principle component analysis (PCA) score plots suggested a distinct separation among the different fasting durations (Figure 3A)
The orthogonal partial least-squaresdiscriminant analysis (OPLS-DA) revealed a clear separation between the non-fasting and fasting groups (Figure 3B–F)
Summary
AMP-activated protein kinase is activated and inhibits the mechanistic target of rapamycin in order to suppress cell growth and activate autophagy [6]. Activated autophagy scavenges cytoplasmic materials for energy production [7] and regulates gut homeostasis [8,9]. It has been reported that anomalous autophagy is associated with inflammatory bowel diseases [10] and impaired absorptive enterocytes [8]. What is more, activated intestinal autophagy triggered by fasting protects against TNF-induced apoptosis during chronic colitis and improves life span [11,12]. It has been reported that the autophagy level varies with fasting durations [13]. The autophagy level in the intestine in response to different fasting durations remain unknown
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