Dietary Glucose Ameliorates Impaired Intestinal Development and Immune Homeostasis Disorders Induced by Chronic Cold Stress in Pig Model

Abstract

Endotherms are easily challenged by chronic cold stress. In this study, the development and injury of the small intestine in the Min pig model and Yorkshire pig model under chronic cold stress, and the molecular mechanisms by which glucose supplementation reduces small intestinal mucosal damage were investigated. The results showed that morphological structure lesions of the jejunal mucosa and ileal mucosa were visible in Yorkshire pigs under chronic cold stress. Meanwhile, the Occludin mRNA and protein expression in jejunal mucosa of Yorkshire pigs was decreased. Chronic cold stress enhanced the expression of Toll-like receptor 4 (TLR4), the myeloid differentiation main response 88 (MyD88), nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3), cleaved caspase-1, mature-IL-1β, and high-mobility group box 1 (HMGB 1) mRNA and protein expression in jejunal mucosa of Yorkshire pigs, whereas the mRNA and protein of Bax was triggered in ileal mucosa. In Min pigs, no such deleterious consequences were observed. Dietary glucose supplementation ameliorates small intestinal mucosal injury, declined TLR4 and MyD88 expression in jejunal mucosa. In conclusion, chronic cold stress induced the small intestinal mucosa damage in Yorkshire pigs, whereas glucose supplementation mitigated the deleterious effects of chronic cold stress on the small intestine.

Dietary full-fat rice bran prevents the risk of heart ferroptosis and imbalance of energy metabolism induced by prolonged cold stimulation

“…54,55 Our previous study showed that prolonged cold stimulation induces inflammation by activating the TLR4/NLRP3 signaling pathway in the small intestinal mucosa and lungs. 18,19 In the present study, there was no effect on the protein expression of MyD88 even though its mRNA expression was enhanced during prolonged cold stimulation. Nevertheless, the protein levels of NLRP3 and mature-Il-1β were promoted.…”

“…18 TLR4 induces nuclear factor-κB (NF-κB) activation and nuclear translocation via MyD88, which leads to the triggering of pro-IL-1β and NLRP3 expression. 18 NLRP3 binds to apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and links to caspase-1 through the CARD structural domain within ASC, as well as forming NLRP3 inflflammasomes. 54 NLRP3 inflammatory vesicles shear pro-IL-1β and pro-IL-18 into their respective mature forms, and promote the formation of the gasdermin D (GSDMD) N-terminal domain, which oligomerizes and moves to the cell membrane to form pores, ultimately resulting in the release of intracellular inflammatory factors and pyroptosis.…”

“…Organs and systems may sustain varying degrees of injury when temperatures drop below the tolerance of humans. 18,19 The heart primarily powers the circulation of blood in the body. Previous studies have shown that shortterm cold stimulation increases heart output and blood flow, helping the body fight the cold.…”

“…When the organism suffers an injury, HMGB1 will be released outside the cell and activate the TLR4/ MyD88 signaling pathway. 18 TLR4 induces nuclear factor-κB (NF-κB) activation and nuclear translocation via MyD88, which leads to the triggering of pro-IL-1β and NLRP3 expression. 18 NLRP3 binds to apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and links to caspase-1 through the CARD structural domain within ASC, as well as forming NLRP3 inflflammasomes.…”

Glucose supplementation improves intestinal amino acid transport and muscle amino acid pool in pigs during chronic cold exposure

“…The results showed that the trypsin activity in jejunal mucosa had a trend toward inhibition in the CSY group, suggesting that protein digestion ability was weakened. Studies have shown that chronic cold stress modulates intestinal inflammatory cell infiltration, intestinal development and mucosal barrier function ( Liu et al., 2019 ; Sun et al., 2022 ). Thus, chronic cold exposure may dilute the ability for the small intestine to digest crude protein by inducing damage to the small intestine.…”