Running Head: Heat Affects Cholesterol and Bile Acid Alterations in Cholesterol and Bile Acids Metabolism in Large White Pigs during Short-Term Heat Exposure.

Wei Fang,Lei Liu,Qingshi Meng,Hongfu Zhang,Jingjing Xie,Xiaobin Wen,Nadia Everaert

doi:10.3390/ani10020359

Abstract

Heat stress influences lipid metabolism independently of nutrient intake. It is not well understood how cholesterol and bile acid (BA) metabolism are affected by heat stress. To investigate the alterations of cholesterol and bile acids when pigs are exposed to short term heat stress, 24 Large White pigs (63.2 ± 9.5 kg body weight, BW) were distributed into one of three environmental treatments: control conditions (CON, 23 °C with ad libitum intake; n = 8), heat stress conditions (HS, 33 °C with ad libitum intake; n = 8), or pair-fed conditions (PF, 23 °C with the same amount to the feed consumed by the HS; n = 8) for three days. Compared with CON pigs, HS pigs reduced the average daily feed intake and average daily gain by 55% and 124%, respectively, and significantly increased rectal temperatures by 0.9 °C and respiration rates more than three-fold. The serum total cholesterol (TC), low-density lipoprotein-cholesterol, and triglycerides (TG) increased (p < 0.05), while hepatic TC, TG, and mRNA of 3-hydroxy-3-methylglutaryl-CoA reductase were reduced on day 3. Furthermore, liver taurine-conjugated BAs (TCBAs), including taurolithocholic acid, taurochenodeoxycholic acid (TCDCA), tauroursodeoxycholic acid, taurohyodeoxycholic acid, and taurocholic acid were elevated in HS pigs compared to CON and PF pigs (p < 0.05), and the level of chenodeoxycholic acid was more significant in the PF group than in the CON and HS groups. The concentration of ursodeoxycholic acid in the serum was higher in HS pigs than CON and PF pigs (p < 0.05), and TCDCA was increased in HS pigs compared with PF pigs (p < 0.05). Altogether, short-term HS reduced hepatic cholesterol levels by decreasing cholesterol synthesis, promoting cholesterol to TCBAs conversion, and cholesterol release to serum in growing pigs. This independently reduced feed intake might serve as a mechanism to protect cells from damage during the early period.

Highlights

Reduced growth performance and increased economic losses in pigs caused by heat stress (HS)have been well documented in animal agriculture [1,2]
Without heat abatement strategies, growing pigs are susceptible to HS [3], which has been shown to decrease feed intake [4], alter metabolism [5], and tissue accretion [6] compared to thermoneutral-reared pigs
We have previously shown that long-term heat exposure decreased cholesterol uptake and taurine-conjugated bile acid (BA) synthesis and uptake in the liver [24,25]

Summary

Introduction

Reduced growth performance and increased economic losses in pigs caused by heat stress (HS)have been well documented in animal agriculture [1,2]. Heat stress impacts lipid metabolism in pigs, mainly by decreasing the lipolytic capacity and increasing fat deposition and triglyceride storage, independent of the heat-induced inadequate feed intake [5,7]. Lipids play an essential role in regulating several biological processes involved in heat stress response [11]. Heat stress induces the fluidization of cellular membranes, which play an essential role in the control of heat sensing and signaling to maintain cellular function [12,13]. Cholesterol is an essential component of most cell membranes, regulating the fluidity of the lipid bilayer and the heat shock protein signaling and contributing to heat adaptation [14,15].

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