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Research
Zhao Hua
Animal Nutrition Institute of Sichuan Agricultural University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0334-4189
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background:
Chronic heat stress (CHS) disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs. Selenium (Se) may regulate the metabolic state through affect selenoprotein. Thus, we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid (HMSeBA) on CHS induced hepatic metabolic disorder in growing pigs, and the corresponding response of selenoprotein.
Methods:
Forty crossbreed growing pigs were randomly assigned to five groups: control group raised in the thermoneutral environment (22 ± 2 oC) with basal diet; four CHS groups raised in hyperthermal condition (33 ± 2 oC) with basal diet and supplied with 0.0, 0.2, 0.4 and 0.6 mg Se/kg HMSeBA, respectively. The trial lasted 28 days. The serum biochemical, hepatic metabolism related enzyme, protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR, ELISA and western blot.
Results:
CHS significantly increased the rectal temperature, respiration rate, serum aspartate aminotransferase (AST) and low-density lipoprotein cholesterol (LDL-C) of pigs, up-regulated hepatic heat shock protein 70 (HSP70) and induced lower liver weight, glycogen content, hepatic glucokinase and glutathione peroxidase (GSH-Px). The CHS-induced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes, and decreased the protein abundance of GCK, GPX4 and SELENOS. HMSeBA improved anti-oxidative capacity of liver. 0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight, glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK. HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes, and enhanced protein expression of GPX1, GPX4 and SELENOS in the liver affected by CHS. CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKα in the liver.
Conclusions:
In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, recovered the liver glycogen content and the processes are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.
Keywords
Chronic heat stress, HMSeBA, Hepatic metabolism, Pigs, Selenoprotein
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Peer Review Timeline
CURRENT STATUS: Under Review
Version 2
Posted 12 Feb, 2021
No community comments so far
Editorial decision: Major revision
On 16 Feb, 2021
Review #2 received
Received 15 Feb, 2021
Reviewer #2 agreed
On 09 Feb, 2021
Reviewer #1 agreed
On 07 Feb, 2021
Review #1 received
Received 07 Feb, 2021
Editor assigned
On 06 Feb, 2021
Reviewers invited
Invitations sent on 06 Feb, 2021
Submission checks complete
On 06 Feb, 2021
Editor invited
On 06 Feb, 2021
No comments provided
Editorial decision: Major revision
On 20 Jan, 2021
Review #1 received
Received 17 Jan, 2021
Review #2 received
Received 10 Jan, 2021
Reviewer #2 agreed
On 08 Jan, 2021
Reviewer #1 agreed
On 06 Jan, 2021
Reviewers invited
Invitations sent on 20 Dec, 2020
First submitted
On 14 Dec, 2020
Editor assigned
On 14 Dec, 2020
Submission checks complete
On 14 Dec, 2020
Editor invited
On 14 Dec, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
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This preprint is under consideration at Journal of Animal Science and Biotechnology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Zhao Hua
Animal Nutrition Institute of Sichuan Agricultural University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0334-4189
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 2
Posted 12 Feb, 2021
No community comments so far
Editorial decision: Major revision
On 16 Feb, 2021
Review #2 received
Received 15 Feb, 2021
Reviewer #2 agreed
On 09 Feb, 2021
Reviewer #1 agreed
On 07 Feb, 2021
Review #1 received
Received 07 Feb, 2021
Editor assigned
On 06 Feb, 2021
Reviewers invited
Invitations sent on 06 Feb, 2021
Submission checks complete
On 06 Feb, 2021
Editor invited
On 06 Feb, 2021
No comments provided
Editorial decision: Major revision
On 20 Jan, 2021
Review #1 received
Received 17 Jan, 2021
Review #2 received
Received 10 Jan, 2021
Reviewer #2 agreed
On 08 Jan, 2021
Reviewer #1 agreed
On 06 Jan, 2021
Reviewers invited
Invitations sent on 20 Dec, 2020
First submitted
On 14 Dec, 2020
Editor assigned
On 14 Dec, 2020
Submission checks complete
On 14 Dec, 2020
Editor invited
On 14 Dec, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background:
Chronic heat stress (CHS) disrupts hepatic metabolic homeostasis and jeopardizes product quality of pigs. Selenium (Se) may regulate the metabolic state through affect selenoprotein. Thus, we investigate the protective effect of dietary hydroxy-4-methylselenobutanoic acid (HMSeBA) on CHS induced hepatic metabolic disorder in growing pigs, and the corresponding response of selenoprotein.
Methods:
Forty crossbreed growing pigs were randomly assigned to five groups: control group raised in the thermoneutral environment (22 ± 2 oC) with basal diet; four CHS groups raised in hyperthermal condition (33 ± 2 oC) with basal diet and supplied with 0.0, 0.2, 0.4 and 0.6 mg Se/kg HMSeBA, respectively. The trial lasted 28 days. The serum biochemical, hepatic metabolism related enzyme, protein and gene expression and 25 selenoproteins in liver tissue were determined by real-time PCR, ELISA and western blot.
Results:
CHS significantly increased the rectal temperature, respiration rate, serum aspartate aminotransferase (AST) and low-density lipoprotein cholesterol (LDL-C) of pigs, up-regulated hepatic heat shock protein 70 (HSP70) and induced lower liver weight, glycogen content, hepatic glucokinase and glutathione peroxidase (GSH-Px). The CHS-induced liver metabolic disorder was associated with the aberrant expression of 6 metabolism-related gene and 11 selenoprotein encoding genes, and decreased the protein abundance of GCK, GPX4 and SELENOS. HMSeBA improved anti-oxidative capacity of liver. 0.4 or 0.6 mg Se/kg HMSeBA supplementation recovered the liver weight, glycogen content and rescue of mRNA abundance of genes related to metabolism and protein levels of GCK. HMSeBA supplementation changed expressions of 15 selenoprotein encoding genes, and enhanced protein expression of GPX1, GPX4 and SELENOS in the liver affected by CHS. CHS alone showed no impact while HMSeBA supplementation increased protein levels of p-AMPKα in the liver.
Conclusions:
In summary, HMSeBA supplementation beyond nutrient requirement mitigates CHS-induced hepatic metabolic disorder, recovered the liver glycogen content and the processes are associated with the activation of AMPK signal and regulation of selenoproteins in the liver of growing pigs.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
This is a list of supplementary files associated with this preprint. Click to download.
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