The role of liver metabolism in compensatory-growth piglets induced by protein restriction and subsequent protein realimentation

2021 ◽  
Vol 74 ◽  
pp. 106512
Author(s):  
M.Y. Zhang ◽  
P. Hu ◽  
D. Feng ◽  
Y.Z. Zhu ◽  
Q. Shi ◽  
...  
2016 ◽  
Vol 11 (S 01) ◽  
Author(s):  
T Laeger ◽  
DC Albarado ◽  
L Trosclair ◽  
J Hedgepeth ◽  
CD Morrison

Aquaculture ◽  
2007 ◽  
Vol 267 (1-4) ◽  
pp. 188-198 ◽  
Author(s):  
Núria Montserrat ◽  
Pedro Gómez-Requeni ◽  
Giovanni Bellini ◽  
Encarnación Capilla ◽  
Jaume Pérez-Sánchez ◽  
...  

1968 ◽  
Vol 243 (5) ◽  
pp. 1031-1038 ◽  
Author(s):  
L S Jefferson ◽  
J H Exton ◽  
R W Butcher ◽  
E W Sutherland ◽  
C R Park
Keyword(s):  

BMC Genomics ◽  
2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Maria Ballester ◽  
Marcel Amills ◽  
Olga González-Rodríguez ◽  
Tainã F. Cardoso ◽  
Mariam Pascual ◽  
...  

2014 ◽  
Vol 307 (1) ◽  
pp. G66-G76 ◽  
Author(s):  
Hae-Ki Min ◽  
Silvia Sookoian ◽  
Carlos J. Pirola ◽  
Jianfeng Cheng ◽  
Faridoddin Mirshahi ◽  
...  

PNPLA3 was recently associated with the susceptibility to nonalcoholic fatty liver disease, a common cause of chronic liver disease characterized by abnormal triglyceride accumulation. Although it is established that PNPLA3 has both triacylglycerol lipase and acylglycerol O-acyltransferase activities, is still unknown whether the gene has any additional role in the modulation of the human liver metabolome. To uncover the functional role of PNPLA3 on liver metabolism, we performed high-throughput metabolic profiling of PNPLA3 siRNA-silencing and overexpression of wild-type and mutant Ile148Met variants (isoleucine/methionine substitution at codon 148) in Huh-7 cells. Metabolomic analysis was performed by using GC/MS and LC/MS platforms. Silencing of PNPLA3 was associated with a global perturbation of Huh-7 hepatoma cells that resembled a catabolic response associated with protein breakdown. A significant decrease in amino- and γ-glutamyl-amino acids and dipeptides and a significant increase in cysteine sulfinic acid, myo-inositol, lysolipids, sphingolipids, and polyunsaturated fatty acids were observed. Overexpression of the PNPLA3 Met148 variant mirrored many of the metabolic changes observed during gene silencing, but in the opposite direction. These findings were replicated by the exploration of canonical pathways associated with PNPLA3 silencing and Met148 overexpression. Overexpression of the PNPLA3 Met148 variant was associated with a 1.75-fold increase in lactic acid, suggesting a shift to anaerobic metabolism and mitochondrial dysfunction. Together, these results suggest a critical role of PNPLA3 in the modulation of liver metabolism beyond its classical participation in triacylglycerol remodeling.


2015 ◽  
Vol 114 (4) ◽  
pp. 519-532 ◽  
Author(s):  
Huan Wang ◽  
Gabriel J. Wilson ◽  
Dan Zhou ◽  
Stéphane Lezmi ◽  
Xiuwen Chen ◽  
...  

The aim of the present study was to investigate the mechanistic basis of protein deficiency during pregnancy in mother that is transduced to offspring. To this end, timed-pregnant Sprague–Dawley rats were fed either a control (20 % of energy from protein) or low-protein (LP, 8 % of energy from protein) diet during gestation. Tissues were collected after delivery from rat dams, and skeletal muscle was collected at postnatal day 38 from the offspring. Quantitative RT-PCR and Western blot analyses were performed to determine mRNA and protein levels. Histological analysis was performed to evaluate myofibre size. LP dams gained significantly less weight during pregnancy, developed muscle atrophy, and had significantly lower circulating threonine and histidine levels than control dams. The mRNA expression of the well-known amino acid response (AAR) pathway-related target genes was increased only in the skeletal muscle of LP dams, as well as the protein expression levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiation factor 2α (p-eIF2α). The mRNA expression of autophagy-related genes was significantly increased in the skeletal muscle of LP dams. Moreover, the mRNA expression of genes involved in both AAR and autophagy pathways remained elevated and was memorised in the muscle of LP offspring that consumed a post-weaning control diet. Additionally, the LP diet increased an autophagy marker, microtubule-associated proteins 1A/1B light chain 3B (LC3B) protein expression in the skeletal muscle of rat dams, consistent with the initiation of autophagy. The LP diet further increased ATF4 binding at the predicted regions of AAR and autophagy pathway-related genes. Increased binding of ATF4 unveils the crucial role of ATF4 in the activation of autophagy in response to protein restriction. Our data suggest that molecular changes in maternal muscle are memorised in the offspring long after gestational protein restriction, reinforcing the role of maternal signalling in programming offspring health.


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