TY - JOUR
T1 - Chronic psychosocial defeat differently affects lipid metabolism in liver and white adipose tissue and induces hepatic oxidative stress in mice fed a high-fat diet
AU - Giudetti, Anna M.
AU - Testini, Mariangela
AU - Vergara, Daniele
AU - Priore, Paola
AU - Damiano, Fabrizio
AU - Gallelli, Cristina Anna
AU - Romano, Adele
AU - Villani, Rosanna
AU - Cassano, Tommaso
AU - Siculella, Luisa
AU - Gnoni, Gabriele V.
AU - Moles, Anna
AU - Coccurello, Roberto
AU - Gaetani, Silvana
PY - 2018
Y1 - 2018
N2 - It is widely accepted that chronic stress may alter the homeostatic mechanisms of body weight control. In this study, we followed the metabolic changes occurring in mice when chronic stress caused by psychosocial defeat (CPD) is associated with ad libitum exposure to a palatable high-fat diet (HFD). In this model, CPD mice consumed more HFD than unstressed (Un) mice without gaining body weight. We focused on metabolic processes involved in weight control, such asde novolipogenesis (DNL),fatty acidb-oxidation(FAO), andthermogenesis.The activity and expression of DNL enzymes were reduced in the liver and white adipose tissue of mice consuming the HFD. Such effects were particularly evident in stressed mice. In both CPD and Un mice, HFD consumption increased the hepatic expression of the mitochondrial FAO enzyme carnitine palmitoyltransferase-1. In the liver of mice consuming the HFD, stress exposure prevented accumulation of triacylglycerols; however, accumulation of triacylglycerols was observed inUn mice underthe same dietary regimen. In brown adipose tissue, stress increased the expression of uncoupling protein-1, which is involved in energy dissipation, both in HFD and control diet-fed mice. We consider increased FAO and energy dissipation responsible for the antiobesity effect seen in CPD/HFD mice. However, CPD associated with HFD induced hepatic oxidative stress.
AB - It is widely accepted that chronic stress may alter the homeostatic mechanisms of body weight control. In this study, we followed the metabolic changes occurring in mice when chronic stress caused by psychosocial defeat (CPD) is associated with ad libitum exposure to a palatable high-fat diet (HFD). In this model, CPD mice consumed more HFD than unstressed (Un) mice without gaining body weight. We focused on metabolic processes involved in weight control, such asde novolipogenesis (DNL),fatty acidb-oxidation(FAO), andthermogenesis.The activity and expression of DNL enzymes were reduced in the liver and white adipose tissue of mice consuming the HFD. Such effects were particularly evident in stressed mice. In both CPD and Un mice, HFD consumption increased the hepatic expression of the mitochondrial FAO enzyme carnitine palmitoyltransferase-1. In the liver of mice consuming the HFD, stress exposure prevented accumulation of triacylglycerols; however, accumulation of triacylglycerols was observed inUn mice underthe same dietary regimen. In brown adipose tissue, stress increased the expression of uncoupling protein-1, which is involved in energy dissipation, both in HFD and control diet-fed mice. We consider increased FAO and energy dissipation responsible for the antiobesity effect seen in CPD/HFD mice. However, CPD associated with HFD induced hepatic oxidative stress.
KW - Fatty acids
KW - Lipogenesis
KW - Liver steatosis
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UR - http://www.scopus.com/inward/citedby.url?scp=85059247153&partnerID=8YFLogxK
U2 - 10.1096/fj.201801130R
DO - 10.1096/fj.201801130R
M3 - Article
C2 - 30133327
AN - SCOPUS:85059247153
VL - 33
SP - 1428
EP - 1439
JO - FASEB Journal
JF - FASEB Journal
SN - 0892-6638
IS - 1
ER -