Weight gain induced by high-fat feeding involves increased liver oxidative stress.
OBJECTIVE
To assess the effects of high-fat feeding on white adipose tissue gene expression and liver oxidative stress.


METHODS
Male Wistar rats were fed on standard pelleted or high-fat diet to produce a diet-induced obesity model. Therefore, body composition, serum biochemical values and liver malondialdehyde (MDA) were determined after 56 days of feeding. Expression (mRNA) values of three genes were also determined by reverse transcriptase-polymerase chain reaction in white adipose tissue.


RESULTS
Animals fed on the high-fat diet showed more body weight, higher fat deposition and total liver weight, and increased energy intake compared with those on the standard-fat diet. Serum fasting measurements (glucose, insulin, leptin) and homeostasis model assessment insulin resistance index were significantly increased by the high-fat diet consumption. As an indicator of oxidative stress, peroxide decomposition in liver was analyzed, showing an increase of MDA concentrations in rats fed on high-fat diet in comparison with control rats. Interestingly, liver MDA levels correlated positively with body weight gain, serum leptin, and homeostasis model assessment. Finally, leptin and glycerol-3-phosphate dehydrogenase mRNA levels, but not fatty acid synthase, were increased by high-fat diet in comparison with the control-fed group.


CONCLUSIONS
These results show a link among increased fat depots, insulin resistance, and liver oxidative stress. Thus, liver oxidative stress probably contributes to hepatic disorders and aggravates the metabolic syndrome, which is accompanied by a stimulation of the esterification of fatty acids as measured by glycerol-3-phosphate dehydrogenase in the adipose tissue, providing support to the hypothesis that not only calories count in the induction of weight gain or metabolic syndrome and that other factors such as oxidative stress may be involved.
Milagro
Fermín I
FI
Department of Physiology and Nutrition, University of Navarra, C/Irunlarrea s/n, 31008 Pamplona, Spain.
Campión
Javier
J
Martínez
J Alfredo
JA
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001823:Body Composition / Q000502:physiology; D004041:Dietary Fats / Q000008:administration & dosage*; D015870:Gene Expression; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008099:Liver / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015430:Weight Gain
D004041:Dietary Fats; D020738:Leptin; D012333:RNA, Messenger; D008315:Malondialdehyde