A High-Sucrose Isocaloric Pair-Fed Model Induces Obesity and Impairs NDUFB6 Gene Function in Rat Adipose Tissue

Abstract

Background/Aim: Changes in dietary macronutrient content are involved in altered energy metabolism and obesity development. However, there are controversial views about the obesogenic effects of high-sucrose (HS) diets, which usually lead to obesity and insulin resistance but are sometimes associated with reduced weight gain. The aim of this study was to investigate the effect of consumption of a pair-fed HS diet on weight gain and energy homeostasis in rats, as well as to assess the effects on expression of the NADH dehydrogenase (ubiquinone) 1β subcomplex 6 (NDUFB6) gene in adipose tissue. Methods/Results: Although both dietary groups, i.e. HS and control, were pair-fed (isoenergetic feeding), the HS diet increased adiposity and decreased plasma total and high-density lipoprotein cholesterol levels. While no significant differences were found with regard to serum glucose, insulin, adiponectin, free fatty acids and liver malondialdehyde, a slight increase in serum and liver triglycerides was observed. Interestingly, the gene expression of NDUFB6, an inner mitochondrial membrane protein involved in mitochondrial electron transport, was reduced in epididymal adipose tissue when compared to the control-fed group. Conclusion: These results suggest, apparently for the first time, that high-sugar diets appear to induce mitochondrial dysfunction in adipose tissue, which may be related to greater weight gain and metabolic impairment.

High Fatty Diet Effects on Rat Liver

“…It was found in other studies (34)(35)(36)(37)(38), high-carbohydrate diet caused to increase of adipose tissue and hepatic steatosis (39).…”

“…Lomba et al (34) compared with high-sucrose (HS) diet and isocaloric control diet. HS diet increased adiposity, decreased plasma total cholesterol and HDL levels.…”

“…Also, it was determined that high-carbohydrate diet increased hepatic fat synthesis, caused to the accumulation of triglyceride in the liver, rise of ALT, AST levels, and caused mitochondrial dysfunction in adipose tissue (31)(32)(33)(34)(35)(36)(37)(38).…”

Ketohexokinase C blockade ameliorates fructose-induced metabolic dysfunction in fructose-sensitive mice

“…It is commonly thought that the association between sugar consumption and metabolic syndrome is merely due to the hypercaloric effect of fructose and sugar as a consequence of excessive intake (45,46). However, there are isocaloric data to the contrary that highlight the peculiarity of fructose and its metabolism (47,48). Importantly, here we show, using AldoB-KO mice, that even when fructose cannot be directly metabolized into triglycerides, glucose, or glycogen, it can induce specific harmful metabolic effects in the organism, including fatty liver and liver inflammation, which would underscore the importance of the particular metabolism of fructose in disease.…”

Combined compared to dissociated oral and intestinal sucrose stimuli induce different brain hedonic processes

“…Sucrose remains the leading added sugar consumed in the American diet and the leading source of fructose, although a rapid increase in fructose consumption has been noticed in the last decades (Tappy and Le, 2010). Yet, chronic consumption of high-sugar diets has been proved to induce metabolic, neurophysiological and brain alterations leading to eating disorders and obesity in humans, pigs and rats (Zhao et al, 2005; Lomba et al, 2009; Benton, 2010; Val-Laillet et al, 2010, 2011). Consequently, the characterization of the brain networks that contribute to the processing of oral and/or post-oral sugar signals in animal models, by leading to a better understanding of impaired eating behaviors like the onset of exacerbated sugar preferences in humans, might fulfill the current needs in human nutrition and health research.…”