Antioxidant enzymes induced by repeated intake of excess energy in the form of high-fat, high-carbohydrate meals are not sufficient to block oxidative stress in healthy lean individuals

Abstract

It has been reported that high-fat, high-carbohydrate (HFHC) meals increase oxidative stress and inflammation. We examined whether repeated intake of excess energy in the form of HFHC meals alters reactive oxygen species (ROS) generation and the expression levels of antioxidant enzymes and mitochondrial proteins in mononuclear cells, and to determine whether this is associated with insulin resistance. We recruited healthy lean individuals (n 10). The individuals were divided into two groups: one group (n 5) ingested 10878·4 kJ/d (2600 kcal/d; 55-70 % carbohydrate, 9·5-16 % fat, 7 -20 % protein) recommended by the Dietary Reference Intake for Koreans for 4 d and the other group (n 5) ingested a HFHC meal containing 14 644 kJ/d (3500 kcal/d). Then, measurements of blood insulin and glucose levels, together with suppressor of cytokine signalling-3 (SOCS-3) expression levels, were performed in both groups. Also, cellular and mitochondrial ROS levels as well as malondialdehyde (MDA) levels were measured. Expression levels of cytosolic and mitochondrial antioxidant enzymes, and mitochondrial complex proteins were analysed. Repeated intake of HFHC meals induced an increase in homeostasis model of assessment-insulin resistance (HOMA-IR), together with an increase in SOCS-3 expression levels. While a single intake of the HFHC meal increased cytosolic and mitochondrial ROS, repeated intake of HFHC meals reduced them and increased the levels of MDA, cytosolic and mitochondrial antioxidant enzymes, and several mitochondrial complex proteins. Repeated intake of HFHC meals induced cellular antioxidant mechanisms, which in turn increased lipid peroxidation (MDA) and SOCS-3 expression levels, induced hyperinsulinaemia and increased HOMA-IR, an index of insulin resistance. In conclusion, excess energy added to a diet can generate detrimental effects in a short period.

Remission of pre-diabetes to normal glucose tolerance in obese adults with high protein versus high carbohydrate diet: randomized control trial

“…A study showed antioxidant enzymes induced by repeated intake of excess energy in the form of high-fat, HC diets are not sufficient to block oxidative stress and inflammation in healthy human subjects. 37 Thus, the fact that our HP diet had a significantly greater reduction in ROS and inflammation markers than the HC diet in pre-diabetes subjects is of great health importance.…”

Inflammatory and Oxidative Stress Responses to High-Carbohydrate and High-Fat Meals in Healthy Humans

“…The postprandial phase has been described as pro-oxidative [15, 16, 37–39] with the magnitude of the oxidative stress response linked to the carbohydrate content of the meal and the level of hyperglycaemia and hyperinsulinemia evoked [16]. However, data gathered in obese humans has been controversial, with studies reporting either increased [35] or decreased [40] ROS emission from skeletal muscle mitochondria ex vivo in the postprandial state.…”

“…However, the available literature is conflicting as to whether circulating inflammatory cytokines change in response to meals, although a consensus is generally reached in respect to stimulation of postprandial IL6 [11–14]. Whether high-fat and high-carbohydrate meals differentially modulate the inflammatory or oxidative stress responses in humans is also debated [15, 16]. Therefore, the aim of this study was to examine circulating and skeletal muscle gene expression of inflammation and oxidative stress markers in the fasting state and after a physiological challenge by a high-carbohydrate or high-fat meal in healthy, non-obese, normoglycemic individuals, 7 of whom reported a family history of type 2 diabetes.…”

Factors associated with oxidative stress and cancer risk in the Breast and Prostate Cancer Cohort Consortium

“…Ozone and cigarette smoke [3], absorption of heavy metal particles [4], high dietary fat intake [5], and alcohol consumption [6, 7, 8] are environmental and lifestyle factors contributing to increased ROS production. Endogenous factors, and in particular genomic variations, may also play a key role in the regulation of ROS balance.…”