Nozickova 2017 MiP2017
Low-carbon diet, usually referred to as a sugar-free diet, is a modern and very popular way to lose weight . Low-carbon diet is defined as a diet with carbohydrate content lower than 26% of daily energy intake . In this diet the main energy substrates are fat and proteins instead of sugars. We used a commercial high fat diet to simulate conditions of low-carbon diet. In this study we investigate the early effect of high fat diet on liver mitochondrial functions of rats.
Male Wistar rats were fed ad libitum for 1 to 6 weeks by standard diet (control; energy content 14.6 kJ/g; 66% carbohydrates, 24% proteins, 10% fat) or by high fat diet (HFD; energy content 23.5 kJ/g; 15% carbohydrates, 15% proteins, 70% fat + 1.25% cholesterol). Liver samples were analyzed histologically, biochemically and liver mitochondrial functions were investigated using high-resolution respirometry (Oroboros O2k-FluoRespirometry, Innsbruck, Austria) and reference respiratory protocols.
We found no significant difference in caloric intake between HFD group and control group over the whole duration of this experiment. Rats in the control group exhibited greater weight increase in comparison to HFD group. We observed a significant liver steatosis in HFD group in comparison to control group already after 1 week of feeding confirmed histologically and biochemically by the content of triglycerides and cholesterol. After 6 weeks of HFD feeding we observed an inhibition of total respiratory capacity of liver mitochondria. This decrease in mitochondrial respiration however was not linear and after three weeks of HFD we found an increase in oxidative capacity. The beta-oxidation and ketogenesis of liver mitochondria increased already after 1 week of HFD feeding and were significantly higher over the whole duration of experiment.
To conclude, HFD leads to lower body mass of rats but at the same time to development of liver steatosis. During this process liver mitochondria exhibit an adaptation of their function to higher lipid turnover by increased activity of lipid metabolic pathways with subsequent inhibition of total oxidative capacity.
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Organism: Rat Tissue;cell: Liver
- Dept Physiol, Faculty Medicine Hradec Kralove, Charles Univ, Czech Republic. - email@example.com
- Accurso A, Bernstein RK, Dahlqvist A, Draznin B, Feinman RD, Fine EJ, Gleed A, Jacobs DB, Larson G, Lustig RH, Manninen AH, McFarlane SI, Morrison K, Nielsen JV, Ravnskov U, Roth KS, Silvestre R, Sowers JR, Sundberg R, Volek JS, Westman EC, Wood RJ, Wortman J and Vernon MC (2008) Dietary carbohydrate restriction in type 2 diabetes mellitus and metabolic syndrome: time for a critical appraisal. Nutr Metab (Lond) 5:9
- Meng Y, Bai H, Wang S, Li Z, Wang Q and Chen L (2017) Efficacy of low carbohydrate diet for type 2 diabetes mellitus management: A systematic review and meta-analysis of randomized controlled trials. Diabetes Res Clin Pract 131:124-31.