Treating fructose-induced metabolic changes in mice with high-intensity interval training: insights in the liver, white adipose tissue, and skeletal muscle

Abstract

Fructose-rich caloric sweeteners induce adverse changes in the metabolism of humans. The study evaluated the effects of high-intensity interval training (HIIT) on a fructose feeding model, focusing on the liver, white adipose tissue (WAT), skeletal muscle, and their interplay. Male C57BL/6 mice were fed for 18 wk one of the following diets: control (C; 5% of total energy from fructose) or fructose (F; 55% of total energy from fructose). In the 10th week, for an additional 8-wk period, the groups were divided into nontrained (NT) or HIIT groups, totaling four groups: C-NT, C-HIIT, F-NT, and F-HIIT. At the end of the experiment, fructose consumption in the F-NT group led to a high systolic blood pressure, high plasma triglycerides, insulin resistance with glucose intolerance, and lower insulin sensitivity. We also observed liver steatosis, adipocyte hypertrophy, and diminished gene expressions of peroxisome proliferator-activated receptor-γ coactivator 1-α and fibronectin type III domain containing 5 (FNDC5; irisin) in this F-NT group. These results were accompanied by decreased gene expressions of nuclear respiratory factor 1 and mitochondrial transcription factor A (markers of mitochondrial biogenesis), and peroxisome proliferator-activated receptor-α and carnitine palmitoyltransferase 1 (markers of β-oxidation). HIIT improved all of these data in the C-HIIT and F-HIIT groups. In conclusion, in mice fed a fructose diet, HIIT improved body mass, blood pressure, glucose metabolism, and plasma triglycerides. Liver, WAT, and skeletal muscle were positively modulated by HIIT, indicating HIIT as a coadjutant treatment for diseases affecting these tissues. We investigated the effects of high-intensity interval training (HIIT) in mice fed a fructose-rich diet and the resulting severe negative effect on the liver, white adipose tissue (WAT), and skeletal muscle, which reduced the expression of fibronectin type III domain containing 5 (FNDC5, irisin) and PGC1α and, consequently, affected markers of mitochondrial biogenesis and β-oxidation. Because HIIT may block these adverse effects in all of these three tissues, it might be suggested that it functions as a coadjutant treatment in combatting the alterations caused by high-fructose intake.

High-intensity interval training improves metabolic syndrome and body composition in outpatient cardiac rehabilitation patients with myocardial infarction

“…With respect to skeletal muscle, we have previously shown that 4-weeks of aerobic exercise can enhance skeletal muscle mitochondrial biogenesis and function in male mice [49]. Motta et al [50] also showed that HIIT ameliorated fructose-induced metabolic dysfunction in male mice through mitochondrial biogenesis and β-oxidation, via irisin and PGC1 α in skeletal muscle. Moreover, several recent trials have demonstrated that 3–12 weeks of HIIT can significantly increase resting metabolic rate [51] and post-exercise oxygen consumption in healthy adults [52], and fat oxidation in obese adolescents [53].…”

The potential role of FNDC5/irisin in various liver diseases: awakening the sleeping beauties

“…found liver steatosis develops with adipocyte hypertrophy, and these detrimental events were relevant to altered gene expressions including FNDC5 , PGC1α and PGC1β , all of which were efficiently prevented upon high-intensity interval training (HIIT) (Ref. 37). The authors concluded that the beneficial influences of HIIT, in parallel to the medicinal properties of metformin, may partially alleviate the liver injury and prevent progressive NAFLD from more advanced pathological stages.…”

O Papel Do Psicopedagogo Frente Aos Disturbios E Transtornos Causados Pela Ansiedade

“…Segundo Motta, et al (2017) um estudo avaliou os efeitos de treinamento de alta intensidade intervalado (HIIT) em um modelo alimentar com frutose. Ratos machos foram alimentados por 18 semanas com as seguintes dietas: controle (C: 5% do total de energia com fructose), frutose (F: 55% do total energético de frutose).…”