Fructose ingestion impairs expression of genes involved in skeletal muscle’s adaptive response to aerobic exercise

Abstract

BackgroundThe inverse relationship between exercise capacity and its variation over time and both cardiovascular and all-cause mortality suggests the existence of an etiological nexus between cardiometabolic diseases and the molecular regulators of exercise capacity. Coordinated adaptive responses elicited by physical training enhance exercise performance and metabolic efficiency and possibly mediate the health benefits of physical exercise. In contrast, impaired expression of genes involved in mitochondrial biogenesis or protein turnover in skeletal muscle—key biological processes involved in adaptation to physical training—leads to insulin resistance and obesity. Ingestion of fructose has been shown to suppress the exercise-induced GLUT4 response in rat skeletal muscle. To evaluate in greater detail how fructose ingestion might blunt the benefits of physical training, we investigated the effects of fructose ingestion on exercise induction of genes that participate in regulation of mitochondrial biogenesis and protein turnover in rat’s skeletal muscle.MethodsEight-week-old Wistar rats were randomly assigned to sedentary (C), exercise (treadmill running)-only (E), fructose-only (F), and fructose + exercise (FE) groups and treated accordingly for 8 weeks. Blood and quadriceps femoris were collected for biochemistry, serum insulin, and gene expression analysis. Expression of genes involved in regulation of mitochondrial biogenesis and autophagy, GLUT4, and ubiquitin E3 ligases MuRF-1, and MAFbx/Atrogin-1 were assayed with quantitative real-time polymerase chain reaction.ResultsAerobic training improved exercise capacity in both E and FE groups. A main effect of fructose ingestion on body weight and fasting serum triglyceride concentration was detected. Fructose ingestion impaired the expression of PGC-1α, FNDC5, NR4A3, GLUT4, Atg9, Lamp2, Ctsl, Murf-1, and MAFBx/Atrogin-1 in skeletal muscle of both sedentary and exercised animals while expression of Errα and Pparδ was impaired only in exercised rats.ConclusionsOur results show that fructose ingestion impairs the expression of genes involved in biological processes relevant to exercise-induced remodeling of skeletal muscle. This might provide novel insight on how a dietary factor contributes to the genesis of disorders of glucose metabolism.

Tricarboxylic acid (TCA) cycle, sphingolipid, and phosphatidylcholine metabolism are dysregulated inT. gondiiinfection-induced cachexia

“…Fructose, which is metabolized in the liver, was also elevated in the sera of cachectic mice. Fructose has been shown to regulate the muscle specific E3 ubiquitin ligases Murf-1 and Atrogin-1 which drive muscle atrophy during cachexia 45 . We also observed increased abundance of diet-derived metabolites including the antiinflammatory di-saccharide trehalose; pinatol, a plant methylated inositol; and the bacterial metabolite L-ribonate, which has been observed in the sera of diabetic mice after exercise 46 .…”

Chronic aerobic exercise prevents high-fructose diet-induced impairment in blood pressure in healthy young adults: a double-blind, randomised clinical trial

“…Participants were randomised to groups based on VO 2peak because the literature shows that the greater the oxygen consumption of the individual, the greater the cardiometabolic protection (38) . Therefore, it is possible to suggest that individuals with lower values of VO 2peak would be more vulnerable to the effects of fructose consumption (39,40) . In addition, researchers and outcome assessors who were not involved in the preparation and delivery of drinks to volunteers were blinded throughout the data collection and analysis period.…”

Fructose Induced Changes in Rat Serum Lipids and Adipose Tissue Gene Expression and Preventive Effects of Agrimonia Eupatoria Aqueous Infusion Intake

“…For example, fructose supplementation has been reported to increase blood TC and TG content, as well as adipose tissue hypertrophy and body weight gain [1,3,4,8,35]. Tissue gene expression profiles also significantly changed representing its effect on overall metabolism and physiology [14,15,25]. Adipose tissue is important target of fructose effects and gene expression changes indicate adipogenic consequences and impaired signalization and lipid metabolism [37,38].…”