Effects of exercise on biological trace element concentrations and selenoprotein P expression in rats with fructose-induced glucose intolerance

Abstract

In the present study, we investigated the effects of exercise intended to prevent or treat lifestyle related diseases on the glucose tolerance, insulin level, lactic acid utilization, muscle glycogen synthesis, hepatic and renal oxidative stress, hepatic selenoprotein P and biological trace element levels in organs of obese, glucose intolerant rats. We fed normal, healthy rats a 20% casein diet while the glucose intolerant, obese rats received a high fructose diet. They were forced to run for one hour per day, six days per week, for ten weeks. Exercise reduced visceral fat and ameliorated glucose tolerance in the high fructose group, lowered blood lactic acid levels, improved lactic acid usage efficiency, and increased oxidative stress and hepatic levels of Mn, Fe, Cu, and Zn in the normal and high fructose groups. Addi tionally, exercise significantly upregulated hepatic selenoprotein P expression in both groups, however, its effect was remarkable in healthy group. On the other hand, muscle glycogen synthesis was not markedly enhanced in high fructose diet rats but in normal diet rats in response to exercise. It is concluded that exercise conditions rather than exercise load must be customized and optimized for each health and disease states in advance before starting exercise training intended to prevent or treat lifestyle related diseases.

The selenoprotein P 3’ untranslated region is an RNA binding protein platform that fine tunes selenocysteine incorporation

“…We expect future work to reveal conditions where PTBP1 function is required to regulate SELENOP levels in vivo. For example, SELENOP mRNA levels have been reported to dramatically increase in response to exercise stress in mice fed a normal diet but not those fed a high fat diet [19]. We expect the molecular pathways that regulate such a response to work at least in part through the mechanisms uncovered in this report.…”

Bright and dark sides of exercise effects on biological responses such as energy metabolism and renal function in rats with renal failure and fructose-induced glucose intolerance

“…Additionally, exercise decreased T-cho and TG which participate in lipid metabolism, however, the reductions of these lipid metabolism parameters in the plasma levels were relatively small ( Table 2), suggesting that enhancement of glucose and lipid metabolism based on AMPK activation (31) is reduced in response to continuous exercise in the case of DM with renal failure compared to DM state without renal failure. (14) Earlier studies on obese rats reported that exercise increased blood and pancreatic zinc levels (32) and altered hepatic element distribution. (33) We determined biological trace metals in the plasma, liver, kidney, and pancreas by ICP-MS because several trace metals are associated with exercise and diabetes.…”

“…In our previous paper, (14) we have indicated that the salutary and beneficial effects of exercise were substantially more pronounced in healthy condition than in glucose intolerance and obesity condition induced by high-fructose diet. Exercise for health maintenance was found to affect much differently on either healthy or diseased rats.…”

“…Therefore, exercise conditions and regimens are strongly suggested to be adapted to health states of individual, which includes nutritional status, in advance before starting the systematic exercise training intended to prevent or treat lifestylerelated diseases. (14) From other studies, (15,16) exercise has been reported to increase both the insulin sensitivity by enhancing insulin-independent glucose uptake and type I skeletal muscle fiber density rich in GLUT4 and mitochondrial mass, and exercise-mediated skeletal muscle transformation would also enhance insulin sensitivity. This mechanism is mediated by muscle contraction-induced activation of AMP-activated protein kinase (AMPK) and glucose transporter 4 (GLUT4) which govern transmembrane glucose transport.…”

The Selenoprotein P 3’ untranslated region is an RNA binding protein platform that fine tunes selenocysteine incorporation

“…We expect future work to reveal conditions where PTBP1 function is required to regulate SELENOP levels in vivo. For example, SELENOP mRNA levels have been reported to dramatically increase in response to exercise stress in mice fed a normal diet but not those fed a high fat diet [16] . We expect the molecular pathways that regulate such a response to work at least in part through the mechanisms uncovered in this report.…”