Chronic elevated lactate levels are associated with insulin resistance in patients with type 2 diabetes mellitus (T2DM). Furthermore, lactacidosis plays a role in limiting physical performance. Erythrocytes, which take up lactate via monocarboxylate transporter (MCT) proteins, may help transport lactate within the blood from lactate-producing to lactate-consuming organs. This study investigates whether cycling endurance training (3 times/week for 3 months) alters the basal erythrocyte content of MCT-1, and whether it affects lactate distribution kinetics in the blood of T2DM men (n = 10, years = 61 ± 9, body mass index = 31 ± 3 kg/m(2)) following maximal exercise (WHO step-incremental cycle ergometer test). Immunohistochemical staining indicated that basal erythrocyte contents of MCT-1 protein were up-regulated (+90%, P = 0.011) post-training. Erythrocyte and plasma lactate increased from before acute exercise (= resting values) to physical exhaustion pre- as well as post-training (pre-training: +309%, P = 0.004; +360%, P < 0.001; post-training: +318%, P = 0.008; +300%, P < 0.001), and did not significantly decrease during 5 min recovery. The lactate ratio (erythrocytes:plasma) remained unchanged after acute exercise pre-training, but was significantly increased after 5 min recovery post-training (compared with the resting value) (+22%, P = 0.022). The results suggest an increased time-delayed influx of lactate into erythrocytes following an acute bout of exercise in endurance-trained diabetic men.
Type 2 diabetes mellitus (T2DM) is associated with an increased release of free radicals which play an important role in the manifestation of diabetes and in the progression of diabetic complications. Peroxiredoxins are thought to be essential components of the erythrocyte antioxidative defense. Therefore, we compared peroxiredoxin isoform contents (PRDX1-6 immuno-histochemial stainings) in the erythrocytes of overweight/obese T2DM men (n = 6) and of BMI-matched non-diabetic male control subjects (n = 6). Only erythrocyte PRDX1 and PRDX2 proteins were detectable using immunohistochemical methods. PRDX1 was significantly increased in T2DM men relative to control subjects (+95.9%, P ≤ 0.05). Furthermore, we studied the influence of a 3-month endurance training program (3 times a week, cycling at 75% maximal heart rate) on erythrocyte PRDX1 and PRDX2 contents in overweight/obese T2DM men (n = 11). Training significantly increased PRDX2 at rest (+96%, P ≤ 0.05). The up-regulation of the peroxiredoxin system may help counteract free radicals in the erythrocytes of T2DM patients.
It has been demonstrated that alterations of adipocytokines can alter immune status in type 2 diabetes. The present study investigated changes of adipocytokine plasma concentrations and cellular immune status in overweight men, suffering from non-insulin dependent type 2 diabetes (n=14, age 61.0±8.7 years, BMI 31.1±3.5 kg/cm2). Subjects underwent a 3 months endurance exercise intervention (twice per week for up to 45 min) cycling at a heart rate corresponding to a 2 mmol/l lactate threshold. Before and after the intervention testing for adipocytokines (leptin, adiponectin, resistin) and cellular immune status (including T memory-cells and regulative T-cells) was performed by RIA and FACS accordingly.The exercise intervention improved anthropometric and metabolic parameters of all subjects. We observed a significant decline for resistin and for the CD19+ B-cells. The CD4+CD25+CD127low Treg-cells decreased, however not statistically significant. All other parameters remained unchanged.In conclusion, even though only training twice a week, the exercise affected parts of the cellular immune system as well as resistin levels in men suffering from non-insulin dependent type 2 diabetes.
Patients suffering from type 2 diabetes mellitus (T2DM) often exhibit chronic elevated lactate levels which can promote peripheral insulin resistance by disturbing skeletal muscle insulin-signaling. Monocarboxylate transporter (MCT) proteins transfer lactate molecules through cellular membranes. MCT-1 and MCT-4 are the main protein isoforms expressed in human skeletal muscle, with MCT-1 showing a higher affinity (lower Km) for lactate than MCT-4. T2DM patients have reduced membranous MCT-1 proteins. Consequently, the lactate transport between muscle cells and the circulation as well as within an intracellular lactate shuttle, involving mitochondria (where lactate can be further metabolized), can be negatively affected. This study investigates whether moderate cycling endurance training (3 times per week for 3 months) can change skele-tal muscle MCT contents in T2DM men (n=8, years=56±9, body mass index (BMI)=32±4 kg/m(2)). Protein content analyses (immuno-histochemical stainings) were performed in bio-psies taken from the vastus lateralis muscle. Intracellular MCT-1 proteins were up-regulated (relative increase+89%), while intracellular MCT-4 contents were down-regulated (relative decrease - 41%) following endurance training. Sarcolemmal MCT-1 and MCT-4 did not change. The question of whether the training-induced up-regulation of intracellular MCT-1 leads to an improved lactate transport (and clearance) in T2DM patients requires further research.
This study investigates whether regular physical activity (moderate endurance or resistance training twice a week for 3 months) influences the key regulatory molecules of mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α), nuclear respiratory factor-1 (NRF1), and mitochondrial transcription factor A (TFAM)) in patients suffering from non-insulin-dependent type 2 diabetes mellitus (T2DM) (n = 16, years = 62 ± 7, body mass index (BMI) = 30 ± 4 kg/m(2)). Seven T2DM men took part in endurance training, and 9 men participated in resistance training. BMI-matched non-diabetic male control subjects (CON) (n = 7, years = 53 ± 6, BMI = 30 ± 4 kg/m(2)) were studied for comparison. The protein contents of PGC1α, NRF1, and TFAM were determined using immunohistochemical staining methods on biopsies taken from the musculus vastus lateralis. At baseline, no differences were observed in NRF1-density between the T2DM men and the CON, while the contents of PGC1α and TFAM were decreased in the T2DM men. PGC1α and TFAM contents were not changed in the T2DM patients after the training period, but NRF1 was decreased. The down-regulation of mitochondrial signaling molecules might explain the patho-physiological reduction in mitochondrial biogenesis found in T2DM. Physical training, as performed in our study, did not reverse the down-regulation of mitochondrial signaling molecules--at least not after 3 months. [corrected].
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.