Cree-Green 2018 Diabetes
|Cree-Green M, Scalzo RL, Harrall K, Newcomer BR, Schauer IE, Huebschmann AG, McMillin S, Brown MS, Orlicky D, Knaub L, Nadeau KJ, Mcclatchey PM, Bauer TA, Regensteiner JG, Reusch JEB (2018) Supplemental oxygen improves in-vivo mitochondrial oxidative phosphorylation flux in sedentary obese adults with type 2 diabetes. Diabetes 67:1369-79.|
Abstract: Type 2 diabetes is associated with impaired exercise capacity. Alterations in both muscle perfusion and mitochondrial function can contribute to exercise impairment. We hypothesized that impaired muscle mitochondrial function in type 2 diabetes is mediated, in part, by decreased tissue oxygen delivery and would improve with oxygen supplementation. Ex vivo muscle mitochondrial content and respiration assessed from biopsy samples demonstrated expected differences in obese individuals with (N=18) and without (N=17) diabetes. Similarly, in vivo mitochondrial oxidative phosphorylation capacity measured in the gastrocnemius muscle via 31-Phosphorus magnetic resonance spectroscopy (31P MRS) indicated an impairment in the rate of ADP depletion with rest (27±6 seconds diabetes, 21±7 controls; p=0.008) and oxidative phosphorylation (p=0.046) in type 2 diabetes following isometric-calf exercise compared to controls. Importantly, the in vivo impairment in oxidative capacity resolved with oxygen supplementation in adults with diabetes (ADP depletion rate 5.0 seconds faster; p=0.012, oxidative phosphorylation 0.046±0.079 mmol/L/sec faster, p=0.027). Multiple in vivo mitochondrial measures related to HbA1C. These data suggest that oxygen availability is rate-limiting for in vivo mitochondrial oxidative exercise recovery measured with 31-P MRS in individuals with uncomplicated diabetes. Targeting muscle oxygenation could improve exercise function in type 2 diabetes.
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style Pathology: Diabetes, Obesity
Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase
Coupling state: LEAK, OXPHOS, ET Pathway: F, N, NS HRR: Oxygraph-2k