Whole-body vibration (WBV) provides gained attention like a potential exercise mimetic,

Whole-body vibration (WBV) provides gained attention like a potential exercise mimetic, but direct comparisons with the metabolic effects of exercise are scarce. moderate effects of TE and WBV on bone geometry, mineralization, and biomechanics may reflect delicate raises in osteoblast activity in multiple areas of the skeleton. Taken collectively, these observations show that WBV recapitulates the effects of exercise on rate of metabolism in type 2 diabetes. Disruption of bone formation and turnover has been reported in a range of metabolic disorders, including obesity and type 2 diabetes. Although a significant body of literature suggests that obesity reduces risk of osteopenia and osteoporosis (1, 2), there are also several recent reports that obesity and its comorbidities reduce bone formation (3C6). Obesity is accompanied by ectopic lipid deposition in multiple cells, including the skeleton, where infiltration of adipocytes into the bone marrow market may negatively effect bone formation (7, 8). Bone marrow stem cells express receptors for multiple adipokines, including the adipose-derived hormone leptin INK 128 cost (9, 10). Data from leptin-deficient rodent models possess exposed regionally specific effects within the skeleton, with reports of cortical bone atrophy in weight-bearing long bones like the femur and tibia (11C16). Leptin-deficient (ob/ob) mice also show lower femoral cortical bone mineral denseness (BMD) and strength compared with wild-type (WT) littermates (13). Bone loss in models of leptin or leptin receptor deficiency has been linked with lower osteoblast activity (9, 14), suggesting that cellular leptin resistance in obesity might reduce bone formation. Participation in regular physical activity protects against bone loss (12, 17), and increasing evidence suggests that whole-body vibration (WBV) elicits related effects in certain patient populations (18C20). Bone is definitely a mechanically responsive cells (21, 22), and musculoskeletal loading with WBV or exercise promotes bone formation in animal models (12, 21C26). Bone formation is accompanied by increased levels of osteocalcin, a hormone produced primarily by osteoblasts during matrix synthesis (7, 27, 28). Circulating osteocalcin also enhances insulin secretion by pancreatic cells and raises levels of the insulin-sensitizing hormone adiponectin (29, 30). Circulating osteocalcin levels are reduced in humans and in rodent models of obesity and insulin resistance (16, 20, 31C34), and this effect is particularly prominent in models with coincident obesity and bone loss, such as Zucker rats (12) and leptin receptorCdeficient (db/db) mice (16). However, no studies possess directly compared the metabolic and skeletal effects of WBV in parallel with physical exercise. Given that exercise and WBV place biomechanical weight within the skeleton, we hypothesized that both interventions would Rabbit Polyclonal to ADCK2 promote bone formation, and that osteogenic responses would be associated with improvements in glycemic control and lipid rate of metabolism in db/db mice. Both interventions modestly reduced body weight, and in leptin receptorCdeficient (db/db) mice, treadmill machine exercise (TE) INK 128 cost and WBV restored muscle mass dietary fiber diameters to within the range of WT mice. Musculoskeletal loading with TE or WBV reduced adipocyte hypertrophy in visceral extra fat and attenuated hepatic steatosis. Although effects on bone structure and biomechanics were minimal, TE and WBV both increased circulating levels of osteocalcin in db/db mice. This association, if proven to be causal in subsequent studies, would support the utility of WBV as an exercise mimetic. Materials and Methods Animal care, TE, and WBV Male db/db mice and WT controls on the C57Bl6/J background were obtained from Jackson Laboratories (Bar Harbor, ME) at 5 weeks of age. All animals were housed two per cage with access to food and water. Mice from each genotype were assigned to sedentary (SED), WBV, or TE conditions, with each group balanced for an equal distribution of starting weights (n = 14 to 16 per condition). The first week consisted of habituation INK 128 cost to the experimental apparatus, followed by 12 weeks of TE or WBV, as previously described (35, 36). In brief,.