After Roux-en-Y gastric bypass, there was evidence of calcium and vitamin D malabsorption. Bone turnover increased, and hip bone density rapidly declined. The decline in hip BMD was strongly associated with weight loss itself. Vigilance for nutritional deficiencies and bone loss in patients both before and after bariatric surgery is crucial.

Chronic kidney disease (CKD) patients may have high rates of bone loss and fractures, but microarchitectural and biochemical mechanisms of bone loss in CKD patients have not been fully described. In this longitudinal study of 53 patients with CKD Stages 2-5D, we used dual energy X-ray absorptiometry (DXA), high resolution peripheral quantitative computed tomography (HRpQCT) and biochemical markers of bone metabolism to elucidate effects of CKD on the skeleton. Median follow-up was 1.5 years (Range 0.9 to 4.3 years); bone changes were annualized and compared to baseline. By DXA, there were significant declines in areal bone mineral density (BMD) of the total hip and ultradistal radius: −1.3% (95% CI: −2.1 to −0.6) and −2.4% (95% CI: −4.0 to −0.9), respectively. By HRpQCT at the distal radius, there were significant declines in cortical area, density and thickness, and increases in porosity: −2.9% (95% CI −3.7 to −2.2), −1.3% (95% CI −1.6 to −0.6), −2.8% (95% CI −3.6 to −1.9), and +4.2% (95% CI 2.0 to 6.4) respectively. Radius trabecular area increased significantly: +0.4% (95% CI 0.2 to 0.6), without significant changes in trabecular density or microarchitecture. Elevated time-averaged levels of parathyroid hormone (PTH) and bone turnover markers predicted cortical deterioration. Higher levels of serum 25-hydroxyvitamin D predicted decreases in trabecular network heterogeneity. These data suggest that significant cortical loss occurs with CKD, which is mediated by hyperparathyroidism and elevated turnover. Future investigations are required to determine whether these cortical losses can be attenuated by treatments that reduce PTH levels and remodeling rates.

13 male subjects were studied and placed in 3 groups. Each group exercised one leg with sprint (S), or endurance (E) training and the other leg oppositely or not at all (NT). Oxygen uptake (Vo2), heart rate and blood lactate were measured for each leg separately and for both legs together during submaximal and maximal bicycle work before and after 4 weeks of training with 4-5 sessions per week. Muscle samples were obtained from the quadriceps muscle and assayed for succinate dehydrogenase (SDH) activity, and stained for myofibrillar ATPase. In addition, eight of the subjects performed after the training two-legged exercise at 70% Vo2 max for one hour. The measurements included muscle glycogen and lactate concentrations of the two legs as well as the blood flow and the a-v difference for O2, glucose and lactate.

Summary We compared skeletal parameters in type 2 diabetic (T2DM) and non-diabetic postmenopausal women. Bone structure by dual energy x-ray absorptiometry (DXA) and HR-pQCT was not different, although procollagen type 1 amino-terminal propeptide (P1NP) and osteocalcin levels were lower in T2DM. Introduction T2DM is associated with increased fracture risk, but, paradoxically, with higher cross-sectional bone density (BMD) as measured by DXA. We sought explanations to this puzzle by investigating detailed structural and biochemical skeletal parameters in T2DM. Methods Cross-sectional comparison of 25 postmenopausal T2DM women and 25 matched controls using DXA, high-resolution peripheral quantitative computed tomography (HR-pQCT) and biochemical bone turnover markers. Results BMD by DXA did not differ between T2DM and controls. HR-pQCT assessment also did not differ, with the exception of cortical area at the tibia, which tended to be lower in the diabetics (difference of 12±6 [mean ± SD] mm, p=0.06). P1NP and osteocalcin levels were lower in T2DM as compared to controls (P1NP, 34.3±16 vs. 57.3±28 ng/ml; p=0.005; osteocalcin, 4.5±2 vs. 6.2±2 nmol/L; p=0.001). Conclusions Postmenopausal women with T2DM had lower levels of bone formation markers as compared to controls. Aside from a possible decrease in cortical bone area at a weight-bearing site, bone structure was not altered in T2DM. Lower bone turnover may be a skeletal parameter that is present in T2DM.

After bariatric surgery, hip bone loss reflects skeletal unloading and cortical bone loss reflects secondary hyperparathyroidism. This study highlights deterioration of cortical bone loss as a novel mechanism for bone loss after bariatric surgery.