Search Results (41)

Background: Inherited metabolic disorders (IMDs) are a heterogeneous group of genetic diseases, some of which require lifelong disease-specific dietary management. Children with phenylketonuria (PKU), organic acidemias (OAs), and glycogen storage diseases (GSDs) are particularly susceptible to nutritional imbalances and metabolic disturbances that may adversely affect bone metabolism and skeletal health. However, data regarding bone turnover markers and bone health in these pediatric IMD populations remain limited. Objective: This study aimed to evaluate bone metabolism by assessing biochemical parameters, bone turnover markers, and bone mineral density in children with PKU, OA, and GSD receiving long-term dietary treatment. Methods: This cross-sectional study included 95 children, comprising 25 patients with PKU, 20 patients with organic acidemias, 20 patients with glycogen storage diseases, and 30 healthy age-matched controls. Demographic characteristics, anthropometric measurements, and dietary intake were recorded. Biochemical evaluation included serum calcium, phosphorus, alkaline phosphatase (ALP), parathyroid hormone (PTH), and 25-hydroxyvitamin D levels. Bone turnover was assessed using C-terminal telopeptide of type I collagen (CTX), procollagen type I N-terminal propeptide (P1NP), and osteocalcin (OC) levels. Bone mineral density was evaluated by dual-energy X-ray absorptiometry (DXA). Results: Age and sex distributions were similar among the groups. Height was lower in OA than in controls and PKU, and in GSD than in PKU; weight and BMI were lower in both OA and GSD than in controls and PKU (p < 0.05). Significant differences were observed in dietary energy and macronutrient intake according to disease-specific nutritional regimens. Serum calcium, phosphorus, and 25-hydroxyvitamin D levels were significantly lower in all IMD groups compared with healthy controls (p < 0.001). ALP and PTH levels were significantly higher in PKU, OA, and GSD patients than in controls (p < 0.001). Among bone turnover markers, P1NP and osteocalcin levels significantly differed among groups, with the highest values observed in PKU patients (p = 0.006 and p = 0.028, respectively). CTX levels did not significantly differ among the groups (p = 0.183). DXA Z-scores were significantly lower in all IMD groups than in controls, with the lowest mean Z-scores observed in GSD patients. Conclusions: Children with PKU, OA, and GSD receiving long-term dietary treatment exhibited significant alterations in bone metabolism, characterized by lower vitamin D, calcium, and phosphorus levels, higher ALP and PTH concentrations, differences in bone formation markers, and lower DXA Z-scores compared with controls. Significant differences were observed in the bone formation markers P1NP and osteocalcin, whereas CTX levels remained comparable among the study groups. These findings underscore the importance of regular assessment of bone health and optimization of nutritional management in children under dietary treatment, while acknowledging that disease-specific mechanisms of skeletal involvement may differ among these conditions. Full article

Background: Bone disease remains a major long-term complication after kidney transplantation. However, the relationship between circulating bone turnover markers (BTMs) and densitometric skeletal parameters in kidney transplant recipients (KTRs) remains incompletely understood. Methods: This single-center, cross-sectional comparative study included 50 stable adult KTRs and 56 non-transplanted individuals with dual-energy X-ray absorptiometry (DXA)-confirmed osteopenia or osteoporosis. Serum bone formation markers, bone-specific alkaline phosphatase (BALP) and procollagen type I N-terminal propeptide (P1NP), and bone resorption markers, β-C-terminal telopeptide of type I collagen (β-CTX) and tartrate-resistant acid phosphatase 5b (TRAP5b), were quantified by enzyme-linked immunosorbent assay (ELISA). Bone mineral density (BMD), Z-scores, and Fracture Risk Assessment Tool (FRAX) estimates were obtained by DXA. Between-group comparisons were adjusted for age, sex, body mass index (BMI) and postmenopausal status, with sensitivity analyses restricted to participants with low bone mass. An exploratory receiver operating characteristic (ROC) analysis was performed to assess the association of BTMs with KTR status. Results: KTRs showed lower DXA-derived Z-scores at the total hip, femoral neck and lumbar spine despite being younger. After adjustment for age, sex, BMI and postmenopausal status, KTRs had significantly higher BALP (adjusted Δ = 129.96 ng/mL, p < 0.001) and PTH, and lower eGFR and magnesium than the reference group, whereas unadjusted differences in P1NP and lumbar spine BMD did not persist; β-CTX and TRAP5b did not differ between groups. BALP remained significantly higher in KTRs across the low-bone-mass restricted and propensity-score overlap analyses. BTMs showed no significant correlations with DXA parameters in KTRs. In the exploratory ROC analysis of study-group status, BALP showed the strongest separation between KTRs and the reference group (AUC = 0.808, p < 0.001). Conclusions: Long-term KTRs exhibit a distinct bone remodeling profile characterized most consistently by elevated BALP, which remained significant after adjustment and showed the strongest separation regarding KTR status. The limited BTM–DXA associations require confirmation in longitudinal studies. Full article

Background/Objectives: Peak cough flow (PCF) is an objective measure of cough effectiveness after stroke, but biomarkers reflecting physiological vulnerability related to reduced PCF are not well established. We investigated whether bone turnover markers (BTMs)—C-terminal telopeptide of type I collagen (CTX) and procollagen type 1 N-terminal propeptide (P1NP)—were associated with PCF in subacute ischemic stroke. Methods: In this retrospective study, 112 patients admitted within 21 days of stroke onset had fasting morning CTX and P1NP measured by electrochemiluminescence immunoassay, and PCF measured within 72 h of admission. Associations were assessed using Spearman correlation and multivariable linear regression with BTMs standardized (per 1 standard deviation increase), adjusting for age, sex, body mass index, onset-to-admission days, National Institutes of Health Stroke Scale score, Korean version of the Modified Barthel Index, estimated glomerular filtration rate, smoking status, and brainstem lesion. Results: CTX showed an inverse correlation with PCF (rho = −0.469; p < 0.001) and remained independently associated with lower PCF after multivariable adjustment (β = −42.32 L/min; 95% confidence interval, −56.12 to −28.52; p < 0.001), whereas P1NP showed weaker associations. In secondary outcome analyses, higher CTX was associated with low PCF (PCF < 160 L/min), aspiration pneumonia, and longer length of stay. Conclusions: Higher CTX levels were independently associated with lower peak cough flow and selected respiratory-related outcomes in this retrospective cohort. These findings are hypothesis-generating, do not imply prognostic validation, and warrant confirmation in prospective multicenter studies assessing incremental predictive value. Full article

Glucose-dependent insulinotropic polypeptide (GIP) was the first incretin hormone identified, best known for promoting glucose-stimulated insulin secretion. Increasing evidence has expanded its physiological relevance beyond glucose metabolism, revealing a significant role for GIP in the gut–bone axis. In vitro studies demonstrate that GIP inhibits osteoclast differentiation and activity while promoting osteoblastic bone formation. Findings from genetic animal models and human variant analyses further support the essential role of endogenous GIP signaling in maintaining bone mass and quality. Exogenous administration of GIP suppresses the bone-resorption marker C-terminal telopeptide of type I collagen (CTX) and increases the bone-formation marker procollagen type I N-terminal propeptide (P1NP) in healthy individuals, reflecting an acute shift toward reduced bone resorption and enhanced bone formation. Moreover, GIP confers protection against bone deterioration in multiple pathological conditions, including postmenopausal osteoporosis, inflammatory bone loss, obesity, and diabetes, etc., suggesting therapeutic potential beyond physiological contexts. Recent evidence also shows that GIP attenuates orthodontic tooth movement by limiting mechanically induced osteoclast activity, highlighting its broader skeletal actions. In this review, we summarize recent advances regarding the role of GIP in bone metabolism, integrating evidence from cellular studies, animal models and human investigations, and discuss future directions for GIP-based interventions. Full article

Background: Impaired bone health is a recognized complication of type 1 diabetes. This study evaluated the effects of low-carbohydrate (LC) and Mediterranean (MED) diets on bone turnover markers in adolescents and young adults. Methods: In a 24-week randomized controlled trial, 40 individuals aged 12–21 years, with type 1 diabetes, were assigned to an LC or MED intervention (20 participants per group). C-terminal telopeptide (CTX) and procollagen type 1 N-terminal propeptide (P1NP) were measured at baseline and 24 weeks. Results: The groups had similar baselines. At 24 weeks, the between-group difference in delta glucose time in range was not statistically significant; median daily carbohydrate intake was 86 g (68–95) in LC and 130 g (102–173) in MED (p < 0.001). Comparing LC to MED, the median BMI z-score was lower (−0.1 [−0.3 to −0.1] vs. 0.0 [−0.1 to −0.1], p = 0.10), and calcium (p = 0.035) and magnesium intakes (p = 0.030) were lower. These associations did not remain statistically significant after false-discovery-rate correction. The median-adjusted alkaline phosphatase level decreased significantly in the LC group (p = 0.009). The median CTX changed following LC from 395 pg/mL (232–591) to 423 pg/mL (289–591) (p = 0.278); and following MED, from 357 pg/mL (244–782) to 296 pg/mL (227–661) (p = 0.245). P1NP changed in LC from 95 ng/mL (68–112) to 88 ng/mL (62–97) (p = 0.056) and in MED from 76 ng/mL (54–198) to 71 ng/mL (55–122) (p = 0.594). Conclusions: Exploratory analyses of bone turnover markers showed insignificant differences following LC and MED diets. Full article

Objective: The aim was to evaluate the effects of two high-resistance training (RT) protocols combined with curcumin supplementation on antioxidant capacity, systemic inflammation, bone and muscle health, and body composition. Methods: Eighty-one apparently healthy older adults [(68.2 ± 4.6 years (57% women); BMI 26.4 ± 4.8 kg/m²; minimally active according to IPAQ] were randomly allocated to accentuated eccentric (Aecc), maximal strength (Max), or a non-training control (C). Additionally, participants received either a bio-optimized curcumin formulation (Cur) or a placebo (Pla), resulting in six study groups: Aecc-Cur, Aecc-Pla, Max-Cur, Max-Pla, C-Cur, and C-Pla. Participants underwent pre- and post-intervention assessments of oxidative stress, inflammation, and bone health parameters, whole-body composition, and muscle function. Aecc and Max performed six familiarization sessions and a 16-week intervention. Participants in the curcumin groups received 500 mg/day of a bio-optimized curcumin formulation (Cursol^TM; 2 × 250 mg capsules per day, corresponding to 10.50 mg/day of curcumin) throughout the intervention. Data were analyzed using three-way repeated-measures ANOVA/ANCOVA with time (pre–post) as the within-subject factor and training group and supplementation as between-subject factors, with Least Significant Difference post hoc comparisons and effect sizes (Hedges’ g, ηp²) reported, and the significance level set at p < 0.05. Results: Aecc was the most effective in improving antioxidant capacity (glutathione; F = 25.57, p ≤ 0.001, ηp² = 0.262) and bone biomarkers (serum-procollagen type I N-propeptide—P1NP, p ≤ 0.001, ηp² = 0.504; serum beta C-terminal cross-linked telopeptide of type I collagen—β-CTX—p = 0.022, ηp² = 0.074, and their ratio—P1NP/β-CTX—p ≤ 0.001, ηp² = 0.605). Interleukin-6 (IL-6) decreased more in Aecc (p ≤ 0.001, ηp² = 0.584) and tumor necrosis factor-alpha (TNF-α) in Max (p ≤ 0.001, ηp² = 0.471). Both groups similarly improved body composition and muscle function. Bone mineral density was generally unchanged. Overall, curcumin supplementation enhanced the benefits of high-RT programs (further glutathione increase in Aecc [Hedge’s g: 0.49]; IL-6 decrease in both modalities [Hedge’s g: 0.48–1.27]; decrease in TNF-α in controls [Hedge’s g: 0.47]; better outcomes in P1NP/β-CTX in all groups [Hedge’s g: 0.46–1.46]; among others). Conclusions: Aecc is recommended for supporting antioxidant capacity and bone health, while the choice between Aecc and Max may depend on the individual’s inflammatory profile. Curcumin supplementation further amplifies the benefits of both RT protocols across most outcome variables. Full article

The present study aimed to determine the acute effects of high-intensity dynamic resistance training (HI-DRT) and whole-body electromyostimulation (WB-EMS) on markers of bone formation and resorption in young healthy women. Using a crossover design, 17 students of dentistry (26.5 ± 4.0 years, 21.5 ± 2.5 kg/m²) were randomly assigned to begin either with HI-DRT (five exercises, three sets to repetition maximum) or 20 min of non-superimposed, low-frequency (85 Hz), intermitted (6 s impulse/4 s impulse break) WB-EMS. The study outcome parameters were total Procollagen Type-1 N-Terminal Propeptide (P1NP) and Type-I Collagen Cross-Linked C-Telopeptide (CTX), which were sampled immediately prior to and 15 min post intervention. ANCOVA was applied to determine the main effects, i.e., differences in pre–post changes in CTX and P1NP between the interventions. No participant was lost to follow-up or reported adverse effects related to the exercises. Briefly, we observed significant differences (p = 0.019, d′ = 1.19) for changes in P1NP that were maintained in the HI-DRT (p = 0.446) and decreased in the WB-EMS group (p = 0.002). In contrast, we did not observe differences for HI-DRT- vs. WB-EMS-induced CTX changes (p = 0.509; d′ = 0.134). In summary, while HI-DRT provides significantly more favorable effects on bone formation markers compared to WB-EMS, the clinical significance of this finding in predicting the general effectiveness of an exercise protocol on bone strength remains to be determined. (Clinical trials.gov; registration date: 2025-02-06; ID: NCT06813092.) Full article

Maintaining muscle health is essential for preserving mobility, independence, and quality of life with age. As muscle mass and function decline, the risk of frailty, chronic disease, and disability increases. Sarcopenia, characterized by the progressive loss of muscle mass, strength, and function, is a major contributor to these adverse outcomes in older adults. Early identification and monitoring of sarcopenia are critical for timely intervention to prevent irreversible decline. Muscle biomarkers offer a promising approach for detecting muscle deterioration and guiding treatment strategies. This review explores key biomarkers—including insulin-like growth factor 1 (IGF-1), myostatin, interleukin-6 (IL-6), irisin, interleukin 15 (IL-15), and procollagen type III N-terminal propeptide (P3NP)—that reflect underlying processes such as muscle anabolism, inflammation, metabolism, and remodeling. Alterations in these markers are associated with muscle health status. Furthermore, hormonal status, biological sex, and nutritional factors all modulate biomarker levels, emphasizing the need for personalized assessments. Integrating biomarker analysis into clinical practice has the potential to enhance early diagnosis, inform personalized interventions, and ultimately promote healthy aging by maintaining muscle function and reducing disability risk. Full article

Background/Objectives: Increasing evidence suggests that metabolic dysfunction-associated steatotic liver disease (MASLD) and hypertension (HTN), a well-established cardiometabolic risk factor, both negatively impact bone metabolism. This study aimed to investigate the associations between bone turnover markers (BTMs)—namely, osteopontin (OPN) and procollagen type 1 N-terminal propeptide (P1NP)—and metabolic health indicators, non-invasive measures of liver disease severity, as well as skeletal muscle mass (SMM), muscle strength, and bone mineral density (BMD) in patients with MASLD and HTN. Methods: We enrolled 117 patients diagnosed with MASLD and HTN and conducted anthropometric measurements, laboratory analyses, abdominal ultrasound, and point shear-wave elastography. Muscle strength was evaluated using grip strength measurements and the Five Times Sit-to-Stand Test (FTSST). SMM and BMD were quantified using dual-energy X-ray absorptiometry (DEXA). Serum OPN and P1NP concentrations were quantified using enzyme-linked immunosorbent assays (ELISAs). Results: Serum OPN concentrations below 2.89 ng/mL were associated with significantly elevated levels of AST (p = 0.001), ALT (p = 0.006), and GGT (p = 0.025), while serum P1NP concentrations above 47.5 pg/mL were associated only with significantly elevated GGT levels (p = 0.024). In addition, patients with MASLD and HTN with lower serum OPN levels had higher liver stiffness values (p = 0.003). Serum OPN concentrations were inversely associated with the following metabolic health indicators: waist circumference (WC, p < 0.001) and epicardial fat thickness (EFT, p = 0.001). In addition, they were significantly elevated in patients with MASLD and HTN who had decreased spinal BMD (p = 0.017). In turn, serum P1NP levels were reduced in patients with decreased SMM (p = 0.023). Conclusions: These findings in patients with MASLD and HTN suggest an association between serum P1NP levels and SMM, and between OPN levels and spinal BMD, indicating a potential interplay among liver function, muscle mass, and bone health. Furthermore, OPN appeared to be strongly associated with overall metabolic health indicators, such as WC and EFT, whereas P1NP exhibited a stronger association with muscle mass. Full article

Childhood leukemia survivors are at risk of long-term complications. Data on bone remodeling in childhood acute lymphoblastic leukemia (ALL) are limited. This 2-year prospective longitudinal study investigated bone remodeling and bone turnover markers at diagnosis, during treatment, and until stopping treatment, in ALL patients < 18 years, to clarify the influence of leukemia itself and/or chemotherapy on bone. Methods: A total of 22 ALL children (12 males, age 5.5 ± 3.6 years) underwent blood sampling at the 5 time point (T0−T4). Osteoprotegerin (OPG), receptor-activator-NF-B-ligand (RANKL), osteocalcin (OC), C-terminal-telopeptide-type-I-collagen (CTX), bone-alkaline-phosphatase (bALP), tartrate-resistant acid-phosphatase-5b (TRACP5b), procollagen-type-I-N-terminal-propeptide (P1NP), Dickkopf-1 (DKK-1), and sclerostin were assessed. Data from patients at T0 were compared to a control group of healthy children. We used the principal component analysis (PCA) for statistics. Results: Levels of CTX, OC, P1NP, and bALP resulted lower in ALL children than controls (p = 0.009 for CTX and p < 0.001 for the others), also DKK1 and sclerostin (p < 0.0001 and p = 0.023). RANKL ed OPG were higher in patients. During T0−T4, CTX, OC, P1NP, TRACP5b, and bALP showed a significant increase, in particular at T0−T1 (end-of-induction). Less evident changes were detected onwards. Conclusions: The onset of leukemia has been revealed as a key point in determining a slowing of bone remodeling in ALL children. Full article

Background/Objectives: Osteoporosis is a major public health concern, due to its high risk of fractures and disability and associated medical costs. Romosozumab, an anabolic agent, has been approved for the treatment of osteoporosis in postmenopausal women at high risk of fractures. However, limited data exist on its long-term effects in the Korean population, particularly regarding its impact on bone mineral density (BMD), bone turnover markers, and body composition. This study aimed to evaluate the 12-month effects of romosozumab treatment on BMD, bone turnover markers, and body composition in postmenopausal Korean women with high-fracture-risk osteoporosis (T-scores ≤ −3.0). Additionally, the impact of concomitant postmenopausal hormone therapy (MHT) on BMD changes was assessed. Methods: This multicenter, retrospective observational study included 50 postmenopausal women diagnosed with osteoporosis (T-scores ≤ −3.0) who received 12 monthly doses of romosozumab (210 mg) at two hospitals in Korea. Changes in BMD in the lumbar spine, femoral neck, and total hip were assessed using dual-energy X-ray absorptiometry (DXA). Bone turnover markers, including procollagen type 1 N-terminal propeptide (P1NP) and C-terminal telopeptide of type 1 collagen (CTX), were measured at baseline and at 3, 6, and 12 months. Changes in body composition, including the skeletal muscle index (SMI), body mass index (BMI), and visceral adipose tissue (VAT), were also analyzed. Results: After 12 months of romosozumab treatment, BMD significantly increased at the lumbar spine (14.65%), femoral neck (6.58%), and total hip (4.19%) (p < 0.05). P1NP levels increased significantly at 3 months (+37.9%), but returned to baseline at 6 months, while CTX levels continuously decreased (−27.8%) over 12 months. No significant changes were observed in SMI or BMI, but the VAT showed a slight decreasing trend (p < 0.05). Additionally, patients receiving concomitant MHT demonstrated a significantly greater increase in lumbar spine BMD compared to those receiving romosozumab alone (p < 0.05), while no significant differences were observed in femoral neck and total hip BMD. Conclusions: This study demonstrated that 12 months of romosozumab treatment significantly improved BMD and bone turnover markers in postmenopausal Korean women with severe osteoporosis. The combination of romosozumab and MHT further enhanced lumbar spine BMD gains. These findings support the use of romosozumab as an effective treatment for high-risk osteoporotic fractures in postmenopausal Korean women, and suggest potential benefits of a combined therapeutic approach. Full article

Background/Objectives: Type 2 diabetes and weight loss are associated with detrimental skeletal health. Incretin-based therapies (GLP-1 receptor agonists, and dual GIP/GLP-1 receptor agonists) are used clinically to treat diabetes and obesity. The potential effects of semaglutide and tirzepatide on bone metabolism in type 2 diabetic mice remain uncertain. Methods: Combined streptozotocin and high fat feeding were employed in female C57BL/6J mice to promote hyperglycemia. Mice were administered for 4 weeks with a saline vehicle (sc., once-daily), semaglutide (40 μg/kg/d, sc., every three days), or tirzepatide (10 nmol/kg, sc., once-daily). Bone strength was assessed by three-point bending. Femur microarchitecture was determined by micro-CT, and bone formation and resorption parameters were measured by histomorphometric analysis. Serum was collected to measure bone resorption (C-telopeptide fragments of type I collagen, CTX) and formation (procollagen type 1 N-terminal propeptide, P1NP) biomarkers, respectively. The expression of bone metabolism-related genes was evaluated in the bone using RT-PCR. Results: Glucose levels significantly reduced after 4 weeks of semaglutide and tirzepatide treatment (both p < 0.05) compared with vehicle treatment. Tirzepatide led to more weight loss than semaglutide. Compared to saline-treated diabetic mice, the mean femur length was shorter in the tirzepatide group. After treatment with tirzepatide or semaglutide, cortical bone and trabecular bone parameters did not change significantly compared to saline-treated diabetic mice, except that cortical thickness was lower in the semaglutide group compared to the saline group (p = 0.032). Though CTX and P1NP levels decreased, however, the change in CTX and P1NP levels did not differ among the four groups during the 4 weeks of treatment (all p > 0.05). Semaglutide affected RANKL and OPG mRNA expression and increased the ratio of OPG/RANKL. No significant difference was found in the quantity of Col1a1, RANKL, OPG, and RUNX2 between tirzepatide- and saline-treated diabetic mice. Conclusions: The 4-week treatment with semaglutide and tirzepatide had a neutral effect on bone mass compared with the controls, and most of the bone microarchitecture parameters were also comparable between groups in diabetic mice. A better understanding of incretin-based therapies on bone metabolism in patients with diabetes requires further evaluation in large clinical trials. Full article

The role of bone and muscle as endocrine organs may be important contributing factors for children’s growth and development. Myokines, secreted by muscle cells, play a role in regulating bone metabolism, either directly or indirectly. Conversely, markers of bone metabolism, reflecting the balance between bone formation and bone resorption, can also influence myokine secretion. This study investigated a panel of serum myokines and their relationships with bone metabolism markers in children following vegetarian and omnivorous diets. A cohort of sixty-eight healthy prepubertal children, comprising 44 vegetarians and 24 omnivores, participated in this study. Anthropometric measurements, dietary assessments, and biochemical analyses were conducted. To evaluate the serum concentrations of bone markers and myokines, an enzyme-linked immunosorbent assay (ELISA) was used. The studied children did not differ regarding their serum myokine levels, except for a higher concentration of decorin in the vegetarian group (p = 0.020). The vegetarians demonstrated distinct pattern of bone metabolism markers compared to the omnivores, with lower levels of N-terminal propeptide of type I procollagen (P1NP) (p = 0.001) and elevated levels of C-terminal telopeptide of type I collagen (CTX-I) (p = 0.018). Consequently, the P1NP/CTX-I ratio was significantly decreased in the vegetarians. The children following a vegetarian diet showed impaired bone metabolism with reduced bone formation and increased bone resorption. Higher levels of decorin, a myokine involved in collagen fibrillogenesis and essential for tissue structure and function, may suggest a potential compensatory mechanism contributing to maintaining bone homeostasis in vegetarians. The observed significant positive correlations between myostatin and bone metabolism markers, including P1NP and soluble receptor activator of nuclear factor kappa-B ligand (sRANKL), suggest an interplay between muscle and bone metabolism, potentially through the RANK/RANKL/OPG signaling pathway. Full article

Boron supplementation may improve the musculoskeletal health of pullets before entering the lay phase. This study aimed to evaluate the effects of different boron amounts on the performance, muscle deposition, tibia cross-sectional area (CSA) and mineral density (BMD), ash percent, breaking strength, and bone mineralization (bone-specific alkaline phosphatase [BALP] and pro-collagen type 1 n-terminal propeptide [P1NP]) of a white-feathered strain of pullets. A total of 528 Hy-Line W-36 pullets were distributed across 24 pens and fed basal diets containing varying amounts of boron (C: 0 mg/kg; L: 50 mg/kg; M: 100 mg/kg; H: 150 mg/kg) for 17 weeks. Performance parameters (body weight, average daily weight gain/bird, and average daily feed intake/bird) were measured at weeks 4, 7, 10, 13, and 16, while all other measures were taken at 11 and 17 weeks of age. Performance was not impacted by boron supplementation. Pectoralis major weights were higher in H pullets at 11 weeks of age, and we also observed higher pectoralis major, minor, and leg muscle weights in H pullets at 17 weeks of age. Pullets fed the H diet had larger cortical CSA than the other treatment groups at 11 weeks of age. At 17 weeks of age, both the H and M groups had larger cortical CSA than the L and C groups, but the M group had slightly smaller cortical CSA. Pullets fed the H diet had higher BMD values than the other treatment groups at 11 weeks of age. At 17 weeks of age, pullets fed the H diet had the highest total BMD values compared to the other treatment groups, and cortical BMD increased with increasing boron inclusion. Pullets fed the H diet had the highest tibia ash percentages and concentrations of BALP and P1NP. Pullets fed the M and H diets had greater failure load and maximum bending moment than pullets fed the L or C diet at 11 weeks of age, with H pullets having greater stiffness values than other groups. At 17 weeks of age, pullets fed the H diet had greater failure load and maximum bending moment compared to all other treatment groups. Our results suggest that providing boron within the diet at 150 mg/kg can improve the musculoskeletal characteristics of Hy-Line W-36 pullets up to 17 weeks of age, without impacting performance parameters. Full article

Osteoporosis is a bone-debilitating disease, demonstrating a higher prevalence in post-menopausal women due to estrogen deprivation. One of the main mechanisms underlying menopause-related bone loss is oxidative stress. S-allylmercapto-N-acetylcysteine (ASSNAC) is a nuclear factor erythroid 2-related factor 2 (Nrf2) activator and cysteine supplier, previously shown to have anti-oxidation protective effects in cultured cells and animal models. Here, we studied the therapeutic potential of ASSNAC with and without Alendronate in ovariectomized (OVX) female mice. The experimental outcome included (i) femur and L3 lumbar vertebra morphometry via Micro-Computed Tomography (μCT); (ii) bone remodeling (formation vs. resorption); and (iii) oxidative stress markers in bone marrow (BM) cells. Four weeks after OVX, there was a significant bone loss that remained evident after 8 weeks, as demonstrated via µCT in the femur (cortical and trabecular bone compartments) and vertebra (trabecular bone). ASSNAC at a dose of 50 mg/Kg/day prevented bone loss after the four-week treatment but had no significant effect after 8 weeks, while ASSNAC at a dose of 20 mg/Kg/day significantly protected against bone loss after 8 weeks of treatment. Alendronate prevented ovariectomy-induced bone loss, and combining it with ASSNAC further augmented this effect. OVX mice demonstrated high serum levels of both C-terminal cross-linked telopeptides of type I collagen (CTX) (bone resorption) and procollagen I N-terminal propeptide (P1NP) (bone formation) after 2 weeks, and these returned to control levels after 8 weeks. Alendronate, ASSNAC and their combination decreased CTX and increased P1NP. Alendronate induced oxidative stress as reflected by decreased glutathione and increased malondialdehyde (MDA) levels, and combining it with ASSNAC partially attenuated these changes. These results portray the therapeutic potential of ASSNAC for the management of post-menopausal osteoporosis. Furthermore, ASSNAC ameliorates the Alendronate-associated oxidative stress, suggesting its potential to prevent Alendronate side effects as well as improve its bone-protective effect. Full article