Unlabelled: Nutrition influences peak bone mass development in early adulthood. The effect of high dietary phosphate intake on the growing skeleton of 1-month-old male rats (n = 30) was assessed in an 8-week intervention. High dietary phosphate intake increased bone remodeling and impaired bone material properties, diminishing bone mechanical strength.
Introduction: High dietary phosphate intake is typical in the Western diet. Abundant phosphate intake enhances parathyroid secretion and bone metabolism. To study the influence of high dietary phosphate intake on growing bone homeostasis and structure, we submitted growing rats to experimental diets that varied in their phosphate content.
Materials And Methods: One-month-old intact male rats (n = 30) were fed a control diet (Ca:P 1:1) or an experimental diet of either Ca:P 1:2 or Ca:P 1:3 for 8 weeks. At the beginning and the end of the study period, the right femurs were measured using DXA. Double labeling with tetracycline injection was performed 12 and 2 days before death. After death, hind legs were cut loose. Left femurs were processed for histomorphometry. Right femurs were measured with pQCT. Mechanical testing was performed on the right femoral neck and tibial shaft. Six right tibias were analyzed with microCT. Serum PTH, calcium, and phosphate contents were analyzed.
Results: High-phosphate intake impaired growth of the animal, limited bone longitudinal growth, and restricted femur BMC and BMD build-up. Osteoclast number, osteoblast perimeter, and mineral apposition rate were increased, and trabecular area and width were decreased. Phosphate decreased femur midshaft total bone BMD, cortical bone BMD, and mean cortical thickness. High-phosphate diet reduced femoral neck and tibial shaft ultimate strength and tibia stiffness and toughness. In addition, serum PTH increased.
Conclusions: High dietary phosphate intake reduced growth, skeletal material, and structural properties and decreased bone strength in growing male rats. Adequate calcium could not overcome this.
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http://dx.doi.org/10.1359/jbmr.061009 | DOI Listing |
Citrin Deficiency (CD) is caused by inactivation of SLC25A13, a mitochondrial membrane protein required to move electrons from cytosolic NADH to the mitochondrial matrix in hepatocytes. People with CD do not like sweets. We discovered that SLC25A13 loss causes accumulation of glycerol-3-phosphate (G3P), which activates carbohydrate response element binding protein (ChREBP) to transcribe FGF21, which acts in the brain to restrain intake of sweets and alcohol, and to transcribe key genes of lipogenesis.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Key Laboratory of Polymer Ecomaterials, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, 5625 Renmin Street, Changchun, 130022, P. R. China.
Dentin hypersensitivity (DH), marked by exposed dentinal tubules, presents as a sharp toothache triggered by stimuli and subsides when the stimuli are removed. To address the limitations of current commercial desensitizers in terms of acid resistance, friction resistance, and stability, a black phosphorus nanosheet-composited methacrylate gelatin hydrogel (GelMA/BP) is developed for DH treatment, leveraging the synergistic effects of photothermal therapy and biomineralization. Incorporating the BP nanosheet provided GelMA/BP with a stable photothermal response and the continuous release of phosphate anions, which blocked dentinal tubules by converting light energy into heat and initiating biomineralization.
View Article and Find Full Text PDFEur Eat Disord Rev
January 2025
ACUTE Center for Eating Disorders and Severe Malnutrition at Denver Health, Denver, Colorado, USA.
Objective: Refeeding oedema, believed to result from the effects of insulin on renal sodium retention and subsequent oedema formation, typically occurs during the first 2 weeks after reintroduction of nutrition in individuals with severe malnutrition and can intensify body image distress in patients with eating disorders (EDs). Phosphate supplements have been found to increase insulin sensitivity, and it is hypothesised that they may also contribute to refeeding oedema in patients with EDs.
Method: In this retrospective cohort study of 633 patients with severe malnutrition due to anorexia nervosa (AN) or avoidant restrictive food intake disorder (ARFID), the impact of phosphate supplementation on the rate of weight gain was investigated.
Gut Microbes
December 2025
Hypertension Research Laboratory, School of Biological Sciences, Faculty of Science, Monash, Clayton, Australia.
The gut microbiota is a crucial link between diet and cardiovascular disease (CVD). Using fecal metaproteomics, a method that concurrently captures human gut and microbiome proteins, we determined the crosstalk between gut microbiome, diet, gut health, and CVD. Traditional CVD risk factors (age, BMI, sex, blood pressure) explained < 10% of the proteome variance.
View Article and Find Full Text PDFEnviron Res
December 2024
Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai, 200237, China. Electronic address:
Background: As a class of synthetic chemicals, organophosphate esters (OPEs) were shown to have thyroid hormones (THs) disrupting potentials in animal studies, while epidemiological evidence on gestational exposure to OPEs and thyroid disruption is limited. Besides, assessment on the safety threshold of OPEs exposure during gestation is especially scarce.
Methods: Based on the Shanghai Minhang Birth Cohort Study, we measured maternal urine concentration of 8 OPE metabolites and THs levels in cord plasma and examined their associations using multiple linear regression and quantile g-computation (QGC) models.
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