Plasma Hydroxyproline Levels Research Articles

Meta-omics profiling of the gut-lung axis illuminates metabolic networks and host-microbial interactions associated with elevated lung elastance in a murine model of obese allergic asthma.

Obesity and associated changes to the gut microbiome worsen airway inflammation and hyperresponsiveness in asthma. Obesogenic host-microbial metabolomes have altered production of metabolites that may influence lung function and inflammatory responses in asthma. To understand the interplay of the gut microbiome, metabolism, and host inflammation in obesity-associated asthma, we used a multi-omics approach to profile the gut-lung axis in the setting of allergic airway disease and diet-induced obesity. We evaluated an immunomodulator, nitro-oleic acid (NO2-OA), as a host- and microbial-targeted treatment intervention for obesity-associated allergic asthma. Allergic airway disease was induced using house dust mite and cholera toxin adjuvant in C57BL6/J mice with diet-induced obesity to model obesity-associated asthma. Lung function was measured by flexiVent following a week of NO2-OA treatment and allergen challenge. 16S rRNA gene (from DNA, taxa presence) and 16S rRNA (from RNA, taxa activity) sequencing, metabolomics, and host gene expression were paired with a Treatment-Measured-Response model as a data integration framework for identifying latent/hidden relationships with linear regression among variables identified from high-dimensional meta-omics datasets. Targeting both the host and gut microbiota, NO2-OA attenuated airway inflammation, improved lung elastance, and modified the gut microbiome. Meta-omics data integration and modeling determined that gut-associated inflammation, metabolites, and functionally active gut microbiota were linked to lung function outcomes. Using Treatment-Measured-Response modeling and meta-omics profiling of the gut-lung axis, we uncovered a previously hidden network of interactions between gut levels of amino acid metabolites involved in elastin and collagen synthesis, gut microbiota, NO2-OA, and lung elastance. Further targeted metabolomics analyses revealed that obese mice with allergic airway disease had higher levels of proline and hydroxyproline in the lungs. NO2-OA treatment reduced proline biosynthesis by downregulation of pyrroline-5-carboxylate reductase 1 (PYCR1) expression. These findings are relevant to human disease: adults with mild-moderate asthma and BMI ≥ 25 had higher plasma hydroxyproline levels. Our results suggest that changes to structural proteins in the lung airways and parenchyma may contribute to heightened lung elastance and serve as a potential therapeutic target for obese allergic asthma.

Does dietary intake of acrylamide affect hydroxyproline levels? An animal study

Acrylamide is a chemical that occurs due to high temperatures during cooking. It consists of an amino acid found in foods and sugars. Studies have shown that cancer formation occurs within the scope of oxidant reagents and DNA damage due to exposure to acrylamide. Our study aims to examine the effects of dietary acrylamide intake on plasma hydroxyproline levels in rats. In this study, 4 groups were formed with 8 rats in each group (total number=32). Blood samples were collected on days 14 and 28. Acrylamide solution was applied to each rat in the treatment group by gastric gavage process at 5 mg/kg three times a week. Hydroxyproline levels in rats’ plasma samples were measured. The median (IQR) hydroxyproline levels were 7.40(2.45) µg/L in group 1 (14. days control group) and 7.98(3.34) µg/L in group 2 (14. days acrylamide applied) who received acrylamide. The mean hydroxyproline levels were 7.25(1.96) µg/L in group 3 (28. days control group) and 9.76(2.64) µg/L in group 4 (28. days acrylamide applied) who received acrylamide. No difference was observed between the groups. Dietary acrylamide intake did not have a significant effect on hydroxyproline levels at the application dose and duration in our study.

Fishmeal replacement by mixed plant proteins and maggot meal on growth performance, target of rapamycin signalling and metabolism in juvenile turbot (Scophthalmus maximus L.)

Fishmeal could only be replaced by plant proteins at limited levels in aquafeeds, especially for carnivorous fish. In this study, an experiment was designed to evaluate the possibility of improving the utilization of plant proteins by maggot meal supplementation in turbot diet. Five diets were formulated: a reference diet (FM) containing 63% fishmeal and four experimental diets (35(0%), 35(3%), 40(0%), 40(3%)) in which fishmeal was substituted at different levels by plant proteins with 0–3% maggot meal. Turbot (4.90 ± 0.03 g) was fed with these diets for 9 weeks. Fishmeal was successfully replaced by plant proteins in turbot diet without growth reduction at 35% but not 40%. However, maggot supplementation (3%) at 40% plant protein replacement level achieved comparable growth performance with that of fishmeal. Maggot meal supplementation improved apparent digestibility coefficients, plasma hydroxyproline levels, intestine trypsin activities and activated target of rapamycin (TOR) signalling, all of which were decreased or down-regulated after high plant protein replacement. Therefore, this study demonstrated maggot meal, a potential valuable protein source for turbot.

Elevated plasma hydroxyproline. A possible risk factor associated with connective tissue injuries during overuse.

Basal plasma hydroxyproline was measured in 104 male Navy Seal candidates 1 week into their intense physical training program, which lasted 7 weeks, and correlated to the incidence of connective tissue injuries incurred later in the training program. Eleven subjects (10.6%) were diagnosed as having connective tissue injuries. Those subjects with connective tissue injuries had a significantly higher (P less than 0.05) mean plasma hydroxyproline value (4.02 micrograms/ml) than subjects without injury (3.10 micrograms/ml). The majority of graduates (75%) had plasma hydroxyproline values less than 3.3 micrograms/ml. These graduates represented the strongest and most enduring injury-free subjects. Of the subject pool who incurred connective tissue injuries, only 27% had plasma hydroxyproline values less than 3.3 micrograms/ml. The majority of the injured subjects (73%) had plasma hydroxyproline values greater than or equal to 3.3 micrograms/ml. In conclusion, there is a relationship between initial training basal plasma hydroxyproline levels and connective tissue injuries later incurred in an intense physical training program. These data suggest that elevated plasma hydroxyproline levels may represent a risk factor associated with connective tissue injuries.

Acute responsiveness to calcitonin in chronic renal failure.

The acute effect of porcine calcitonin was tested in 17 patients undergoing chronic haemodialysis. In normal adults calcitonin has no effect on plasma calcium or phosphate levels, but in nine patients both concentrations were substantially reduced after calcitonin. This hypocalcaemic and hypophosphataemic effect was a function of the initial plasma phosphate level but was unrelated to the initial plasma calcium level. Plasma hydroxyproline levels were not significantly different in the two groups an were unaffected by calcitonin. In 11 patients fasting plasma calcitonin levels were undetectable with an assay sensitive to 0-1 mug/1. Calcitonin seems to have an acute effect in chronic renal failure which may not operate by arresting bone resorption but is dependent on the plasma phosphate concentration.

Acute Responsiveness to Calcitonin in Chronic Renal Failure

The acute effect of porcine calcitonin was tested in 17 patients undergoing chronic haemodialysis. In normal adults calcitonin has no effect on plasma calcium or phosphate levels, but in nine patients both concentrations were substantially reduced after calcitonin. This hypocalcaemic and hypophosphataemic effect was a function of the initial plasma phosphate level but was unrelated to the initial plasma calcium level. Plasma hydroxyproline levels were not significantly different in the two groups an were unaffected by calcitonin. In 11 patients fasting plasma calcitonin levels were undetectable with an assay sensitive to 0-1 mug/1. Calcitonin seems to have an acute effect in chronic renal failure which may not operate by arresting bone resorption but is dependent on the plasma phosphate concentration.

Adaptation of the Bergman and Loxley technique for hydroxyproline determination to the autoanalyzer and its use in determining plasma hydroxyproline in the domestic fowl.

The adaptation of a manual technique for hydroxyproline determination to the AutoAnalyzer is described. The method can be used to determine standard solutions to within 2·6 per cent. and to deal with successive concentration differences of up to 10 µg ml–1. The concentration range for optimum accuracy is 2·5 to 15·0 µg ml–1. Application of the technique to the study of plasma hydroxyproline levels in the domestic fowl is described, and comparison with isotope-dilution analysis demonstrates the lack of gross interference.

Influence of the Parathyroids on Plasma Hydroxyproline Levels

Plasma levels of hydroxypro line were studied in rats subjected to dietary limitation, parathyroidectomy, nephrectomy and combinations of these conditions. Total hydroxyproline levels were determined on hydrolyzed samples and compared with the amounts observed without hydrolysis in aliquots of the same samples. Parathyroidectomy consistently lowered plasma hydroxyproline levels, although the changes were minimal in hydrolyzed plasma samples taken from animals maintained on normal diets. Nephrectomy lowered the values of nonhydrolyzed plasma samples, but increased markedly the total hydroxyproline content as determined by hydrolysis. It is suggested that one source of plasma hydroxyproline was collagen which was broken down as a result of parathyroid-bone interactions in the process of maintaining a constant plasma calcium level. Nephrectomy, which increases endogenous parathyroid activity, appears to increase the breakdown of bone collagen, transferring the hydroxyproline residues to plasma in a bound form.