In order to investigate whether the oral ingestion of collagen peptide affects the extracellular matrix of tendon, two doses (0.2 g/kg and 1.0 g/kg body weight) were orally administered daily for 56 d to a rabbit, and both the size of collagen fibrils and the amount of glycosaminoglycans in the Achilles tendon were measured in comparison with those in a rabbit fed with a control protein, lactalbumin, or water alone. Ingestion of collagen peptide or lactalbumin induced a significant increase in collagen fibril diameter and a decrease in fibril density except for a high dose of lactalbumin compared with the water control. A histogram pattern of fibril diameter in a high dose of collagen peptide showed a peak at 160-180 nm, which was not observed in other groups. However the percentage of diameters over 200 nm was the lowest in this group but highest in the low-dose group of collagen peptide. The mean fibril diameter and mass average diameter of a high dose of collagen peptide were significantly smaller than those in a low dose. The amount of dermatan sulphate increased in the high-dose groups, while the amount of hyaluronic acid decreased in rabbits fed with collagen peptide or lactalbumin at either dose. These results suggest that the ingestion of collagen peptide affects the size of collagen fibrils and composition of glycosaminoglycans in the Achilles tendon and thus may improve the mechanical properties of the Achilles tendon.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3177/jnsv.51.169 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mathematical modeling of impacts of patient differences on renin-angiotensin system and applications to COVID-19 lung fibrosis outcomes.
Comput Biol Med
January 2025
Department of Chemical and Biological Engineering, University at Buffalo, The State University of New York, Buffalo, NY, 14260, USA; Department of Biomedical Engineering, University at Buffalo, The State University of New York, Buffalo, NY, 14260, USA; Institute for Artificial Intelligence and Data Science, University at Buffalo, The State University of New York, Buffalo, NY, 14260, USA; Witebsky Center for Microbial Pathogenesis and Immunology, University at Buffalo, The State University of New York, Buffalo, NY, 14203, USA; Department of Pharmaceutical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, 14215, USA. Electronic address:
Patient-specific premorbidity, age, and sex are significant heterogeneous factors that influence the severe manifestation of lung diseases, including COVID-19 fibrosis. The renin-angiotensin system (RAS) plays a prominent role in regulating the effects of these factors. Recent evidence shows patient-specific alterations of RAS peptide homeostasis concentrations with premorbidity and the expression level of angiotensin-converting enzyme 2 (ACE2) during COVID-19.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of North Dakota, Grand Forks, ND, USA.
Background: Alzheimer's disease (AD) is an age-related neurodegenerative disorder affecting nearly 50 million individuals worldwide. Besides aging, various comorbidities can increase the risk of AD, such as asthma. However, the molecular mechanism(s) underlying this asthma-associated AD exacerbation is unknown.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Amsterdam UMC, location VUmc, Department of Anatomy and Neurosciences, Section Clinical Neuroanatomy and Biobanking, Amsterdam, Netherlands.
Background: Recent studies highlight distinct patterns of cortical atrophy between amnestic (typical) and non-amnestic (atypical, with subtypes: behavioural, dysexecutive, logopenic and visuospatial) clinical phenotypes of Alzheimer's disease (AD). The current study aimed to assess regional MRI patterns of cortical atrophy across AD phenotypes, and their association with amyloid-beta (Aβ), phosphorylated tau (pTau), axonal degeneration (NfL) and microvascular deterioration (COLIV).
Method: Postmortem In-situ 3DT1 3T-MRI data was collected for 33 AD (17 typical, 16 atypical) and 16 control brain donors.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Homi Bhabha National Institute, Mumbai, Maharashtra, India.
Background: Receptor Tyrosine kinase-mediated signaling is indispensable for the cell's normal functioning, the perturbation of which leads to disease conditions. The altered expression and activity of several Receptor Tyrosine kinases (RTKs) are known to regulate the pathophysiology of Alzheimer's disease (AD). However, the mechanistic details remain illusive.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Mounting evidence suggests that acute and past exposure to the environmental toxicant lead (Pb) results in longitudinal decline in cognitive function and brain atrophy. In animals, chronic Pb exposure can increase brain Aβ deposition. However, it remains unclear how Pb induces different natures of amyloid depositions and underlying mechanisms to contribute to the pathogenesis of AD and related dementia.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!