Alkaline phosphatase (ALP) hydrolyzes a variety of monophosphate esters and plays an important role in phosphorus (P) metabolism. Several nutrients in food have been reported to affect intestinal ALP activity in animal models. Previous reports indicated that high levels of P or phosphate in diets decreased intestinal ALP activity in rats. Because potato starch contains considerable amounts of esterified P, unlike other starch-derived plants, we hypothesized that the feeding of potato starch would decrease ALP activity in the intestinal tract. Male Sprague-Dawley rats (7 weeks old) were fed 3 different types of diet containing 60% corn starch or 1 of 2 types of potato starch with different esterified P content for 1 or 5 weeks. Body weight and food intake of each rat were measured every day throughout the experimental periods. At the end of the feeding periods, the small intestine was removed to determine ALP activity in the mucosal tissues. Significant differences were observed in ALP activity in the small intestine between the 2 feeding periods, among the 4 segments of the small intestine, and among the 3 diet groups. Significant positive linear correlations between the amount of P derived from the starch and mucosal ALP activity were obtained in the jejunum and jejunoileum in rats after feeding for 5 weeks. We concluded, contrary to our hypotheses, that the ingestion of potato starch adaptively increases ALP activity in the upper part of the small intestine of growing rats in an esterified P content-dependent manner.
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http://dx.doi.org/10.1016/j.nutres.2010.05.003 | DOI Listing |
Inflammation
January 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Background: DNA methyltransferase 3A (Dnmt3a) is an enzyme that catalyzes the de novo methylation of DNA, and plays essential roles in a wide range of physiological and pathological processes. However, it remains unclear whether Porphyromonas gingivalis affects cementoblasts, the cells responsible for cementum formation, through Dnmt3a.
Methods: The samples were collected from models of mouse periapical lesions and mice of different ages, and the expression of Dnmt3a was detected through immunofluorescence.
Anal Chim Acta
January 2025
Hunan Provincial Key Laboratory of Cytochemistry, School of Chemistry and Chemical Engineering, Changsha University of Science and Technology, Changsha, 410114, PR China.
Alkaline phosphatase (ALP) is a critical biomarker associated with various physiological and pathological processes, making its detection essential for disease diagnosis and biomedical research. In this study, we developed a novel, simple, and portable visual quantification method for ALP activity in cells using an efficient CuZnS nanomaterial with peroxidase-like properties, integrated into a smartphone-based platform for enhanced usability. The CuZnS nanomaterial catalyzes the breakdown of H₂O₂, generating ·OH radicals that oxidize the colorless substrate TMB into blue oxTMB, which is subsequently reduced back to TMB by ascorbic acid (AA).
View Article and Find Full Text PDFBiomed Mater
January 2025
Biomechanics Research Centre (BMEC), School of Engineering, University of Galway, University Road, Galway, H91 TK33, IRELAND.
Bioabsorbable textile scaffolds are promising for bone tissue engineering applications. Their tuneable, porous, fibre based architecture resembles that of native extracellular matrix, and they can sustain tissue growth while being gradually absorbed in the body. In this work, immortalized mouse calvaria preosteoblast MC3T3-E1 cells were cultured in vitro on two warp-knitted bioabsorbable spacer fabric scaffolds made of poly(lactic acid) (PLA) and poly-4-hydroxybutyrate (P4HB), to investigate their osteogenic properties.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA
Background: Autophagy‐lysosomal pathway (ALP) efficiency declines Alzheimer’s disease (AD). In AD mouse models expressing a fluorescent autophagy and pH probe, autolysosomes pH elevation, resulting from deficient v‐ATPase activity, causes autophagy substrates, including Aβ and APP‐βCTF, to build up selectively within autolysosomes before extracellular amyloid deposits. In the most compromised but still intact neurons, massive numbers of Aβ‐positive autolysosomes pack into huge petal‐like blebs bulging out from the perikaryal membrane (PANTHOS).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA
Background: Autophagy‐lysosomal pathway (ALP) dysfunction emerges early in Alzheimer’s disease(AD). In mouse AD models, lysosomal acidification deficits impair ALP in neurons, in some inducing massive autolysosome accumulations, intraneuronal amyloid plaque, and early neuronal death yielding an extracellular amyloid plaque. This distinctive neurodegenerative pattern (PANTHOS) emerges in early‐stage AD and is recapitulated in human late‐onset AD (accompanying poster).
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