acid-phosphatase and Metabolic-Diseases

An 8-week feeding trial was conducted, where turbot were fed four experimental diets, containing different LPC levels (0%, 0.1%, 0.25%, and 0.5%, named LPC0, LPC0.1, LPC0.25, and LPC0.5, respectively). The intestinal morphology results showed that there were no widened lamina propria and mixed inflammatory cells in the LPC-supplemented groups. Dietary LPC remarkably decreased the expression of TLRs (TLR3, TLR8, TLR9, and TLR22), MyD88, and signaling molecules (NF-κB, JNK, and AP-1). Similarly, diets with LPC supplementation markedly depressed the gene expression of NF-κB and JNK signaling pathway downstream genes (TNF-α, IL-1β, Bax, Caspase9, and Caspase-3). Furthermore, dietary LPC modified the intestinal microbial profiles, increasing the relative abundance of short-chain fatty acids-producers, lactic acid bacteria, and digestive enzyme-producing bacteria. Predictive functions of intestinal microbiota showed that turbot fed LPC diets had a relatively higher abundance of functions, such as lipid metabolism and immune system, but a lower abundance of functions, such as metabolic diseases and immune system diseases. The activities of intestinal acid phosphatase and alkaline phosphatase were also increased by dietary LPC. In conclusion, LPC supplementation could regulate the intestinal mucosal barrier via the TLR signaling pathway and alter the intestinal microbiota profile of turbot fed high-lipid diets.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animal Feed; Animals; bcl-2-Associated X Protein; Caspase 3; Diet; Dietary Supplements; Flatfishes; Lysophosphatidylcholines; Metabolic Diseases; Myeloid Differentiation Factor 88; NF-kappa B; Toll-Like Receptor 3; Toll-Like Receptor 8; Toll-Like Receptor 9; Transcription Factor AP-1; Tumor Necrosis Factor-alpha

Topics: Acid Phosphatase; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelet Disorders; Blood Platelets; Glucose-6-Phosphatase; Glucosephosphate Dehydrogenase Deficiency; Glycogen; Hemorrhagic Disorders; Humans; Metabolic Diseases; Microscopy, Electron; Platelet Adhesiveness

Topics: Acid Phosphatase; Endoplasmic Reticulum; Fibroblasts; Histiocytes; Histocytochemistry; Humans; Leprosy; Metabolic Diseases; Microscopy, Electron; Mycobacterium leprae

Topics: Acid Phosphatase; Culture Techniques; Fibroblasts; Glycosaminoglycans; Humans; Metabolic Diseases; Skin; Vitamin A

In a Chinese population 1,000 full-term male neonates and a further 117 jaundiced neonates of both sexes were studied in an investigation of the frequency of deficiency of erythrocyte glucose-6-phosphate dehydrogenase (G6PD). This enzyme was found to be deficient in 3.6% of male neonates. Correlation of the results with the birthplace of the 602 mothers who were known to come from Kwangtung province showed no significant differences in the frequency of the deficiency between certain parts of the province.The deficiency of G6PD in hemizygous males is profound but it is not associated with erythrocyte acid monophosphoesterase deficiency in Chinese in Hong Kong. The G6PD deficiency accounts for 15.4% of all the 117 cases of neonatal jaundice. The relative importance of G6PD deficiency as a cause of neonatal jaundice does not differ materially in male and female mutants. Neonatal jaundice can occur in all genotypes of G6PD mutation in Chinese.

Topics: Acid Phosphatase; Adult; Asian People; Erythrocytes; Female; Glucosephosphate Dehydrogenase Deficiency; Hong Kong; Humans; Infant, Newborn; Jaundice, Neonatal; Kernicterus; Male; Metabolic Diseases

Topics: Acid Phosphatase; Adolescent; Alkaline Phosphatase; Aminohydrolases; Brain; Carotenoids; Child; Chondroitin; Diffuse Cerebral Sclerosis of Schilder; Gangliosides; Glucosyltransferases; Histocytochemistry; Humans; Infant; Kidney; Lipid Metabolism; Liver; Metabolic Diseases; Mucopolysaccharidosis I; Phosphotransferases; Rats; Research; Sulfatases; Sulfates; Sulfur Isotopes; Tuberous Sclerosis