Abstract

D-Glucosamine hydrochloride (GlcN∙HCl) is an endogenous amino monosaccharide synthesized from glucose that is useful in the treatment of joint diseases in both humans and animals. The aim of this study was to examine amino acid metabolism in dogs after oral administration of GlcN∙HCl. Accelerated fumarate respiration and elevated plasma levels of lactic acid and alanine were observed after administration. These results suggest that oral administration of GlcN∙HCl induces anaerobic respiration and starvation in cells, and we hypothesize that these conditions promote cartilage regeneration. Further studies are required to evaluate the expression of transforming growth factor-beta (TGF-β).

Highlights

  • Glucosamine (GlcN) is a derivative of cellular glucose metabolism and is a component of glycosaminoglycans, hyaluronic acid, and proteoglycans in the cartilage matrix that form the ends of bones

  • The Principal component analysis (PCA) score plots of each dog changed in a similar manner before (O1, N1, W1) and after (O2, N2, W2) oral administration of

  • The results revealed that the individual variability in the change in amino acid metabolism was small

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Summary

Introduction

Glucosamine (GlcN) is a derivative of cellular glucose metabolism and is a component of glycosaminoglycans, hyaluronic acid, and proteoglycans in the cartilage matrix that form the ends of bones. Exogenous GlcN primarily exists in two forms, D-GlcN hydrochloride (HCl) and GlcN sulfate [1]. Both forms are immediately ionized into GlcN, and D-GlcN·HCl and GlcN sulfate. Mar. Drugs 2012, 10 are largely redundant [2]. In Japan, GlcN sulfate is a medical agent but not used as a nutritional supplement. In the Glucosamine/Chondroitin Arthritis Intervention Trial (GAIT), GlcN·HCl supplements were used, and based on that, we chose the same form for our study [3]

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