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Glucosamine-induced insulin resistance in 3T3-L1 adipocytes
| Title | Glucosamine-induced insulin resistance in 3T3-L1 adipocytes |
| Publication Type | Journal Article |
| Year of Publication | 2000 |
| Authors | |
| Journal | Am J Physiol Endocrinol Metab |
| Volume | 278 |
| Issue | 1 |
| Pagination | E103-12 |
| Date Published | Jan |
| Publication Language | eng |
| ISBN Number | 0193-1849 (Print) |
| Accession Number | 10644543 |
| Key Words | Receptor, Insulin/metabolism, Proto-Oncogene Proteins c-akt, Proto-Oncogene Proteins/metabolism, *Protein-Serine-Threonine Kinases, Phosphorylation/drug effects, Mice, Intracellular Signaling Peptides and Proteins, *Insulin Resistance, Insulin Receptor Substrate Proteins, Insulin/pharmacology, Glucosamine/*pharmacology, Dose-Response Relationship, Drug, Animals, Phosphoproteins/metabolism, *Muscle Proteins, Monosaccharide Transport Proteins/metabolism, Glucose Transporter Type 4, Deoxyglucose/pharmacokinetics, Cell Membrane/metabolism, Adipocytes/*drug effects/*physiology, 3T3 Cells, 1-Phosphatidylinositol 3-Kinase/metabolism, Tyrosine/metabolism, Ribosomal Protein S6 Kinases/metabolism |
| Abstract | To study molecular mechanisms for glucosamine-induced insulin resistance, we induced complete and reversible insulin resistance in 3T3-L1 adipocytes with glucosamine in a dose- and time-dependent manner (maximal effects at 50 mM glucosamine after 6 h). In these cells, glucosamine impaired insulin-stimulated GLUT-4 translocation. Glucosamine (6 h) did not affect insulin-stimulated tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 and -2 and weakly, if at all, impaired insulin stimulation of phosphatidylinositol 3-kinase. Glucosamine, however, severely impaired insulin stimulation of Akt. Inhibition of insulin-stimulated glucose transport was correlated with that of Akt activity. In these cells, glucosamine also inhibited insulin stimulation of p70 S6 kinase. Glucosamine did not alter basal glucose transport and insulin stimulation of GLUT-1 translocation and mitogen-activated protein kinase. In summary, glucosamine induced complete and reversible insulin resistance in 3T3-L1 adipocytes. This insulin resistance was accompanied by impaired insulin stimulation of GLUT-4 translocation and Akt activity, without significant impairment of upstream molecules in insulin-signaling pathway. |
| Notes | R29-DK-51015/DK/NIDDK NIH HHS/United StatesJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United states |
| URL | http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10644543 |
| Citation Key | 362 |
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- *Insulin Resistance
- *Muscle Proteins
- *Protein-Serine-Threonine Kinases
- 1-Phosphatidylinositol 3-Kinase/metabolism
- 3T3 Cells
- Adipocytes/*drug effects/*physiology
- Animals
- Cell Membrane/metabolism
- Deoxyglucose/pharmacokinetics
- Dose-Response Relationship, Drug
- Glucosamine/*pharmacology
- Glucose Transporter Type 4
- Insulin Receptor Substrate Proteins
- Insulin/pharmacology
- Intracellular Signaling Peptides and Proteins
- Mice
- Monosaccharide Transport Proteins/metabolism
- Phosphoproteins/metabolism
- Phosphorylation/drug effects
- Proto-Oncogene Proteins c-akt
- Proto-Oncogene Proteins/metabolism
- Receptor, Insulin/metabolism
- Ribosomal Protein S6 Kinases/metabolism
- Tyrosine/metabolism