Induction of insulin resistance by glucosamine reduces blood flow but not interstitial levels of either glucose or insulin
Abstract
To study the effects of a glucosamine infusion on skeletal muscle metabolism, microdialysis was performed in the medial femoral muscle in Sprague-Dawley rats during a euglycemic-hyperinsulinemic clamp (insulin infusion 18 mU x kg(-1) x min(-1)). During steady-state clamping conditions (70 min), an infusion of glucosamine (30 micromol x kg(-1) x min(-1)) or saline was given for 240 min. Blood flow was measured by the microsphere technique at the end of the clamp. An approximately 36% (P < 0.001) reduction in the glucose infusion rate was seen after 170 min in the glucosamine-treated rats compared with control rats. There were no significant differences in interstitial or plasma levels of either insulin or glucose between the two groups. Both interstitial (2.31 +/- 0.18 vs. 1.71 +/- 0.24 mmol/l, P < 0.05) and arterial plasma lactate concentrations (1.29 +/- 0.09 vs. 0.79 +/- 0.09 mmol/l, P < 0.01) were significantly higher in control rats compared with glucosamine-treated rats. Blood flow was significantly reduced in hind limb femoral muscles in the glucosamine-treated rats compared with control rats. The most pronounced reduction in blood flow was seen in the Soleus muscle (27.6 +/- 3.4 vs. 14.7 +/- 2.0 ml x 100 g(-1) x min(-1), P < 0.01). These results demonstrate that induction of insulin resistance by glucosamine results in a reduction of the blood flow rate as well as the uptake of glucose and the production of lactate in skeletal muscle. As a result of the inhibited glucose metabolism, the interstitial glucose concentration was unchanged despite the reduced blood flow after glucosamine administration. The data suggest the importance of regulation of blood flow by nonoxidative metabolism of glucose in resting muscle.
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Experimental induction of insulin resistance in rats and in humans resulted in reductions in blood flow responses.
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From Improved Endothelial Function With Metformin in Type 2 Diabetes Mellitus (2001) · cites this paper as [31]
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- Authors
- Holmäng, A., Nilsson, C., Niklasson, M., Larsson, B. M., & Lönroth, P.
- Affiliations
- Sahlgrenska University Hospital (SE)
- Wallenberg Laboratory, Sahlgrenska University Hospital, Göteborg, Sweden. agneta.holmang@wlab.wall.gu.se
- ORCID
- Holmäng, A
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1999-01-01
- Volume
- 48
- Issue
- 1
- Pages
- 106-111
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2064332050
- Cited by
- 51
- References
- 0
- Citations by year
- 2021: 1 · 2017: 1 · 2014: 1 · 2013: 1 · 2012: 2
- FWCI
- 3.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- glucosamine, insulin resistance, skeletal muscle blood flow, glucose uptake, interstitial glucose, lactate, soleus muscle, nonoxidative glucose metabolism, hyperinsulinemic-euglycemic clamp, microdialysis, femoral muscle
- MeSH terms
- Animals, Extracellular Space, Female, Glucosamine, Glucose, Insulin, Insulin Resistance, Regional Blood Flow, Rats, Sprague-Dawley, Microdialysis, Muscle, Skeletal, Rats
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