Effects of glucosamine infusion on insulin secretion and insulin action in humans
Effects of glucosamine infusion on insulin secretion and insulin action in humans. T Monauni , M G Zenti , A Cretti , M C Daniels , G Targher , B Caruso , M Caputo , D McClain , S Del Prato , A Giaccari , M Muggeo , E Bonora and R C Bonadonna Division of Endocrinology and Metabolic Diseases, Univers...
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Published in | Diabetes (New York, N.Y.) Vol. 49; no. 6; pp. 926 - 935 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.06.2000
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Subjects | |
Online Access | Get full text |
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Summary: | Effects of glucosamine infusion on insulin secretion and insulin action in humans.
T Monauni ,
M G Zenti ,
A Cretti ,
M C Daniels ,
G Targher ,
B Caruso ,
M Caputo ,
D McClain ,
S Del Prato ,
A Giaccari ,
M Muggeo ,
E Bonora and
R C Bonadonna
Division of Endocrinology and Metabolic Diseases, University of Verona School of Medicine, Italy.
Abstract
Glucose toxicity (i.e., glucose-induced reduction in insulin secretion and action) may be mediated by an increased flux through
the hexosamine-phosphate pathway. Glucosamine (GlcN) is widely used to accelerate the hexosamine pathway flux, independently
of glucose. We tested the hypothesis that GlcN can affect insulin secretion and/or action in humans. In 10 healthy subjects,
we sequentially performed an intravenous glucose (plus [2-3H]glucose) tolerance test (IVGTT) and a euglycemic insulin clamp
during either a saline infusion or a low (1.6 micromol x min(-1) x kg(-1)) or high (5 micromol x min(-1) x kg(-1) [n = 5])
GlcN infusion. Beta-cell secretion, insulin (SI*-IVGTT), and glucose (SG*) action on glucose utilization during the IVGTT
were measured according to minimal models of insulin secretion and action. Infusion of GlcN did not affect readily releasable
insulin levels, glucose-stimulated insulin secretion (GSIS), or the time constant of secretion, but it increased both the
glucose threshold of GSIS (delta approximately 0.5-0.8 mmol/l, P < 0.03-0.01) and plasma fasting glucose levels (delta approximately
0.3-0.5 mmol/l, P < 0.05-0.02). GlcN did not change glucose utilization or intracellular metabolism (glucose oxidation and
glucose storage were measured by indirect calorimetry) during the clamp. However, high levels of GlcN caused a decrease in
SI*-IVGTT (delta approximately 30%, P < 0.02) and in SG* (delta approximately 40%, P < 0.05). Thus, in humans, acute GlcN
infusion recapitulates some metabolic features of human diabetes. It remains to be determined whether acceleration of the
hexosamine pathway can cause insulin resistance at euglycemia in humans. |
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ISSN: | 0012-1797 1939-327X |
DOI: | 10.2337/diabetes.49.6.926 |