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Metabolic fate of plasma glucose during hyperglycemia in impaired glucose tolerance: evidence for further early defects in the pathogenesis of type 2 diabetes.
Am J Physiol Endocrinol Metab. 2009 Mar; 296(3):E440-4.AJ

Abstract

We examined the intracellular metabolic fate of plasma glucose during a hyperglycemic clamp in impaired glucose-tolerant (IGT; n = 21) and normal glucose-tolerant subjects (n = 10) using a combination of [3-(3)H]glucose infusion with measurement of [(3)H]water formation and indirect calorimetry. IGT was associated with approximately 35% reduced first-phase insulin responses, normal second-phase insulin response, and 25-30% reduced insulin sensitivity, resulting in approximately 35% reduced plasma glucose disposal. This was coupled with approximately 55% reduced storage of plasma glucose (P < 0.01) and approximately 15-20% reduced glycolysis of plasma glucose (P < 0.03), accounting for approximately 75 and 25% of the reduction in glucose disposal, respectively. Decreased glucose oxidation accounted for virtually all the decrease in glycolysis. Therefore, nonoxidative glycolysis of plasma glucose in IGT was similar to that in NGT (P > 0.9) and accounted for an increased proportion of systemic glucose disposal (P < 0.05). We conclude that, in IGT, decreased disposal of plasma glucose involves mainly decreased glycogen synthesis and to a lesser extent decreased glycolysis, which is accounted for by decreased glucose oxidation. An increased proportion of plasma glucose hence undergoes nonoxidative glycolysis, representing a novel early abnormality in the pathogenesis of T2DM.

Authors+Show Affiliations

Department of Endocrinology, Carl T. Hayden VA Medical Center, Phoenix, AZ 85012, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

19141691

Citation

Bokhari, Syed, et al. "Metabolic Fate of Plasma Glucose During Hyperglycemia in Impaired Glucose Tolerance: Evidence for Further Early Defects in the Pathogenesis of Type 2 Diabetes." American Journal of Physiology. Endocrinology and Metabolism, vol. 296, no. 3, 2009, pp. E440-4.
Bokhari S, Emerson P, Israelian Z, et al. Metabolic fate of plasma glucose during hyperglycemia in impaired glucose tolerance: evidence for further early defects in the pathogenesis of type 2 diabetes. Am J Physiol Endocrinol Metab. 2009;296(3):E440-4.
Bokhari, S., Emerson, P., Israelian, Z., Gupta, A., & Meyer, C. (2009). Metabolic fate of plasma glucose during hyperglycemia in impaired glucose tolerance: evidence for further early defects in the pathogenesis of type 2 diabetes. American Journal of Physiology. Endocrinology and Metabolism, 296(3), E440-4. https://doi.org/10.1152/ajpendo.90505.2008
Bokhari S, et al. Metabolic Fate of Plasma Glucose During Hyperglycemia in Impaired Glucose Tolerance: Evidence for Further Early Defects in the Pathogenesis of Type 2 Diabetes. Am J Physiol Endocrinol Metab. 2009;296(3):E440-4. PubMed PMID: 19141691.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Metabolic fate of plasma glucose during hyperglycemia in impaired glucose tolerance: evidence for further early defects in the pathogenesis of type 2 diabetes. AU - Bokhari,Syed, AU - Emerson,Peter, AU - Israelian,Zarmen, AU - Gupta,Anchal, AU - Meyer,Christian, Y1 - 2009/01/13/ PY - 2009/1/15/entrez PY - 2009/1/15/pubmed PY - 2009/4/21/medline SP - E440 EP - 4 JF - American journal of physiology. Endocrinology and metabolism JO - Am J Physiol Endocrinol Metab VL - 296 IS - 3 N2 - We examined the intracellular metabolic fate of plasma glucose during a hyperglycemic clamp in impaired glucose-tolerant (IGT; n = 21) and normal glucose-tolerant subjects (n = 10) using a combination of [3-(3)H]glucose infusion with measurement of [(3)H]water formation and indirect calorimetry. IGT was associated with approximately 35% reduced first-phase insulin responses, normal second-phase insulin response, and 25-30% reduced insulin sensitivity, resulting in approximately 35% reduced plasma glucose disposal. This was coupled with approximately 55% reduced storage of plasma glucose (P < 0.01) and approximately 15-20% reduced glycolysis of plasma glucose (P < 0.03), accounting for approximately 75 and 25% of the reduction in glucose disposal, respectively. Decreased glucose oxidation accounted for virtually all the decrease in glycolysis. Therefore, nonoxidative glycolysis of plasma glucose in IGT was similar to that in NGT (P > 0.9) and accounted for an increased proportion of systemic glucose disposal (P < 0.05). We conclude that, in IGT, decreased disposal of plasma glucose involves mainly decreased glycogen synthesis and to a lesser extent decreased glycolysis, which is accounted for by decreased glucose oxidation. An increased proportion of plasma glucose hence undergoes nonoxidative glycolysis, representing a novel early abnormality in the pathogenesis of T2DM. SN - 0193-1849 UR - https://www.unboundmedicine.com/medline/citation/19141691/Metabolic_fate_of_plasma_glucose_during_hyperglycemia_in_impaired_glucose_tolerance:_evidence_for_further_early_defects_in_the_pathogenesis_of_type_2_diabetes_ L2 - https://journals.physiology.org/doi/10.1152/ajpendo.90505.2008?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -