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Cited by 61Diabetes, Cardiovascular Risks, and LipoproteinsMetabolism, Diabetes, and CancerDiabetes Treatment and Management

Normalization of Plasma Glucose Concentration by Insulin Therapy Improves Insulin-Stimulated Glycogen Synthesis in Type 2 Diabetes

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Pratipanawatr, Thongchai, Cusi, Kenneth, Ngo, Peter, Pratipanawatr, Wilailak, Mandarino, Lawrence J., DeFronzo, Ralph A.·2002·Diabetes
DOI 10.2337/diabetes.51.2.462
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Abstract

Considerable evidence suggests that skeletal muscle insulin resistance is an inherent feature of type 2 diabetes and contributes to the pathogenesis of the disease. In patients with poorly controlled diabetes, hyperglycemia is thought to produce additional insulin resistance in muscle. The magnitude and nature of hyperglycemia-induced insulin resistance is not known. The purpose of the present study was to determine the biochemical mechanisms responsible for increased insulin-stimulated glucose disposal after the achievement of tight glycemic control with a mixed-split regimen. We performed hyperinsulinemic-euglycemic clamps with indirect calorimetry and vastus lateralis muscle biopsies in eight type 2 diabetic patients who had poor glycemic control (HbA1c 10.1%) and again after 3 months of intensive insulin therapy designed to produce near-normoglycemia (HbA1c 6.6%). Improved glycemic control increased insulin-stimulated glucose disposal (5.16 ± 0.32 vs. 3.69 ± 0.33 mg · kg−1 · min−1; P < 0.01); nonoxidative glucose disposal, which primarily reflects glycogen synthesis (2.11 ± 0.26 vs. 0.90 ± 0.16 mg · kg−1 · min−1; P < 0.01); and glycogen synthase fractional velocity (0.094 ± 0.017 vs. 0.045 ± 0.007; P < 0.05). There was no improvement in insulin-stimulated glucose oxidation (3.05 ± 0.25 vs. 2.79 ± 0.20 mg · kg−1 · min−1), hexokinase II mRNA expression (increase over basal values), or hexokinase II enzymatic activity (0.51 ± 0.16 vs. 0.42 ± 0.18 pmol · min−1 · μg−1 protein). All of the increase in insulin-stimulated glucose disposal could be accounted for by increased glycogen synthesis, which is likely attributable to increased activation of glycogen synthase by insulin.

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  • Most studies show insulin does not increase glycogen synthase mRNA or protein expression in human muscle.

    “Most studies have demonstrated that insulin does not increase glycogen synthase mRNA or protein expression in human muscle [201, 220, 221].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [220]

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Authors
Pratipanawatr, T., Cusi, K., Ngo, P., Pratipanawatr, W., Mandarino, L. J., & DeFronzo, R. A.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2002-02-01
Volume
51
Issue
2
Pages
462-468
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.51.2.462
OpenAlex
W2169654705
Cited by
61
References
71
Citations by year
2020: 1 · 2019: 1 · 2018: 3 · 2017: 1 · 2015: 2 · 2014: 2 · 2013: 5 · 2012: 1
FWCI
3.61
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • U.S. Department of Veterans Affairs
  • National Institutes of Health (5r01dk041075-03)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK41075, DK 24092)
  • National Center for Research Resources (M01RR01346, M01RR001346, RR-01346)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
type 2 diabetes, insulin therapy, glycemic control, hyperglycemia, insulin resistance, skeletal muscle, glycogen synthesis, glycogen synthase, insulin-stimulated glucose disposal, hyperinsulinemic-euglycemic clamp, hexokinase 2, nonoxidative glucose disposal, glucose oxidation
MeSH terms
Blood Glucose, Body Weight, Diabetes Mellitus, Type 2, Female, Glycogen, Glycogen Synthase, Hexokinase, Humans, Insulin, Male, Middle Aged, Osmolar Concentration, Reference Values, RNA, Messenger

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