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Citations to this article

Multiple defects in muscle glycogen synthase activity contribute to reduced glycogen synthesis in non-insulin dependent diabetes mellitus.
A W Thorburn, … , G Brechtel, R R Henry
A W Thorburn, … , G Brechtel, R R Henry
Published February 1, 1991
Citation Information: J Clin Invest. 1991;87(2):489-495. https://doi.org/10.1172/JCI115022.
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Research Article

Multiple defects in muscle glycogen synthase activity contribute to reduced glycogen synthesis in non-insulin dependent diabetes mellitus.

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Abstract

To define the mechanisms of impaired muscle glycogen synthase and reduced glycogen formation in non-insulin dependent diabetes mellitus (NIDDM), glycogen synthase activity was kinetically analyzed during the basal state and three glucose clamp studies (insulin approximately equal to 300, 700, and 33,400 pmol/liter) in eight matched nonobese NIDDM and eight control subjects. Muscle glycogen content was measured in the basal state and following clamps at insulin levels of 33,400 pmol/liter. NIDDM subjects had glucose uptake matched to controls in each clamp by raising serum glucose to 15-20 mmol/liter. The insulin concentration required to half-maximally activate glycogen synthase (ED50) was approximately fourfold greater for NIDDM than control subjects (1,004 +/- 264 vs. 257 +/- 110 pmol/liter, P less than 0.02) but the maximal insulin effect was similar. Total glycogen synthase activity was reduced approximately 38% and glycogen content was approximately 30% lower in NIDDM. A positive correlation was present between glycogen content and glycogen synthase activity (r = 0.51, P less than 0.01). In summary, defects in muscle glycogen synthase activity and reduced glycogen content are present in NIDDM. NIDDM subjects also have less total glycogen synthase activity consistent with reduced functional mass of the enzyme. These findings and the correlation between glycogen synthase activity and glycogen content support the theory that multiple defects in glycogen synthase activity combine to cause reduced glycogen formation in NIDDM.

Authors

A W Thorburn, B Gumbiner, F Bulacan, G Brechtel, R R Henry

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Total citations by year

Year: 2025 2024 2020 2017 2016 2015 2014 2013 2012 2011 2010 2009 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 1995 1994 1993 1992 1991 1988 1957 Total
Citations: 2 1 2 3 2 2 1 2 6 1 4 1 1 1 1 1 7 5 8 5 6 3 6 5 7 7 9 5 2 1 1 108
Citation information
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Citations to this article in year 2012 (6)

Title and authors Publication Year
Hyperglycaemia normalises insulin action on glucose metabolism but not the impaired activation of AKT and glycogen synthase in the skeletal muscle of patients with type 2 diabetes
BF Vind, JB Birk, SG Vienberg, B Andersen, H Beck-Nielsen, JF Wojtaszewski, K Højlund
Diabetologia 2012
Early Diagnosis of Pancreatic Adenocarcinoma: Role of Stroma, Surface Proteases, and Glucose-Homeostatic Agents
P Fric, M Zavoral
Pancreas 2012
Effect of acute exercise on glycogen synthase in muscle from obese and diabetic subjects
J Jensen, P Tantiwong, JT Stuenæs, M Molina-Carrion, RA DeFronzo, K Sakamoto, N Musi
American journal of physiology. Endocrinology and metabolism 2012
Effect of acute exercise on glycogen synthase in muscle from obese and diabetic subjects
J Jensen, P Tantiwong, JT Stuenæs, M Molina-Carrion, RA DeFronzo, K Sakamoto, N Musi
American journal of physiology. Endocrinology and metabolism 2012
Placental Restriction Reduces Insulin Sensitivity and Expression of Insulin Signaling and Glucose Transporter Genes in Skeletal Muscle, But Not Liver, in Young Sheep
MJ Blasio, KL Gatford, ML Harland, JS Robinson, JA Owens
Endocrinology 2012
Prevention of Type 2 Diabetes
D LeRoith
2012

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