OBJECTIVE: Hypoglycemia is the most important acute complication in patients with type 1 diabetes. Liver glycogen is an important storage form of glucose and thus important for maintaining glucose homeostasis. To test the hypothesis whether abnormal storage of glycogen in the liver is contributing to the risk of hypoglycemia in type 1 diabetic children and adolescents, liver glycogen was measured. STUDY DESIGN: Hepatic glycogen concentrations were measured in 19 type 1 diabetic children and adolescents as well as in 19 age-matched controls, following overnight fasting and 4 h after two standardized meals. Hepatic glycogen was assessed by natural abundance 13C nuclear magnetic resonance spectroscopy (MRS). RESULTS: Mean (+/- SEM) fasting hepatic glycogen concentrations measured in arbitrary units (au) were similar in type 1 diabetic subjects and controls (4.98 +/- 0.36 vs. 4.48 +/- 0.33 au; p = 0.31). Both groups presented with an increase in liver glycogen concentrations 4 h after the standardized meals (diabetic subjects 5.70 +/- 0.37 au, p = 0.01; controls 5.78 +/- 0.47 au, p < 0.01). Hepatic glycogen accumulation after feeding was 19.1% in diabetic children and adolescents compared with 35.8% in controls, but this difference did not reach significance. CONCLUSION: In children and adolescents with moderately controlled type 1 diabetes, hepatic glycogen stores after fasting and feeding are comparable to those of matched controls.
OBJECTIVE:Hypoglycemia is the most important acute complication in patients with type 1 diabetes. Liver glycogen is an important storage form of glucose and thus important for maintaining glucose homeostasis. To test the hypothesis whether abnormal storage of glycogen in the liver is contributing to the risk of hypoglycemia in type 1 diabeticchildren and adolescents, liver glycogen was measured. STUDY DESIGN: Hepatic glycogen concentrations were measured in 19 type 1 diabeticchildren and adolescents as well as in 19 age-matched controls, following overnight fasting and 4 h after two standardized meals. Hepatic glycogen was assessed by natural abundance 13C nuclear magnetic resonance spectroscopy (MRS). RESULTS: Mean (+/- SEM) fasting hepatic glycogen concentrations measured in arbitrary units (au) were similar in type 1 diabetic subjects and controls (4.98 +/- 0.36 vs. 4.48 +/- 0.33 au; p = 0.31). Both groups presented with an increase in liver glycogen concentrations 4 h after the standardized meals (diabetic subjects 5.70 +/- 0.37 au, p = 0.01; controls 5.78 +/- 0.47 au, p < 0.01). Hepatic glycogen accumulation after feeding was 19.1% in diabeticchildren and adolescents compared with 35.8% in controls, but this difference did not reach significance. CONCLUSION: In children and adolescents with moderately controlled type 1 diabetes, hepatic glycogen stores after fasting and feeding are comparable to those of matched controls.
Authors: I Jane Cox; Amar Sharif; Jeremy F L Cobbold; Howard C Thomas; Simon D Taylor-Robinson Journal: World J Gastroenterol Date: 2006-08-14 Impact factor: 5.742
Authors: Mary Courtney Moore; Marta S Smith; Ben Farmer; Guillaume Kraft; Masakazu Shiota; Phillip E Williams; Alan D Cherrington Journal: Diabetes Date: 2017-02-07 Impact factor: 9.461