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The diagnosis of diabetes
Author(s) -
Gray D. Pereira,
Evans P.
Publication year - 2007
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2007.02181.x
Subject(s) - medicine , gray (unit) , citation , diabetes mellitus , gerontology , clinical practice , family medicine , library science , endocrinology , computer science , radiology
© 2007 The Authors. Journal compilation © 2007 Diabetes UK. Diabetic Medicine , 24 , 1049–1052 1051 vs. 40.0 (24.0, 54.8) pg/ml; P = 0.02]. To investigate if the differences in glucagon levels were secondary to glucose tolerance and adiposity, we pair matched 100 normal glucose tolerant relatives and control subjects on the basis of age, sex, waist– hip ratio (WHR), BMI and blood glucose levels as previously reported [6]. The differences between the two groups were no longer present, with median fasting glucagon [72.5 (50.13, 84.88) vs. 60.25 (44.13, 83.00) pg/ml, P = 0.491] and postglucose challenge glucagon [40.0 (28.0, 57.0) vs. 40.0 (24.0, 56.0) pg/ml, P = 0.577] in relatives and control subjects, respectively. Insulin resistance and impaired pancreatic B-cell function are early metabolic characteristics of non-diabetic relatives of Type 2 diabetic patients, and precede the development of abnormal glucose tolerance [6]. We found that fasting and post-glucose load glucagon levels were increased in our non-diabetic first-degree relatives. The question arises as to whether these changes represent a primary metabolic defect or is secondary to other differences between the groups. To remove the potentially confounding effects of adiposity and hyperglycaemia, we therefore pair matched 100 normal glucose tolerant relatives and control subjects. The glucagon levels were no longer raised in the relatives, indicating that the hyperglucagonaemia was indeed a secondary phenomenon. Several recent studies have helped improve our understanding of glucagon metabolism. In an elegant study, Hamaguchi et al . showed that, when high-dose insulin was used to overcome insulin resistance in obese subjects with impaired glucose tolerance (IGT), the abnormal glucagon response to arginine was normalized. They suggested that the exaggerated glucagon response was secondary to impaired insulin action at the pancreatic A-cell independent of glycaemia [9]. Glucose and insulin are potent suppressors of glucagon secretion, and raised glucagon levels in the presence of hyperinsulinaemia and hyperglycaemia is suggestive of inadequate suppression at the A-cell [10]. In conclusion, we have shown that glucagon levels are raised in non-diabetic relatives, but these seem to be secondary to other metabolic changes (glucose intolerance and increased adiposity), and do not appear to represent a primary metabolic defect.