Khalifa, A. (1999). Study of Glucagon Receptors on Monocytes in Type 2 Diabetes Mellitus: A Case Control Study. Journal of High Institute of Public Health, 29(1), 21-34. doi: 10.21608/jhiph.1999.428358
Adel MA. Khalifa. "Study of Glucagon Receptors on Monocytes in Type 2 Diabetes Mellitus: A Case Control Study". Journal of High Institute of Public Health, 29, 1, 1999, 21-34. doi: 10.21608/jhiph.1999.428358
Khalifa, A. (1999). 'Study of Glucagon Receptors on Monocytes in Type 2 Diabetes Mellitus: A Case Control Study', Journal of High Institute of Public Health, 29(1), pp. 21-34. doi: 10.21608/jhiph.1999.428358
Khalifa, A. Study of Glucagon Receptors on Monocytes in Type 2 Diabetes Mellitus: A Case Control Study. Journal of High Institute of Public Health, 1999; 29(1): 21-34. doi: 10.21608/jhiph.1999.428358
Study of Glucagon Receptors on Monocytes in Type 2 Diabetes Mellitus: A Case Control Study
Department of Internal Medicine, Alexandria Faculty of Medicine, Egypt
Abstract
Monocytes glucagon receptors were chosen as a model to study glucagon receptors in newly diagnosed type 2 diabetic patients. 23 adults patients [15 males and 8 females] diagnosed as type 2 diabetes mellitus as a first presentation to the out patients clinic were included in this work. In addition 17 normal adult persons [10 males and 7 females] of matched age [41.3‡4.4 years for diabetics versus 39.91+2.9 years for healthy subjects] and of matched body mass index [BMI 25.21#1.76 for diabetics versus 24.09#1.62 for healthy persons were chosen as a control. Fasting plasma insulin was not significantly different in diabetics [29.2+8.4 p mol/l] when compared with the control [26.1$5.3 p mol/l, P < 0.05]. Fasting plasma glucagon, on the other hand, was found significantly high in diabetic patients compared with the control [149.9115.1 p g/ml in diabetics versus 125.5$9.3 p g/ml in controls, P < 0.05). Binding study of monocytes glucagon receptors using 125l-monoiodoglucagon showed normal affinity of the receptors to glucagon "IC50 30.41#3.3 ng/ml in controls versus 26.95+2.4 ng/ml in diabetics, P < 0.05". Scatchard analysis of these binding data showed normal monocyte glucagon receptor density compared with the control [34.2+3.1 binding sites/cell in diabetics versus 36.3$2.91 binding sites/cell in controls, P < 0.05]. Glucagon receptor responsiveness as measured by glucagon induced cAMP increments were found to be normal in diabetic subjects [IC50 4.86 p mol/2 x10® cells for diabetics verus 4.79 p mol/2 × 10€ cells for control, P < 0.05]. In conclusion, these data indicate that glucagon receptor system appears to be normal in early type 2 diabetics mellitus and the glucagon mediated enhanced hepatic glucose production in diabetic patients could not be explained on receptor basis. However, reviewing the earlier glucagon infusion studies data revealed, that hypergluconemia can induce its characteristic diabetogenic and ketogenic actions only in the presence of associated insulin deficiency or insulin resistance. Therefore, it is the combined effects insulin deficiency and/or resistance and hyperglucagonemia with normal glucagon receptor-effector system that appear to contribute to the pathophysiology of type 2 diabetes mellitus.
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