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Marked Impairment of the Effect of Hyperglycaemia on Glucose Uptake and Glucose Production in Insulin‐dependent Diabetes
Author(s) -
Arnfred J.,
Schmitz O.,
HotherNielsen O.,
Ørskova C.,
BeckNielsen H.,
Hermansen K.,
Christiansen J. S.,
Alberti K. G. M. M.,
Ørskov H.
Publication year - 1988
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.1464-5491.1988.tb01103.x
Subject(s) - medicine , endocrinology , insulin , diabetes mellitus , somatostatin , glucose uptake
The effect of hyperglycaemia per se on glucose utilization and glucose production was evaluated in 12 patients with insulin‐dependent diabetes and in 9 non‐diabetic control subjects. In diabetic patients normoglycaemia was maintained during the night preceding the study by a variable intravenous insulin infusion. During the study endogenous insulin secretion was suppressed by somatostatin (300 μg h −1 ) and replaced by infusion of insulin (0.2 mU kg −1 min −1 ). Glucose utilization and hepatic glucose production rates were quantified at two plasma glucose concentrations (6.7 and 16.7 mmoll −1 ) using the two‐step sequential hyperglycaemic clamp technique in combination with 3‐ 3 H‐glucose tracer infusion. Duration of each step was 120 min. In diabetic patients glucose utilization, at a glucose concentration of 6.7 mmol ***l −1 , was not different from normal (mean ± SE: 2.9±0.2 vs 3.6±0.3 mg kg −1 min −1 , 0.05< p <0.10), but the response to marked hyperglycaemia was significantly reduced (5.4±0.5 vs 9.4±1.0 mg kg −1 min −1 , p <0.01). Hepatic glucose production was also normal at 6.7 mmol l −1 (1.4±0.1 vs 1.4±0.1 mg kg −1 min −1 , NS), but whereas in control subjects glucose production was suppressed during hyperglycaemia of 16.7 mmoll −1 (0.3±0.4 mg kg −1 min −1 , p <0.01), a slight increase was observed in diabetic patients (2.0±0.2 mg kg −1 min −1 , p <0.05). In conclusion we found the effect of hyperglycaemia in both glucose utilization and hepatic glucose production to be reduced in patients with insulin‐dependent diabetes.