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Insulin infusion (GIK) in the treatment of type 2 (non-insulin dependent) diabetes during the perioperative period

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Abstract The effect of surgery on intermediary metabolism has been studied in six non-diabetic subjects, eleven type 2 diabetic subjects untreated during surgery, and nine type 2 diabetic subjects treated by glucose–insulin–potassium (GIK) infusion during surgery. Plasma glucose results were studied in all subjects and other metabolites whenever possible. Initial glucose concentrations were similar in both groups of diabetic subjects. Four hours postoperatively the plasma glucose was lower in the GIK group (10·1 ± 1·0 mmol/l) than in untreated subjects (14·2 ± 1·3 mmol/l, P < 0·05) but still far above levels found in non-diabetic subjects. Lactate concentration was higher in the GIK treated diabetic subjects than in both non-GIK treated diabetic and non-diabetic patients 15 min after induction (1·32 ± 0·07 compared with 0·93 ± 0·09 and 0·89 ± 0·08 mmol/l, P < 0·02). Non-esterified fatty acid (NEFA) was lower one hour postoperatively in the GIK treated diabetic group than in the non-GIK diabetic patients (0·47 ± 0·09 mmol/l compared with 1·09 ± 0·22 mmol/l, P < 0·05). All NEFA concentrations were lower in GIK treated diabetic subjects than in non-diabetic subjects for the time of insulin infusion. Blood 3-hydroxybutyrate was also lower in GIK treated (0·04 ± 0·02) than in untreated diabetic subjects 4h postoperatively (0·25 ± 0·07 mmol/l, P < 0·05). The levels of non-esterified fatty acid and 3-hydroxybutyrate found in the untreated diabetic did not differ from those found in non-diabetic controls. Plasma cortisol levels had risen in all groups 4 h postoperatively (P < 0·01).
Title: Insulin infusion (GIK) in the treatment of type 2 (non-insulin dependent) diabetes during the perioperative period
Description:
Abstract The effect of surgery on intermediary metabolism has been studied in six non-diabetic subjects, eleven type 2 diabetic subjects untreated during surgery, and nine type 2 diabetic subjects treated by glucose–insulin–potassium (GIK) infusion during surgery.
Plasma glucose results were studied in all subjects and other metabolites whenever possible.
Initial glucose concentrations were similar in both groups of diabetic subjects.
Four hours postoperatively the plasma glucose was lower in the GIK group (10·1 ± 1·0 mmol/l) than in untreated subjects (14·2 ± 1·3 mmol/l, P < 0·05) but still far above levels found in non-diabetic subjects.
Lactate concentration was higher in the GIK treated diabetic subjects than in both non-GIK treated diabetic and non-diabetic patients 15 min after induction (1·32 ± 0·07 compared with 0·93 ± 0·09 and 0·89 ± 0·08 mmol/l, P < 0·02).
Non-esterified fatty acid (NEFA) was lower one hour postoperatively in the GIK treated diabetic group than in the non-GIK diabetic patients (0·47 ± 0·09 mmol/l compared with 1·09 ± 0·22 mmol/l, P < 0·05).
All NEFA concentrations were lower in GIK treated diabetic subjects than in non-diabetic subjects for the time of insulin infusion.
Blood 3-hydroxybutyrate was also lower in GIK treated (0·04 ± 0·02) than in untreated diabetic subjects 4h postoperatively (0·25 ± 0·07 mmol/l, P < 0·05).
The levels of non-esterified fatty acid and 3-hydroxybutyrate found in the untreated diabetic did not differ from those found in non-diabetic controls.
Plasma cortisol levels had risen in all groups 4 h postoperatively (P < 0·01).

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