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Journal of Parenteral and Enteral Nutrition
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Original Communications

Glycemia Influences on Glucose Metabolism in Sepsis During Hyperinsulinemic Clamp

Zdenek Rusavy, MD*, Ian A. Macdonald, PhD{dagger}, Vladimir Sramek, MD{ddagger}, Silvie Lacigova, MD, PhD*, Pavel Tesinsky, MD§ and Ivan Novak, MD*

From the * Department of Medicine I, University Hospital, Plzen, Czech Republic; {dagger} Department of Physiology and Pharmacology, Q.M.C. Nottingham, United Kingdom;{ddagger} Department of Anesthesiology and Intensive Care, University Hospital Brno, Czech Republic; and the§ Department of Medicine II, University Hospital, Prague, Czech Republic

Correspondence: Zdenek Rusavy, MD, Department of Medicine I, University Hospital Plzen, Alej Svobody 80, 304 60 Plzen, Czech Republic. Electronic mail may be sent to rusavy{at}fnplzen.cz.

Background: We investigated glucose metabolism in septic patients during hyperglycemic clamps and compared the different levels of insulinemia and glycemia. Methods: In 10 non-diabetic stable septic patients on mechanical ventilation with baseline glycemia >6mmol/L and continuous insulin infusion, 3 steps of hyperinsulinemic clamp were performed after 8 hours without caloric intake. In step 1, the targets were insulinemia of 250 mIU/L and glycemia of 5mmol/L; in step 2, insulinemia of 250 mIU/L and glycemia of 10 mmol/L; in step 3, insulinemia of 1250 mIU/L and glycemia of 5 mmol/L. Glucose uptake was calculated as the amount of glucose per time needed to maintain the target level of glycemia. Glucose oxidation was calculated from indirect calorimetry and urinary nitrogen losses. Values are provided as means ± SD. A two-way analysis of variance and Scheffe's method were used for statistical analysis and p < .05 was considered significant. Results: At step 1, glucose uptake was lower than at step 2 (3.8 ± 2.48 mg/kg/min and 7.9 ± 3.45 mg/kg/min, respectively; p < .001). Glucose oxidation was also lower at step 1 (2.6 ± 0.98 and 4.2 ± 1.85 mg/kg/min, respectively; p < .01). Glucose storage was low at step 1 (0.7 ± 1.39) and increased at step 2 (3.5 ± 2.18; p < .05). In step 3, glucose uptake was 7.0 ± 2.1, oxidation was 3.6 ± 1.37, and storage was 2.9 ± 2.79. There was no significant difference in all these parameters between steps 2 and 3. Energy expenditure between steps 1, 2 and 3 did not change (2294 + 307.42, 2334 + 341.53, and 2342 + 426.67 kcal/day, respectively). Alanine in plasma dropped significantly (p < .05): 10 mmol/L (311 ± 55.88 mmol/L) at glycemia compared with 5 mmol/L (390 ± 76 umol/L) at insulinemia 250 mIU/L. It did not differ significantly from the values obtained at glycemia 5 mmol/L and insulinemia 1250 mIU/L (348 ± 70.68 mmol/L). Even if the level of cytokines in sepsis was higher, there was no correlation between the insulin level in plasma (250 and 1250 mIU/L), glycemia (5 and 10 mmol/L) and cytokine level (IL-1β, IL-2, IL-6, IL-8 and TNF{alpha}). Conclusion: At insulinemia 250 mIU/L, a glucose level of 10 mmol/L seems to increase glucose uptake, oxidation, and storage compared with glycemia 5 mmol/L. This glucose uptake and oxidation at glycemia 10 mmol/L is comparable with the effect of extremely high insulinemia (1250 mIU/L) clamped at glycemia 5 mmol/L. A higher level of blood glucose or a high level of insulinemia significantly increases glucose uptake but not energy expenditure.

Journal of Parenteral and Enteral Nutrition, Vol. 29, No. 3, 171-175 (2005)
DOI: 10.1177/0148607105029003171


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