Literature DB >> 8288698

Lipolysis during abdominal surgery.

G Felländer1, J Nordenström, I Tjäder, J Bolinder, P Arner.   

Abstract

Subcutaneous adipose tissue lipolysis has been monitored with microdialysis during elective cholecystectomy by laparotomy in otherwise healthy nonobese subjects. Eight of the subjects received saline and seven received glucose iv during the operation. In both groups the glycerol level in the microdialysate (lipolysis index) started to increase steadily from the start of the general anesthesia until the abdominal wall was closed. Thereafter it leveled off and remained elevated until after extubation. Plasma glycerol started to rise after the surgical incision. The levels of noradrenaline and adrenaline, but not of insulin, glucagon, and cortisol in plasma, changed in parallel with that of glycerol in the microdialysate. The glycerol response in adipose tissue in the group receiving iv glucose was three times more marked than in the saline group (P = 0.01) in spite of marked hyperinsulinemia, but there was no difference between the groups in plasma glycerol response. The plasma noradrenaline response was 50% higher (P = 0.03) in the glucose group than in the saline group, but there was no difference between the groups in the plasma adrenaline, glucagon, or cortisol responses. Adipose tissue blood flow was measured by the escape of ethanol from the dialysis solvent into the extracellular space. It was constant throughout the experimental period in both groups. In conclusion, the lipolysis rate is accelerated during general anesthesia and abdominal surgery because of increased catecholamine production. Perioperative glucose infusion is associated with a further acceleration of the lipolytic rate in subcutaneous adipose tissue due to an additional activation of the sympathetic nervous activity that overrides the antilipolytic effect of the glucose-induced hyperinsulinemia. Other adipose regions may be less sensitive to glucose infusions and anesthesia.

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Year:  1994        PMID: 8288698     DOI: 10.1210/jcem.78.1.8288698

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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