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Site of insulin resistance after surgery:: the contribution of hypocaloric nutrition and bed rest.
Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
Department of Endocrinology, Karolinska Hospital, Stockholm, Sweden.
Endocrine Research Unit, Mayo Clinic and Foundation, Rochester MN, United States.
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1997 (English)In: Clinical Science, ISSN 0143-5221, E-ISSN 1470-8736, Vol. 93, no 2, p. 137-146Article in journal (Refereed) Published
Abstract [en]

Insulin resistance after surgery has been shown to be related to several important derangements in protein and fat metabolism. However, mechanisms of impaired glucose tolerance after surgery remain ill-defined. 2. Insulinsensitivity and glucose (6,62H2-glucose) were studied in seven before and after elective surgery (surgery group), by two step-hyperinsulinaemic (0.3 and 0.8 munits kg-1min-1), normoglycaemic (4.5 mmol/l) clamps. Six healthy subjects were studied, using the same protocol, before and after a similar period of bed rest and hypocaloric nutrition (fast/bed rest group) to delineate the effects of surgery per se. 3. Basal endogenous glucose production and whole-body glucose disposal was higher after surgery (P < 0.001), whereas no change was found after fast/bed rest. During glucose clamps, the glucose infusion rates required to maintain normoglycaemia and whole-body glucose disposal decreased (P < 0.001) after surgery, while endogenous glucose production increased (P < 0.001). In the control subjects, levels of endogenous glucose production remained unchanged after fast/bed rest. In contrast, glucose infusion rates and whole-body glucose disposal during glucose clamps also decreased after fast/bed rest (P < 0.01). However, the relative decrease in both these parameters was greater after surgery compared with after fast/bed rest (P < 0.01). 4. After surgery, energy expenditure and fat oxidation increased (P < 0.001), whereas glucose oxidation decreased (P < 0.05). No significant change was found in glucose utilization postoperatively. After fast/bed rest, no change was found in energy expenditure. However, fat oxidation increased (P < 0.01), whereas glucose oxidation and glucose utilization decreased (P < 0.05). 5. In conclusion, impaired glucose tolerance develops after surgery as a result of decreased insulin-stimulated whole-body glucose disposal as well as increased endogenous glucose release. Despite the increase in endogenous glucose production, the reduction in endogenous glucose production with each elevation of insulin was unaffected by surgery. Perioperative bed rest and/or hypocaloric nutrition contributed to the decrease in insulin-stimulated whole-body glucose disposal in the postoperative state, whereas these factors have no effects on endogenous glucose production.

Place, publisher, year, edition, pages
Portland Press, 1997. Vol. 93, no 2, p. 137-146
National Category
Endocrinology and Diabetes Physiology
Identifiers
URN: urn:nbn:se:oru:diva-63873DOI: 10.1042/cs0930137ISI: A1997XM80800006PubMedID: 9301428Scopus ID: 2-s2.0-0030849286OAI: oai:DiVA.org:oru-63873DiVA, id: diva2:1171023
Note

Funding agencies:

NIDDK NIH HHS R01 DK-41973 

Available from: 2018-01-05 Created: 2018-01-05 Last updated: 2018-02-05Bibliographically approved

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Ljungqvist, Olle

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