This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (21)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

Michael S. Dahn, MD; Lloyd A. Jacobs, MD; Stuart Smith, PhD; Bijaya Hans, MD; M. Patricia Lange, BSN; Robert A. Mitchell, PhD; John R. Kirkpatrick, MD

Arch Surg. 1985;120(2):166-172.

Abstract
• Basal glucose metabolism was evaluated in eight stable, infected patients by measuring hepatic glucose production rates in relation to stress endocrine profile and by comparing these data to five injured, noninfected patients. All patients exhibited normal total-body oxygen consumptions and cardiac indices. Fasting basal insulin values were similar in both groups (6 µU/cc) despite a significantly higher plasma glucose level in septic patients (106±14 mg/dL) compared to nonseptic patients (88±10 mg/dL). Septic patients exhibited splanchnic glucose production and calculated glucose clearance rates, 53% and 34% higher, than injured nonseptic patients, respectively. In addition, septic patients exhibited a decreased pancreatic insulin secretory response to an intravenous glucose tolerance test as evidenced by a significantly depressed peak insulin value (17 µU/cc) relative to injured patients (77 µU/cc). These findings indicate that insulin suppression is evident in sepsis even in the absence of shock and suggest that sepsisrelated basal hyperglycemia does not appear to be associated with peripheral insulin resistance.

(Arch Surg 1985;120:166-172)

Author Affiliations
From the Departments of Surgery (Drs Dahn and Jacobs), Nuclear Medicine (Dr Smith), Radiology (Dr Hans), and Nursing (Ms Lange), Veterans Administration Medical Center, Allen Park, Mich, and the Departments of Surgery (Drs Dahn, Jacobs, and Kirkpatrick) and Biochemistry (Dr Mitchell), Wayne State University, Detroit.

Footnotes
Accepted for publication Sept 13, 1984.

Read before the Fourth Annual Meeting of the Surgical Infection Society, Montreal, April 30, 1984.

Reprint requests to Department of Surgery, University Health Center, 6-C, Wayne State University, 4201 St Antoine, Detroit, MI 48201 (Dr Dahn).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Hyperglycemia in Children with Meningococcal Sepsis and Septic Shock: The Relation between Plasma Levels of Insulin and Inflammatory Mediators
van Waardenburg et al.
J. Clin. Endocrinol. Metab. 2006;91:3916-3921.
ABSTRACT | FULL TEXT  

Insulin Attenuates the Systemic Inflammatory Response in Endotoxemic Rats
Jeschke et al.
Endocrinology 2004;145:4084-4093.
ABSTRACT | FULL TEXT  

Hepatic and Peripheral Glucose Metabolism in Intensive Care Patients Receiving Continuous High- or Low-Carbohydrate Enteral Nutrition
Tappy et al.
JPEN J Parenter Enteral Nutr 1999;23:260-268.
ABSTRACT  

Manifestations of Sepsis
Harris et al.
Arch Intern Med 1987;147:1895-1906.
ABSTRACT