Increased glucose uptake by intestinal mucosa and muscularis in hypermetabolic sepsis

• Published in: The American journal of physiology Vol. 261; no. 2 Pt 1; p. G287
• Main Authors: Lang, C H, Obih, J C, Bagby, G J, Bagwell, J N, Spitzer, J J
• Format: Journal Article
• Language: English
• Published: United States 01.08.1991
• Subjects: Animals; Escherichia coli Infections - metabolism; Escherichia coli Infections - pathology; Escherichia coli Infections - physiopathology; Glucose - pharmacokinetics; Hemodynamics; Intestinal Diseases - metabolism; Intestinal Diseases - pathology; Intestinal Diseases - physiopathology; Intestinal Mucosa - metabolism; Intestines - blood supply; Intestines - metabolism; Intestines - pathology; Male; Muscle, Smooth - metabolism; Rats; Rats, Inbred Strains; Regional Blood Flow - drug effects; Somatostatin - pharmacology
• ISSN: 0002-9513
• DOI: 10.1152/ajpgi.1991.261.2.g287

The purpose of the present study was to determine the following: 1) whether the sepsis-induced increase in glucose uptake was a generalized response along the entire length of the gastrointestinal tract; 2) the relative contribution of the mucosa and muscularis to the enhanced uptake; and 3) whether reducing intestinal blood flow would attenuate the elevated rate of glucose uptake. Hypermetabolic sepsis increased in vivo glucose uptake in all sections of the gastrointestinal tract (57-93%) except the stomach. The rates of glucose uptake per gram of tissue by the mucosa and muscularis were not different. However, because the mucosa accounted for the majority of the whole intestine mass, this layer was responsible for 76-78% of the glucose uptake by the entire small intestine. Intestinal blood flow, determined with the use of radiolabeled microspheres, increased by 127% in sepsis. In both groups, approximately 70% of the total intestinal blood flow was distributed to the mucosa. Somatostatin was infused to produce splanchnic vasoconstriction and decreased the sepsis-induced increment in intestinal flow to the mucosa and muscularis (38 and 54%), whereas the enhanced rate of glucose uptake was not altered. Somatostatin also produced a severe insulinopenia. These results indicate that hypermetabolic sepsis increases glucose uptake to a similar extent along the length of the small and large intestine and that the majority of this increase is due to an enhanced uptake by the mucosa.