Increased glucose uptake by intestinal mucosa and muscularis in hypermetabolic sepsis

C. H. Lang, J. C A Obih, G. J. Bagby, J. N. Bagwell, J. J. Spitzer

Research output: Contribution to journalArticle

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Abstract

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, ~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. Because somatostatin blunted the elevated intestinal blood flow and significantly reduced circulating insulin levels, while not altering glucose metabolic rate, the sepsis-induced increase in glucose uptake by the gut appears to be mediated by an insulin-independent mechanism that is not dependent on increased blood flow and glucose delivery.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume261
Issue number2 24-2
StatePublished - Jan 1 1991

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Intestinal Mucosa
Sepsis
Glucose
Mucous Membrane
Somatostatin
Small Intestine
Gastrointestinal Tract
Insulin
Viscera
Large Intestine
Vasoconstriction
Microspheres
Intestines
Blood Glucose
Stomach

All Science Journal Classification (ASJC) codes

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

Cite this

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title = "Increased glucose uptake by intestinal mucosa and muscularis in hypermetabolic sepsis",
abstract = "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, ~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. Because somatostatin blunted the elevated intestinal blood flow and significantly reduced circulating insulin levels, while not altering glucose metabolic rate, the sepsis-induced increase in glucose uptake by the gut appears to be mediated by an insulin-independent mechanism that is not dependent on increased blood flow and glucose delivery.",
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Increased glucose uptake by intestinal mucosa and muscularis in hypermetabolic sepsis. / Lang, C. H.; Obih, J. C A; Bagby, G. J.; Bagwell, J. N.; Spitzer, J. J.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 261, No. 2 24-2, 01.01.1991.

Research output: Contribution to journalArticle

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