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This Article Full Text Full Text (PDF) All Versions of this Article: 287/2/E269    most recent 00040.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Camacho, R. C. Articles by Wasserman, D. H. Search for Related Content PubMed PubMed Citation Articles by Camacho, R. C. Articles by Wasserman, D. H.

Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose

Department of Molecular Physiology and Biophysics, and Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232

Submitted 28 January 2004 ; accepted in final form 25 March 2004

The purpose of this study was to determine whether the sedentary dog is able to autoregulate glucose production (R_a) in response to non-insulin-induced changes (<20 mg/dl) in arterial glucose. Dogs had catheters implanted >16 days before study. Protocols consisted of basal (–30 to 0 min) and bilateral renal arterial phloridzin infusion (0–180 min) periods. Somatostatin was infused, and glucagon and insulin were replaced to basal levels. In one protocol (Phl ± Glc), glucose was allowed to fall from t = 0–90 min. This was followed by a period when glucose was infused to restore euglycemia (90–150 min) and a period when glucose was allowed to fall again (150–180 min). In a second protocol (EC), glucose was infused to compensate for the renal glucose loss due to phloridzin and maintain euglycemia from t = 0–180 min. Arterial insulin, glucagon, cortisol, and catecholamines remained at basal in both protocols. In Phl ± Glc, glucose fell by 20 mg/dl by t = 90 min with phloridzin infusion. R_a did not change from basal in Phl ± Glc despite the fall in glucose for the first 90 min. R_a was significantly suppressed with restoration of euglycemia from t = 90–150 min (P < 0.05) and returned to basal when glucose was allowed to fall from t = 150–180 min. R_a did not change from basal in EC. In conclusion, the liver autoregulates R_a in response to small changes in glucose independently of changes in pancreatic hormones at rest. However, the liver of the resting dog is more sensitive to a small increment, rather than decrement, in arterial glucose.

glucose turnover; phloridzin