author_facet Camacho, Raul C.
Lacy, D. Brooks
James, Freyja D.
Coker, Robert H.
Wasserman, David H.
Camacho, Raul C.
Lacy, D. Brooks
James, Freyja D.
Coker, Robert H.
Wasserman, David H.
author Camacho, Raul C.
Lacy, D. Brooks
James, Freyja D.
Coker, Robert H.
Wasserman, David H.
spellingShingle Camacho, Raul C.
Lacy, D. Brooks
James, Freyja D.
Coker, Robert H.
Wasserman, David H.
American Journal of Physiology-Endocrinology and Metabolism
Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
Physiology (medical)
Physiology
Endocrinology, Diabetes and Metabolism
author_sort camacho, raul c.
spelling Camacho, Raul C. Lacy, D. Brooks James, Freyja D. Coker, Robert H. Wasserman, David H. 0193-1849 1522-1555 American Physiological Society Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism http://dx.doi.org/10.1152/ajpendo.00040.2004 <jats:p>The purpose of this study was to determine whether the sedentary dog is able to autoregulate glucose production (R<jats:sub>a</jats:sub>) in response to non-insulin-induced changes (&lt;20 mg/dl) in arterial glucose. Dogs had catheters implanted &gt;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<jats:sub>a</jats:sub>did not change from basal in Phl ± Glc despite the fall in glucose for the first 90 min. R<jats:sub>a</jats:sub>was significantly suppressed with restoration of euglycemia from t = 90–150 min ( P &lt; 0.05) and returned to basal when glucose was allowed to fall from t = 150–180 min. R<jats:sub>a</jats:sub>did not change from basal in EC. In conclusion, the liver autoregulates R<jats:sub>a</jats:sub>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.</jats:p> Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose American Journal of Physiology-Endocrinology and Metabolism
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title Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_unstemmed Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_full Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_fullStr Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_full_unstemmed Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_short Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_sort hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
topic Physiology (medical)
Physiology
Endocrinology, Diabetes and Metabolism
url http://dx.doi.org/10.1152/ajpendo.00040.2004
publishDate 2004
physical E269-E274
description <jats:p>The purpose of this study was to determine whether the sedentary dog is able to autoregulate glucose production (R<jats:sub>a</jats:sub>) in response to non-insulin-induced changes (&lt;20 mg/dl) in arterial glucose. Dogs had catheters implanted &gt;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<jats:sub>a</jats:sub>did not change from basal in Phl ± Glc despite the fall in glucose for the first 90 min. R<jats:sub>a</jats:sub>was significantly suppressed with restoration of euglycemia from t = 90–150 min ( P &lt; 0.05) and returned to basal when glucose was allowed to fall from t = 150–180 min. R<jats:sub>a</jats:sub>did not change from basal in EC. In conclusion, the liver autoregulates R<jats:sub>a</jats:sub>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.</jats:p>
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author Camacho, Raul C., Lacy, D. Brooks, James, Freyja D., Coker, Robert H., Wasserman, David H.
author_facet Camacho, Raul C., Lacy, D. Brooks, James, Freyja D., Coker, Robert H., Wasserman, David H., Camacho, Raul C., Lacy, D. Brooks, James, Freyja D., Coker, Robert H., Wasserman, David H.
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description <jats:p>The purpose of this study was to determine whether the sedentary dog is able to autoregulate glucose production (R<jats:sub>a</jats:sub>) in response to non-insulin-induced changes (&lt;20 mg/dl) in arterial glucose. Dogs had catheters implanted &gt;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<jats:sub>a</jats:sub>did not change from basal in Phl ± Glc despite the fall in glucose for the first 90 min. R<jats:sub>a</jats:sub>was significantly suppressed with restoration of euglycemia from t = 90–150 min ( P &lt; 0.05) and returned to basal when glucose was allowed to fall from t = 150–180 min. R<jats:sub>a</jats:sub>did not change from basal in EC. In conclusion, the liver autoregulates R<jats:sub>a</jats:sub>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.</jats:p>
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spelling Camacho, Raul C. Lacy, D. Brooks James, Freyja D. Coker, Robert H. Wasserman, David H. 0193-1849 1522-1555 American Physiological Society Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism http://dx.doi.org/10.1152/ajpendo.00040.2004 <jats:p>The purpose of this study was to determine whether the sedentary dog is able to autoregulate glucose production (R<jats:sub>a</jats:sub>) in response to non-insulin-induced changes (&lt;20 mg/dl) in arterial glucose. Dogs had catheters implanted &gt;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<jats:sub>a</jats:sub>did not change from basal in Phl ± Glc despite the fall in glucose for the first 90 min. R<jats:sub>a</jats:sub>was significantly suppressed with restoration of euglycemia from t = 90–150 min ( P &lt; 0.05) and returned to basal when glucose was allowed to fall from t = 150–180 min. R<jats:sub>a</jats:sub>did not change from basal in EC. In conclusion, the liver autoregulates R<jats:sub>a</jats:sub>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.</jats:p> Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose American Journal of Physiology-Endocrinology and Metabolism
spellingShingle Camacho, Raul C., Lacy, D. Brooks, James, Freyja D., Coker, Robert H., Wasserman, David H., American Journal of Physiology-Endocrinology and Metabolism, Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose, Physiology (medical), Physiology, Endocrinology, Diabetes and Metabolism
title Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_full Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_fullStr Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_full_unstemmed Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_short Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_sort hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
title_unstemmed Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose
topic Physiology (medical), Physiology, Endocrinology, Diabetes and Metabolism
url http://dx.doi.org/10.1152/ajpendo.00040.2004