Stress induced by central cholinergic stimulation alters regional distribution of glucose uptake

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The purpose of the present study was to determine whether the intracerebroventricular (ICV) injection of carbachol enhances whole body glucose utilization and, if so, how this cholinergic agonist influences in vivo regional glucose uptake. An ICV cannula and vascular catheters were placed in rats prior to the experiment. Whole body glucose flux was assessed in overnight-fasted conscious unrestrained rats using [3-3H]glucose. Hyperglycemia was elicited 30 min after carbachol (50 nmol), and resulted from an increased rate of hepatic glucose production (135%) that exceeded an elevated rate of peripheral glucose uptake (105%). The glucose metabolic clearance rate was not altered by carbachol. Despite the hyperglycemia, no compensatory increase in plasma insulin levels were observed. Carbachol, however, did increase glucagon (64-164%), catecholamines (3.5- to 15-fold), and corticosterone (62-160%). Complete α-and β-adrenergic blockade prevented the carbachol-induced changes in glucose flux. In vivo glucose uptake (Rg) by individual tissues was determined at the peak of the carbachol-induced hyperglycemia, using [2-14C]deoxyglucose. In addition, a separate group of control rats received an intravenous hormone infusion that increased plasma glucose, glucagon, and catecholamine levels to the same extent seen in carbachol-treated rats. The Rg in liver, spleen, and lung was elevated to a similar extent in carbachol-treated (60, 47, and 48%, respectively) and hormone-infused (60, 53, and 70%, respectively) rats. In contrast, whereas the hormone infusion increased Rg by ileum, skin, and kidney (80, 67, and 110%, respectively), no change was observed in these tissues from rats injected with carbachol. Rg by gastrocnemius was increased 141% after carbachol, but only 66% in hormone-infused rats. Brain Rg was enhanced (21%) only in the carbachol-treated animals. These results indicate that carbachol diverts glucose away from specific tissues, as evidenced by the lack of increase in Rg by ileum, skin, and kidney, and preferentially enhances glucose uptake by skeletal muscle and brain. The redistribution of glucose disposal by carbachol can not be explained by the prevailing hyperglycemia and increased circulating levels of stress hormones.

Original languageEnglish (US)
Pages (from-to)36-42
Number of pages7
JournalShock
Volume1
Issue number1
DOIs
StatePublished - Jan 1 1994

Fingerprint

Carbachol
Cholinergic Agents
Glucose
Hyperglycemia
Hormones
Glucagon
Ileum
Catecholamines
Metabolic Clearance Rate
Kidney
Cholinergic Agonists
Vascular Access Devices
Skin
Liver
Deoxyglucose
Brain
Corticosterone
Intravenous Infusions
Adrenergic Agents
Skeletal Muscle

All Science Journal Classification (ASJC) codes

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine

Cite this

@article{66699a78783845b5a36edd947c8be249,
title = "Stress induced by central cholinergic stimulation alters regional distribution of glucose uptake",
abstract = "The purpose of the present study was to determine whether the intracerebroventricular (ICV) injection of carbachol enhances whole body glucose utilization and, if so, how this cholinergic agonist influences in vivo regional glucose uptake. An ICV cannula and vascular catheters were placed in rats prior to the experiment. Whole body glucose flux was assessed in overnight-fasted conscious unrestrained rats using [3-3H]glucose. Hyperglycemia was elicited 30 min after carbachol (50 nmol), and resulted from an increased rate of hepatic glucose production (135{\%}) that exceeded an elevated rate of peripheral glucose uptake (105{\%}). The glucose metabolic clearance rate was not altered by carbachol. Despite the hyperglycemia, no compensatory increase in plasma insulin levels were observed. Carbachol, however, did increase glucagon (64-164{\%}), catecholamines (3.5- to 15-fold), and corticosterone (62-160{\%}). Complete α-and β-adrenergic blockade prevented the carbachol-induced changes in glucose flux. In vivo glucose uptake (Rg) by individual tissues was determined at the peak of the carbachol-induced hyperglycemia, using [2-14C]deoxyglucose. In addition, a separate group of control rats received an intravenous hormone infusion that increased plasma glucose, glucagon, and catecholamine levels to the same extent seen in carbachol-treated rats. The Rg in liver, spleen, and lung was elevated to a similar extent in carbachol-treated (60, 47, and 48{\%}, respectively) and hormone-infused (60, 53, and 70{\%}, respectively) rats. In contrast, whereas the hormone infusion increased Rg by ileum, skin, and kidney (80, 67, and 110{\%}, respectively), no change was observed in these tissues from rats injected with carbachol. Rg by gastrocnemius was increased 141{\%} after carbachol, but only 66{\%} in hormone-infused rats. Brain Rg was enhanced (21{\%}) only in the carbachol-treated animals. These results indicate that carbachol diverts glucose away from specific tissues, as evidenced by the lack of increase in Rg by ileum, skin, and kidney, and preferentially enhances glucose uptake by skeletal muscle and brain. The redistribution of glucose disposal by carbachol can not be explained by the prevailing hyperglycemia and increased circulating levels of stress hormones.",
author = "Lang, {Charles H.}",
year = "1994",
month = "1",
day = "1",
doi = "10.1097/00024382-199401000-00007",
language = "English (US)",
volume = "1",
pages = "36--42",
journal = "Shock",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

Stress induced by central cholinergic stimulation alters regional distribution of glucose uptake. / Lang, Charles H.

In: Shock, Vol. 1, No. 1, 01.01.1994, p. 36-42.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Stress induced by central cholinergic stimulation alters regional distribution of glucose uptake

AU - Lang, Charles H.

PY - 1994/1/1

Y1 - 1994/1/1

N2 - The purpose of the present study was to determine whether the intracerebroventricular (ICV) injection of carbachol enhances whole body glucose utilization and, if so, how this cholinergic agonist influences in vivo regional glucose uptake. An ICV cannula and vascular catheters were placed in rats prior to the experiment. Whole body glucose flux was assessed in overnight-fasted conscious unrestrained rats using [3-3H]glucose. Hyperglycemia was elicited 30 min after carbachol (50 nmol), and resulted from an increased rate of hepatic glucose production (135%) that exceeded an elevated rate of peripheral glucose uptake (105%). The glucose metabolic clearance rate was not altered by carbachol. Despite the hyperglycemia, no compensatory increase in plasma insulin levels were observed. Carbachol, however, did increase glucagon (64-164%), catecholamines (3.5- to 15-fold), and corticosterone (62-160%). Complete α-and β-adrenergic blockade prevented the carbachol-induced changes in glucose flux. In vivo glucose uptake (Rg) by individual tissues was determined at the peak of the carbachol-induced hyperglycemia, using [2-14C]deoxyglucose. In addition, a separate group of control rats received an intravenous hormone infusion that increased plasma glucose, glucagon, and catecholamine levels to the same extent seen in carbachol-treated rats. The Rg in liver, spleen, and lung was elevated to a similar extent in carbachol-treated (60, 47, and 48%, respectively) and hormone-infused (60, 53, and 70%, respectively) rats. In contrast, whereas the hormone infusion increased Rg by ileum, skin, and kidney (80, 67, and 110%, respectively), no change was observed in these tissues from rats injected with carbachol. Rg by gastrocnemius was increased 141% after carbachol, but only 66% in hormone-infused rats. Brain Rg was enhanced (21%) only in the carbachol-treated animals. These results indicate that carbachol diverts glucose away from specific tissues, as evidenced by the lack of increase in Rg by ileum, skin, and kidney, and preferentially enhances glucose uptake by skeletal muscle and brain. The redistribution of glucose disposal by carbachol can not be explained by the prevailing hyperglycemia and increased circulating levels of stress hormones.

AB - The purpose of the present study was to determine whether the intracerebroventricular (ICV) injection of carbachol enhances whole body glucose utilization and, if so, how this cholinergic agonist influences in vivo regional glucose uptake. An ICV cannula and vascular catheters were placed in rats prior to the experiment. Whole body glucose flux was assessed in overnight-fasted conscious unrestrained rats using [3-3H]glucose. Hyperglycemia was elicited 30 min after carbachol (50 nmol), and resulted from an increased rate of hepatic glucose production (135%) that exceeded an elevated rate of peripheral glucose uptake (105%). The glucose metabolic clearance rate was not altered by carbachol. Despite the hyperglycemia, no compensatory increase in plasma insulin levels were observed. Carbachol, however, did increase glucagon (64-164%), catecholamines (3.5- to 15-fold), and corticosterone (62-160%). Complete α-and β-adrenergic blockade prevented the carbachol-induced changes in glucose flux. In vivo glucose uptake (Rg) by individual tissues was determined at the peak of the carbachol-induced hyperglycemia, using [2-14C]deoxyglucose. In addition, a separate group of control rats received an intravenous hormone infusion that increased plasma glucose, glucagon, and catecholamine levels to the same extent seen in carbachol-treated rats. The Rg in liver, spleen, and lung was elevated to a similar extent in carbachol-treated (60, 47, and 48%, respectively) and hormone-infused (60, 53, and 70%, respectively) rats. In contrast, whereas the hormone infusion increased Rg by ileum, skin, and kidney (80, 67, and 110%, respectively), no change was observed in these tissues from rats injected with carbachol. Rg by gastrocnemius was increased 141% after carbachol, but only 66% in hormone-infused rats. Brain Rg was enhanced (21%) only in the carbachol-treated animals. These results indicate that carbachol diverts glucose away from specific tissues, as evidenced by the lack of increase in Rg by ileum, skin, and kidney, and preferentially enhances glucose uptake by skeletal muscle and brain. The redistribution of glucose disposal by carbachol can not be explained by the prevailing hyperglycemia and increased circulating levels of stress hormones.

UR - http://www.scopus.com/inward/record.url?scp=0028367730&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028367730&partnerID=8YFLogxK

U2 - 10.1097/00024382-199401000-00007

DO - 10.1097/00024382-199401000-00007

M3 - Article

VL - 1

SP - 36

EP - 42

JO - Shock

JF - Shock

SN - 1073-2322

IS - 1

ER -