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Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Related Experiment Video

Updated: Jun 8, 2026

Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo
10:35

Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo

Published on: April 6, 2022

Continuous low-dose fructose infusion does not reverse glucagon-mediated decrease in hepatic glucose utilization.

Paulette M Johnson1, Sheng-Song Chen, Tammy S Santomango

  • 1Division of Pediatric Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-0615, USA.

Metabolism: Clinical and Experimental
|October 14, 2010
PubMed
Summary

Continuous fructose infusion does not increase liver glucose uptake during total parenteral nutrition (TPN). It also fails to counteract the inhibitory effects of glucagon on hepatic glucose uptake in TPN-adapted dogs.

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A Model of Chronic Nutrient Infusion in the Rat
08:18

A Model of Chronic Nutrient Infusion in the Rat

Published on: August 14, 2013

Related Experiment Videos

Last Updated: Jun 8, 2026

Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo
10:35

Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo

Published on: April 6, 2022

A Model of Chronic Nutrient Infusion in the Rat
08:18

A Model of Chronic Nutrient Infusion in the Rat

Published on: August 14, 2013

Area of Science:

  • Metabolism
  • Hepatology
  • Nutritional Science

Background:

  • The liver adapts to total parenteral nutrition (TPN) by increasing glucose consumption and lactate release.
  • Elevated glucagon levels, common during inflammatory stress, inhibit hepatic glucose uptake during TPN.
  • Acute fructose infusion can enhance liver glucose uptake, but its effect during continuous TPN with elevated glucagon is unknown.

Purpose of the Study:

  • To investigate if continuous fructose infusion can overcome the glucagon-mediated inhibition of hepatic glucose uptake during TPN.
  • To determine the impact of continuous fructose administration on liver glucose metabolism in a TPN model.

Main Methods:

  • Studies were conducted in conscious, insulin-treated, pancreatectomized dogs adapted to TPN.
  • Animals were assigned to four groups: TPN, TPN + fructose, TPN + glucagon, or TPN + fructose + glucagon for 63 hours.
  • Insulin, fructose, and glucagon were infused portally, with glucose infusion adjusted to maintain euglycemia.

Main Results:

  • Continuous fructose infusion did not significantly enhance net hepatic glucose uptake compared to control TPN.
  • Fructose infusion did not overcome the decrease in hepatic glucose uptake caused by glucagon.
  • Net hepatic glucose uptake was significantly lower in the glucagon groups (GGN and F+GGN) compared to the non-glucagon groups (C and F).

Conclusions:

  • Continuous fructose infusion is ineffective in augmenting liver glucose uptake during TPN.
  • Fructose administration cannot overcome the inhibitory effects of glucagon on hepatic glucose uptake in this model.
  • These findings suggest fructose is not a viable strategy to enhance glucose utilization or counteract glucagon's effects in TPN.