Hepatic parasympathetic (HISS) control of insulin sensitivity determined by feeding and fasting

In response to insulin, a hormone [hepatic insulin sensitizing substance (HISS)] is released from the liver to stimulate glucose uptake in skeletal muscle but not liver or gut. The aim was to characterize dynamic control of HISS action in response to insulin and regulation of release by hepatic para...

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Bibliographic Details
Published in:American journal of physiology: Gastrointestinal and liver physiology 2001-07, Vol.281 (1), p.G29-G36
Main Authors: Lautt, W W, Macedo, M P, Sadri, P, Takayama, S, Duarte Ramos, F, Legare, D J
Format: Article
Language:English
Subjects:
Anesthesia
Animals
Atropine - pharmacology
Autonomic Denervation
Dose-Response Relationship, Drug
Eating - drug effects
Eating - physiology
Enzyme Inhibitors - pharmacology
Fasting - physiology
Hypoglycemic Agents - pharmacology
Insulin - pharmacology
Insulin Resistance - physiology
Liver - enzymology
Liver - innervation
Male
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - metabolism
omega-N-Methylarginine - pharmacology
Parasympathetic Nervous System - physiology
Parasympatholytics - pharmacology
Postprandial Period - drug effects
Postprandial Period - physiology
Rats
Rats, Sprague-Dawley
Stomach - innervation
Stomach - physiology
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Summary:In response to insulin, a hormone [hepatic insulin sensitizing substance (HISS)] is released from the liver to stimulate glucose uptake in skeletal muscle but not liver or gut. The aim was to characterize dynamic control of HISS action in response to insulin and regulation of release by hepatic parasympathetic nerves. Insulin action was assessed by the rapid insulin sensitivity test, where the index is the glucose required (mg/kg) to maintain euglycemia after a bolus of insulin. Blocking HISS release by interruption of the hepatic parasympathetic nerves by surgical denervation, atropine, or blockade of hepatic nitric oxide synthase produced similar degrees of insulin resistance and revealed a similar dynamic pattern of hormone action that began 3--4 min after, and continued for 9--10 min beyond, insulin action (50 mU/kg). HISS action accounted for 56.5 +/- 3.5% of insulin action at insulin doses from 5 to 100 mU/kg (fed). We also tested the hypothesis that HISS release is controlled by the feed/fast status. Feeding resulted in maximal HISS action, which decreased progressively with the duration of fasting.
ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.2001.281.1.g29