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Please use this identifier to cite or link to this item: http://hdl.handle.net/1993/3008

Title: Glucose disposal by insulin, but not IGF-1, is dependent on the hepatic parasympathetic nerves
Authors: Sadri, P
Lautt, WW
Keywords: HISS
RIST
atropine
insulin sensitivity
fasting
GROWTH-FACTOR-I
SENSITIVITY
METABOLISM
RESISTANCE
BLOCKADE
RATS
CIRRHOSIS
Issue Date: 31-Oct-2000
Citation: 0008-4212; CAN J PHYSIOL PHARMACOL, OCT 2000, vol. 78, no. 10, p.807 to 812.
Abstract: Insulin-like growth factor-1 (IGF-1) has many insulin-like activities, including stimulation of glucose uptake in skeletal muscle. However, those with diabetes or chronic liver disease are insulin resistant but show a normal hypoglycemic response to IGF-1. We have previously shown that insulin sensitivity depends on a hepatic parasympathetic reflex release of a hormone from the liver. The hypothesis was tested that insulin action, but not IGF-1 action, is dependent on the hepatic parasympathetic reflex. Glucose disposal in response to three doses of IGF-1 (25, 100, 200 mu g/kg) was determined in rats. IGF-1 at 200 mu g/kg had similar effect on glucose disposal as did 50 mU/kg of insulin. Interruption of the hepatic parasympathetic reflex either by surgical ablation of the anterior nerve plexus or by atropine (1.0 mg/kg) resulted in insulin, but not IGF-1, resistance. Sixteen hours of fasting resulted in insulin, but not IGF-1, resistance. In conclusion, insulin, but not IGF-1, triggers the hepatic parasympathetic dependent release of a putative hepatic insulin sensitizing substance (HISS) that stimulates glucose uptake in skeletal muscle.
URI: http://hdl.handle.net/1993/3008
DOI: http://dx.doi.org/10.1139/y00-060
Appears in Collection(s):Research Publications (UofM Student, Faculty and Staff only access)

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