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Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615
Our aim was to determine whether vagal
transmission is required for the hormonal response to insulin-induced
hypoglycemia in 18-h-fasted conscious dogs. Hollow coils were placed
around the vagus nerves, with animals under general anesthesia, 2 wk before an experiment. On the day of the study they were perfused with
15°C ethanol for the purpose of blocking vagal transmission, either coincident with the onset of insulin-induced hypoglycemia or
after 2 h of established hypoglycemia. In a separate study the coils
were perfused with 37°C ethanol in a sham cooling experiment. The
following parameters were measured: heart rate, arterial plasma glucose, insulin, pancreatic polypeptide, glucagon, cortisol, epinephrine, norepinephrine, glycerol, free fatty acids, and endogenous glucose production. In response to insulin-induced hypoglycemia (42 mg/dl), plasma glucagon peaked at a level that was double the basal
level, and plasma cortisol levels quadrupled. Plasma epinephrine and
norepinephrine levels both rose considerably to 2,135 ± 314 and 537 ± 122 pg/ml, respectively, as did plasma glycerol (330 ± 60%)
and endogenous glucose production (150 ± 20%). Plasma free fatty acids peaked at 150 ± 20% and then returned to basal levels by the end of the study. The hypoglycemia-induced changes were
not different when vagal cooling was initiated after the prior
establishment of hypoglycemia. Similarly, when vagal cooling occurred
concurrently with the initiation of insulin-induced hypoglycemia (46 mg/dl), there were no significant differences in any of the parameters
measured compared with the control. Thus vagal blockade did not prevent
the effect on either the hormonal or metabolic responses to low blood
sugar. Functioning vagal afferent nerves are not required for a normal
response to insulin-induced hypoglycemia.
hepatic glucose production; vagus nerve
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