In conscious dogs with basal insulin, hyperglycemia produced no net hepatic glucose uptake with basal glucagon, but uptake reached 1.5+/-0.2 mg/kg per min after glucagon withdrawal.
In plain wordsIn dogs with basal insulin, raised blood glucose produced liver glucose uptake after glucagon withdrawal, but none with basal glucagon.
- Peptide
- Glucagon
- Outcome
- DecreaseNet hepatic glucose uptake after glucagon withdrawal
- Study
dogn: not reported in source
Conscious dogs receiving somatostatin and basal insulin replacement- Comparator
- Glucagon withdrawal during hyperglycemia with basal insulin
- Outcome group
- Glycemic control · Liver
- Studied dose
- Dose not stated · intraportal infusionAs given in this study (dog).
Measurements
- Net hepatic glucose uptake
- 1.5 mg/kg per min
- glucagon withdrawn; +/-0.2
Source sentences
Under this circumstance, with the insulin level basal (7+/-1 muU/ml) and the glucagon levels reduced (16+/-2 pg/ml), hyperglycemia (mean increment of 130 mg/dl) promoted marked net hepatic glucose uptake (1.5+/-0.2 mg/kg per min) and glycogen deposition.
3 context sentences(design, population, supporting numbers)
The acute induction of hyperglycemia (mean increment of 121 mg/dl) in the presence of basal levels of insulin (7+/-1 muU/ml) and glucagon (76+/-3 pg/ml) resulted in a 56% decrease in net hepatic glucose production but did not cause net hepatic glucose uptake.
The above protocol was repeated with the exception that glucagon was withdrawn (83% decrease in plasma glucagon) coincident with the induction of hyperglycemia.
To accomplish this, glucose was infused into conscious dogs whose basal insulin and glucagon secretion had been replaced by exogenous intraportal insulin and glucagon infusion after somatostatin inhibition of endogenous pancreatic hormone release.