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Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905
People with type 2 diabetes have defects in both
- and 
-cell function. To determine whether lack of suppression of
glucagon causes hyperglycemia when insulin secretion is impaired but
not when insulin secretion is intact, twenty nondiabetic subjects were
studied on two occasions. On both occasions, a "prandial" glucose
infusion was given over 5 h while endogenous hormone secretion was
inhibited. Insulin was infused so as to mimic either a nondiabetic (n = 10) or diabetic
(n = 10) postprandial profile.
Glucagon was infused at a rate of 1.25 ng · kg
1 · min1,
beginning either at time zero to
prevent a fall in glucagon (nonsuppressed study day) or at 2 h to
create a transient fall in glucagon (suppressed study day). During the
"diabetic" insulin profile, lack of glucagon suppression resulted
in a marked increase (P < 0.002) in
both the peak glucose concentration (11.9 ± 0.4 vs. 8.9 ± 0.4 mmol/l) and the area above basal of glucose (927 ± 77 vs. 546 ± 112 mmol · l1 · 6 h) because of impaired (P < 0.001)
suppression of glucose production. In contrast, during the
"nondiabetic" insulin profile, lack of suppression of glucagon
resulted in only a slight increase (P < 0.02) in the peak glucose concentration (9.1 ± 0.4 vs. 8.4 ± 0.3 mmol/l) and the area above basal of glucose (654 ± 146 vs. 488 ± 118 mmol · l1 · 6 h). Of interest, when glucagon was suppressed, glucose concentrations differed only minimally during the nondiabetic and diabetic insulin profiles. These data indicate that lack of suppression of glucagon can
cause substantial hyperglycemia when insulin availability is limited,
therefore implying that inhibitors of glucagon secretion and/or
glucagon action are likely to be useful therapeutic agents in such individuals.
glucose production; glucose disappearance; postprandial hypoglycemia; type 2 diabetes; glucagon; insulin
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