TY - JOUR
T1 - Failure of nocturnal hypoglycemia to cause daytime hyperglycemia in patients with IDDM
AU - Hirsch, Irl B.
AU - Smith, Lori J.
AU - Havlin, Carolyn E.
AU - Shah, Suresh D.
AU - Clutter, William E.
AU - Cryer, Philip E.
PY - 1990/2
Y1 - 1990/2
N2 - To test the hypothesis that nocturnal hypoglycemia causes postprandial hyperglycemia the next day (the Somogyi phenomenon) in patients with insulin-dependent diabetes mellitus (IDDM), we studied 10 moderately well controlled patients, who were on their usual therapeutic regimens, from 2000 to 2000 on three occasions. On a control day, samples were obtained without intervention. On another day, nocturnal hypoglycemia was prevented (by intravenous infusion of glucose, if necessary, from 2200 to 0400 to keep plasma glucose levels at >5.6 mM). On another day, nocturnal hypoglycemia was induced (by stepped intravenous insulin infusions between 2200 and 0200 to reduce plasma glucose levels to <2.8 mM). After nocturnal hypoglycemia (1.9 ± 0.2 mM), fasting (0800), morning (0800-1100), afternoon (1200-1500), evening (1600-2000), and entire-day (0800-2000) plasma glucose concentrations were no higher than those after prevention of nocturnal hypoglycemia or sampling only. On the control day, fasting and daytime plasma glucose levels were directly related to the preceding 2200 (r = 0.723, P < 0.02, and r = 0.762, P = 0.01, respectively) and nocturnal nadir (r = 0.714, P < 0.02, and r = 0.728, P < 0.02) plasma glucose concentrations. Daytime plasma glucose levels were unrelated to peak nocturnal plasma glucagon, epinephrine, norepinephrine, growth hormone, or cortisol concentrations. We conclude that nocturnal hypoglycemia does not appear to cause clinically important daytime hyperglycemia in patients representative of most patients with IDDM.
AB - To test the hypothesis that nocturnal hypoglycemia causes postprandial hyperglycemia the next day (the Somogyi phenomenon) in patients with insulin-dependent diabetes mellitus (IDDM), we studied 10 moderately well controlled patients, who were on their usual therapeutic regimens, from 2000 to 2000 on three occasions. On a control day, samples were obtained without intervention. On another day, nocturnal hypoglycemia was prevented (by intravenous infusion of glucose, if necessary, from 2200 to 0400 to keep plasma glucose levels at >5.6 mM). On another day, nocturnal hypoglycemia was induced (by stepped intravenous insulin infusions between 2200 and 0200 to reduce plasma glucose levels to <2.8 mM). After nocturnal hypoglycemia (1.9 ± 0.2 mM), fasting (0800), morning (0800-1100), afternoon (1200-1500), evening (1600-2000), and entire-day (0800-2000) plasma glucose concentrations were no higher than those after prevention of nocturnal hypoglycemia or sampling only. On the control day, fasting and daytime plasma glucose levels were directly related to the preceding 2200 (r = 0.723, P < 0.02, and r = 0.762, P = 0.01, respectively) and nocturnal nadir (r = 0.714, P < 0.02, and r = 0.728, P < 0.02) plasma glucose concentrations. Daytime plasma glucose levels were unrelated to peak nocturnal plasma glucagon, epinephrine, norepinephrine, growth hormone, or cortisol concentrations. We conclude that nocturnal hypoglycemia does not appear to cause clinically important daytime hyperglycemia in patients representative of most patients with IDDM.
UR - http://www.scopus.com/inward/record.url?scp=0025095195&partnerID=8YFLogxK
U2 - 10.2337/diacare.13.2.133
DO - 10.2337/diacare.13.2.133
M3 - Article
C2 - 2190769
AN - SCOPUS:0025095195
SN - 0149-5992
VL - 13
SP - 133
EP - 142
JO - Diabetes care
JF - Diabetes care
IS - 2
ER -