Changes in plasma leptin during the treatment of diabetic ketoacidosis

To test the hypothesis that insulin regulates leptin, we measured the plasm a leptin concentration before and during treatment of diabetic ketoacidosis (DKA), a condition characterized by extreme insulin deficiency. The study included 17 patients with type 1 diabetes (7 males and 10 females), aged 10 +/- 1 yr (mean +/- se), with a body mass index of 17.6 +/- 1.9 kg/m(2). Pa tients were treated with continuous insulin infusion and fluid and electrol yte replacement. Plasma leptin was measured every 6 h in the first 24 h, du ring which patients received a total insulin dose of 0.6-2.0 U/kg. Plasma l eptin concentrations were also measured in a control group of 29 stable typ e 1 diabetic children (12 males and 17 females) and 25 healthy children (11 males and 14 females), aged 11 +/- 1 yr, with a body mass index of 18.5 +/ - 1.1 kg/m(2). Before treatment, plasma leptin concentrations were signific antly lower in patients with DKA than those in diabetic and healthy control s (4.9 +/- 1.2 us. 9.0 +/- 1.8 and 11.2 +/- 2.1 ng/mL, respectively; P < 0. 05). In the DKA patients, plasma leptin increased to 6.4 +/- 1.5, 7.5 +/- 1 .9, 9.1 +/- 2.7, and 8.9 +/- 2.5 at 6, 12, 18, and 24 h, respectively, afte r starting treatment (P = 0.001). Thus, leptin levels increased by 38 +/- 1 0% and 92 +/- 38% within 6 and 24 h of starting treat ment. There was no di fference in the change in plasma leptin by 24 h between subjects who could eat (n = 7) and those who could not (n = 10). The plasma leptin increase wa s paralleled by a rise in insulin leveland a decline in glucose and cortiso l levels at 6 and 24 h. In conclusion, DKA was associated with decreased pl asma leptin concentrations. Treatment resulted in a significant increase in plasma leptin, which may be due to the effect of insulin on leptin product ion. Our data lend support to the hypothesis that insulin is the link betwe en caloric intake and plasma leptin.