Leptin before and after insulin therapy in children with new-onset type 1 diabetes

被引:48
|
作者
Hanaki, K
Becker, DJ
Arslanian, SA
机构
[1] Univ Pittsburgh, Childrens Hosp Pittsburgh, Div Endocrinol, Pittsburgh, PA 15213 USA
[2] Univ Pittsburgh, Childrens Hosp Pittsburgh, Div Pediat Endocrinol, Pittsburgh, PA 15213 USA
[3] Univ Pittsburgh, Childrens Hosp Pittsburgh, Div Metab, Pittsburgh, PA 15213 USA
[4] Univ Pittsburgh, Childrens Hosp Pittsburgh, Div Diabet Mellitus, Pittsburgh, PA 15213 USA
关键词
D O I
10.1210/jc.84.5.1524
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Serum leptin levels reflect the amount of body fat. However, several reports suggest that insulin may also regulate serum leptin levels. This study was aimed at testing whether leptin levels are low in newly diagnosed patients with type 1 diabetes and increase after institution of insulin therapy. Nineteen children with new-onset type 1 diabetes were studied. Serum leptin levels were measured at presentation before insulin therapy was initiated (day 0), 1 day after insulin therapy (day 1), 3-5 days after insulin therapy (day 3-5), and at 3 months of follow-up (3 months). The control group consisted of 19 healthy children matched for age and body mass index. On day 0 leptin levels were lower in the patients compared with those in controls (3.3 +/- 0.2 us. 6.2 +/- 0.9 ng/mL; P < 0.005). After insulin therapy, leptin levels increased significantly by day 1 without significant weight change and became comparable to control values by days 3-5. Before insulin therapy, leptin did not correlate with weight, body mass index, or hemoglobin A(1c). After insulin therapy, leptin levels on days 3-5 correlated with insulin dose (r = 0.43; P = 0.03). The results of this study demonstrate that children with new-onset type 1 diabetes have low leptin levels before insulin therapy. Leptin levels increase within 24 h of insulin therapy and become comparable to nondiabetic levels by 3-5 days. This rapid increase in leptin after 24 h of insulinization is independent of changes in body weight and is postulated to be due to a stimulatory effect of insulin on leptin production, nutritional replenishment, or both factors together.
引用
收藏
页码:1524 / 1526
页数:3
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