<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Leptin, the gene product of adipose tissue that signals
caloric plentitude <italic>via</italic> central nervous system
receptors, may also have diverse peripheral metabolic
actions. Of paramount interest has been the
potential interaction(s) between leptin and insulin.
Insofar as insulin alters leptin secretion/action (or
<italic>vice versa</italic>), dysregulation of this system could contribute
to disease states such as diabetes.</p> <p>The purpose of this study was to examine the
effect of exogenous insulin on serum leptin in
children with newly-diagnosed Type 1 diabetes.
Since these patients are hypoinsulinemic (insulindeplet.
ed) at diagnosis, they present an ideal
opportunity to examine the effect of insulin repletion
on serum leptin. Seventeen patients were
enrolled. At baseline (prior to insulin therapy),
leptin levels were 4.3 ± 1.1ng/ml; they were not statistically
related to the baseline serum insulin or
illness severity. There was no significant change in
serum leptin before, shortly (1–6 days) or several
weeks (3–26 weeks) after insulin treatment even
when the data was corrected for changes in BMI,
hemoglobin A<sub>1C</sub>, and daily insulin dose. Since
repletion of the insulin deficiency that is present
in non-acidotic, ambulatory patients with new
onset Type 1 diabetes did not alter serum leptin,
these results argue against an effect of insulin on
serum leptin in the absence of the acute diabetic
ketoacidosis. Because as the recuperative months
following the diagnosis of new onset Type 1
diabetes are marked by weight gain, the absence
of a rise in serum leptin might also indicate
either an adaptive (weight permissive) or pathologic
(impaired secretory) deficit.</p>
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Int J Exp Diabetes Res. 2001; 2(2):121-127