Leptin levels in diabetic and nondiabetic subjects

Citation
P. Tatti et al., Leptin levels in diabetic and nondiabetic subjects, ENDOCRINE, 15(3), 2001, pp. 305-308
Citations number
18
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ENDOCRINE
ISSN journal
1355008X → ACNP
Volume
15
Issue
3
Year of publication
2001
Pages
305 - 308
Database
ISI
SICI code
1355-008X(200108)15:3<305:LLIDAN>2.0.ZU;2-C
Abstract
The role of leptin in human pathophysiology elicits considerable interest i n view of its potential role as a treatment tool for obesity and other insu lin resistant states, like type 2 diabetes mellitus (T2DM). Leptin has been extensively studied in obese humans, and much less so in other pathologic conditions. Leptin level has been reported to correlate with percent body f at mass (%FM), fasting serum insulin (FPI), insulin sensitivity and blood p ressure. The aim of this study was to compare the leptin concentration, and its relationship with some anthropometric and biochemical parameters relat ed to insulin resistance in 140 moderately obese type 2 diabetics (T2DM) an d 160 age and weight matched non-diabetic controls in order to get a better insight into the possible role of leptin in the metabolic abnormalities of diabetes. The leptin levels were lower in the diabetic population only whe n both sexes were combined (p < 0.05) and were higher in the females of bot h groups. Among the nondiabetics, the leptin levels appeared to be related to BMI, %FM, HDL and FPI, while this was not the case in the diabetics. Ar correction for BMI, leptin appeared to be correlated with the FPI levels on ly in the non-diabetic female. When plasma leptin was included in a multipl e linear regression model with plasma leptin as a dependent variable, BMI, W:Hr and FPI levels were significantly related to leptin in the non diabeti c population, while no relationship reached the level of statistical signif icance among the diabetics, with the exception of the borderline value for the FPI (p = .052). In conclusion, leptin levels were independent of any of the parameters examined in our diabetic population, possibly due to the pr ogressive loss of the normal mechanisms of leptin regulation with advancing disease. Conclusive data can only be obtained from the longitudinal study of a cohort of newly diagnosed diabetic subjects.