Obesity Surgery, 12, 623-627 © FD-Communications Inc. Obesity Surgery, 12, 2002 623 Background: The authors evaluated the relationship between leptin and the clinical, anthropometric and metabolic variables connected to the metabolic syn- drome in obese individuals. Methods: A large group of patients with different degrees of obesity was investigated: body mass index (BMI) values, serum leptin, fasting glucose and insulin, triglycerides and HDL-cholesterol concen- trations, insulin resistance index and blood pressure were measured. Results: On multiple regression analysis, serum leptin levels appeared to be positively correlated to the BMI and to the serum HDL-cholesterol concen- tration. Principal component factor analysis revealed three factors, explaining 61.3% of the total variance of the sample. General features of these factors were: factor 1 – BMI values and serum leptin and fasting glucose concentration; factor 2 – sys- tolic and diastolic blood pressure and serum triglyc- erides and HDL-cholesterol concentration; factor 3 – fasting serum insulin concentration and insulin resistance index. Conclusions: In obese subjects multiple factors underlie the metabolic syndrome and therefore more than one mechanism may account for the clustering characteristics. In obese patients leptin loads only one factor, and therefore leptin does not appear to be a key feature in the metabolic syndrome. On the contrary, multiple correlation and factor analysis data give rise to the hypothesis that in obese patients, leptin may play a protective role against cardiovascular risk. Key words: Leptin, metabolic syndrome, obesity, morbid obesity Introduction Metabolic syndrome defines a network of interre- lated conditions, the chief of which are overall and central obesity, disturbances of glucose metabo- lism, serum lipid alterations and high blood pres- sure. These conditions, either separately or clus- tered together, carry an increased risk of cardiovas- cular disease, affecting overall morbidity and mor- tality. Leptin is an adipocyte-derived product of the ob gene that is thought to regulate eating in experi- mental animals: leptin acts as a satiety signal, while reduced leptin levels have been suggested to lead to increased hunger. 1-4 Thus, leptin might modulate food intake according to the amount of energy stores. In humans, serum leptin concentra- tion is in a close positive correlation with BMI val- ues and is in an even stronger association with adi- pose tissue size, 5-7 thus indicating the poor reliabil- ity of this simple animal model. It has been specu- lated that a resistance to leptin action develops in obese patients, leading to accumulation of body fat without any effect on energy intake. 8,9 This is con- firmed by the lack of any correlation between rest- ing energy expenditure and serum leptin concen- tration observed in some studies. Furthermore, ani- mal studies suggested that specific HDL-choles- terol catabolic pathways are likely regulated by obesity and/or by leptin signaling; 10 furthermore, serum leptin production in man has been found to be related to arterial hypertension 11 and insulin resistance. 12 These observations led to the hypoth- esis that leptin may play a coordinating role in the metabolic syndrome. 13,14 This study was undertaken to gain insight into Relationships of Serum Leptin to Clinical and Anthropometric Findings in Obese Patients Gian Franco Adami; Dario Civalleri; Franca Cella; Giuseppe Marinari; Giovanni Camerini; Francesco Papadia; Nicola Scopinaro Dipartimento di Discipline Chirurgiche, Università di Genova, Genova, Italy Reprint requests to: Dr. Gian Franco Adami, Dipartimento di Discipline Chirurgiche e Metodologie Integrate, largo R. Benzi, 8, 16132 Genova, Italy. Fax: 39 10 502754; e-mail: adami@unige.it