Circulating leptin correlates with left ventricular mass in morbid (grade III) obesity before and after weight loss induced by bariatric surgery: a potential role for leptin in mediating human left ventricular hypertrophy.
BACKGROUND
Obesity is frequently associated with left ventricular hypertrophy, even when uncomplicated by hypertension or diabetes mellitus. Left ventricular hypertrophy is an important risk factor for congestive heart failure.


OBJECTIVE
The objective of this study was to evaluate the relationship between leptin and left ventricular mass in uncomplicated, morbid (grade 3) obesity and the existence of leptin receptors and intracellular signaling proteins in the human heart.


METHODS
Left ventricular mass (LVM) was calculated through electrocardiogram reading in normotensive grade III obese patients (World Health Organization classification) undergoing bariatric surgery [laparoscopic adjustable gastric banding (LAGB)] at baseline and 1 yr later. The control group was composed of healthy lean normotensive subjects. Leptin receptors were detected by PCR and immunocytochemistry in human heart biopsies.


METHODS
This study was performed at university hospitals.


METHODS
Thirty-one grade 3 obese patients and 30 healthy nonobese normotensive, age- and sex-matched control subjects were studied.


METHODS
Obese subjects underwent LAGB to induce weight loss and were evaluated at baseline and after 1 yr.


RESULTS
LVM, plasma leptin, glucose, insulin levels, and homeostasis model assessment index were higher in obese than in lean controls (P < 0.01); at univariate regression analysis, LVM correlated with body mass index, leptin, and homeostasis model assessment index; at multiple regression analysis, LVM only correlated with leptin levels (P = 0.001). Obese subjects were reevaluated 1 yr after LAGB, when their body mass index changed from 46.2 +/- 1.24 to 36.6 +/- 1.05 kg/m(2) (P < 0.01); the decrease in LVM correlated only with the decrease in leptin levels (P < 0.01). We demonstrated that long and short isoforms of the leptin receptor and intracellular proteins mediating leptin signaling were expressed in human heart by RT-PCR, immunocytochemistry, or both methods.


CONCLUSIONS
These data suggest that leptin could contribute to the left ventricular hypertrophy in humans.
Perego
Lucia
L
Divisione di Medicina Interna, Istituto Scientifico San Raffaele, Via Olgettina 60, 20132 Milan, Italy.
Pizzocri
Pierluigi
P
Corradi
Domenico
D
Maisano
Francesco
F
Paganelli
Michele
M
Fiorina
Paolo
P
Barbieri
Michelangela
M
Morabito
Alberto
A
Paolisso
Giuseppe
G
Folli
Franco
F
Pontiroli
Antonio E
AE
D000328:Adult; D015992:Body Mass Index; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology*; D020738:Leptin / Q000097:blood* / Q000502:physiology; D008297:Male; D009767:Obesity, Morbid / Q000097:blood* / Q000601:surgery; D011956:Receptors, Cell Surface / Q000032:analysis; D054411:Receptors, Leptin; D012044:Regression Analysis; D015431:Weight Loss
C515448:LEPR protein, human; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin