Electrophysiological characterization of left ventricular myocytes from obese Sprague-Dawley rat.
OBJECTIVE
Obesity is a complex multifactorial disease that is often associated with cardiac arrhythmias. Various animal models have been used extensively to study the effects of obesity on physiological functions, but, to our knowledge, no study related to ionic membrane currents has been performed on isolated cardiac myocytes. Therefore, we examined the electrophysiological characteristics of four ionic currents from isolated left ventricular myocytes of a high-energy (HE)-induced obesity rat model.


METHODS
Male Sprague-Dawley rats were fed with either a control diet or a diet containing 33% kcal as fat (HE) for 14 weeks starting at 6 weeks of age. Voltage-clamp experiments were performed on ventricular myocytes. Leptin receptor (ObR) expression was measured using ObR enzyme-linked immunosorbent assay.


RESULTS
In the HE group, rats designated as obese did not develop a cardiac hypertrophy, either at the organ level or at the cellular level. Densities and kinetics of the L-type calcium current, the transient outward potassium current, the delayed rectifier potassium current, and the sodium-calcium exchange current (I(NCX)) were not significantly different between control and obese rats. A down-regulation of ObR expression was evidenced in the heart of obese rats compared with controls. Acute exposure (5 minutes) of leptin (100 nM) did not induce a significant modification in the current densities either in control or in obese rats, except for I(NCX) density measured in control rats.


CONCLUSIONS
The absence of effect of leptin on I(NCX) in obese rats could be a potential arrhythmogenic substrate in obesity.
Ricci
Estelle
E
Unité Mixte de Recherche Centre National de la Recherche Scientifique 5123, Physiologie Intégrative, Cellulaire et Moléculaire, Université Lyon I, Campus La Doua, 69622 Villeurbanne, France.
Smallwood
Sébastien
S
Chouabe
Christophe
C
Mertani
Hichem C
HC
Raccurt
Mireille
M
Morel
Gérard
G
Bonvallet
Robert
R
D052436:Adipose Tissue, White; D050154:Adiposity / Q000187:drug effects; D000818:Animals; D001835:Body Weight / Q000502:physiology; D048429:Cell Size; D004594:Electrophysiology; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D020738:Leptin / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009765:Obesity / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000378:metabolism; D054411:Receptors, Leptin
D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin