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Reduced paraventricular nucleus norepinephrine responsiveness in obesity-prone rats.

Male Sprague-Dawley rats prone to develop diet-induced obesity (DIO-prone) when fed a high-energy diet have several deficits in brain noradrenergic function compared with diet-resistant (DR) rats. To further characterize these deficits, 3-mo-old rats were identified prospectively as being DIO- or DR-prone rats by their high (DIO-prone) or low (DR-prone) 24-h urine norepinephrine (NE) levels. Saturation-binding studies with 0.2-20 nM [3H] paraminoclonidine to alpha 2-adrenoceptors showed 27-54% decreases in maximal binding capacity in the anterior hypothalamic area, paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMN), and basolateral amygdalar nucleus of DIO- vs. DR-prone rats. The areal extent of the VMN was selectively reduced by 15% in DIO-prone rats. Freely moving, catheterized DIO-prone rats had higher basal plasma glucose (9%) and insulin (31%) levels. Bilateral 3 nmol NE infusions over 20 min into the PVN increased plasma NE (175%) and insulin (31%) levels in DR-prone rats but decreased plasma insulin by 17% and did not alter plasma NE levels in DIO-prone rats. PVN NE infusions had no effect on plasma epinephrine or glucose or motor activity in either group. Thus reduced PVN alpha 2-adrenoceptor binding is associated with a selective reduction in NE-induced sympathetic activation and insulin release, suggesting a postsynaptic, noradrenergic deficit in DIO-prone rats.