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Reduced paraventricular nucleus norepinephrine responsiveness in obesity-prone rats
Ist Teil von
American journal of physiology. Regulatory, integrative and comparative physiology, 1996-02, Vol.270 (2), p.456-R461
Ort / Verlag
United States
Erscheinungsjahr
1996
Quelle
MEDLINE
Beschreibungen/Notizen
B. E. Levin
Neurology Service, Department of Veterans Affairs Medical Center, East Orange, New Jersey 07018, USA.
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.