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2014 ; 128
(ä): 126-32
Nephropedia Template TP
Grillo CA
; Mulder P
; Macht VA
; Kaigler KF
; Wilson SP
; Wilson MA
; Reagan LP
Physiol Behav
2014[Apr]; 128
(ä): 126-32
PMID24518861
show ga
Obesity-induced changes in the metabolic and endocrine milieu elicit deficits in
neuroplasticity, including increased risk for development of neuropsychiatric
disorders such as depressive illness. We previously demonstrated that
downregulation of hypothalamic insulin receptors (hypo-IRAS) elicits a phenotype
that is consistent with features of the metabolic syndrome (MetS) and that rats
with this phenotype exhibit deficits in neuronal plasticity, including
depressive-like behaviors such as anhedonia. Since food restriction paradigms
effectively inhibit obesity-induced neuroplasticity deficits, the aim of the
current study was to determine whether food restriction could reverse
obesity-induced anhedonia in hypo-IRAS rats. Compared to hypo-IRAS rats provided
ad lib food access, food restriction paradigms that were initiated either prior
to increases in body weight or following development of the MetS/obesity
phenotype effectively restored sucrose intake in hypo-IRAS rats. Moreover, food
restriction paradigms were able to prevent and reverse the changes in the
endocrine/metabolic/inflammatory milieu observed in hypo-IRAS, such as increases
in plasma leptin and triglyceride levels and increases in pro-inflammatory
cytokines such as IL-1?, IL-6 and C-reactive protein (CRP). Collectively, these
results demonstrate that obesity-induced anhedonia is a reversible process and
identify some potential mechanistic mediators that may be responsible for
co-morbid depression in obesity.
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