Abstract
BackgroundSuppression of body weight and symptom of anorexia are major symptoms of depression. Recently, we reported that chronic social defeat stress (CSDS) induced suppression of body weight gain and anorexic feeding behavior in rats. These abnormalities were the result of disrupted malonyl-coenzyme A (CoA) signaling pathway in the hypothalamus. However, the condition of peripheral leptin and its hypothalamic downstream signal molecules which regulate hypothalamic malonyl-CoA level in the CSDS-exposed rats (CSDS rats) is still unknown.ResultsCSDS rats showed suppressed body weight gain and food intake. The weight of the CSDS rats’ epididymal white adipose tissues was decreased when compared to the control rats. The plasma cholesterol concentration was decreased significantly in the CSDS rats compared to the control rats (P < 0.05). The plasma glucose concentration was slightly decreased in the CSDS rats compared to the control rats (P < 0.1). The expression of leptin mRNA in epididymal white adipose tissues and the plasma leptin concentration were decreased in CSDS rats. Furthermore, the phosphorylation of the hypothalamic downstream signals of leptin, including extracellular signal-regulated kinase 1/2 (ERK1/2) and signal transducer and activator of transcription 3 (STAT3), was decreased in CSDS rats.ConclusionsOur results indicated that decreased peripheral leptin expression in CSDS rats could down-regulate the hypothalamic downstream signaling pathways of leptin while suppressed food intake. These data indicate that CSDS induces the down-regulation of hypothalamic AMPK following the elevation of hypothalamic malonyl-CoA levels and is independent of peripheral leptin and glucose.
Highlights
Suppression of body weight and symptom of anorexia are major symptoms of depression
Because feeding behavior is regulated by the central nervous system, in particular the hypothalamus, we focused on the hypothalamic signal molecules and metabolites that were related to feeding behaviors in chronic social defeat stress (CSDS) rats [4]
We focused on peripheral leptin expression and its downstream hypothalamic signaling pathway and blood plasma components including protein, triglycerides, cholesterol and glucose in CSDS rats to elucidate the effectors for hypothalamic Adenosine monophosphate-activated protein kinase (AMPK) and malonyl-coenzyme A (CoA) signaling pathways in CSDS-induced symptom of anorexia
Summary
We reported that chronic social defeat stress (CSDS) induced suppression of body weight gain and anorexic feeding behavior in rats. These abnormalities were the result of disrupted malonyl-coenzyme A (CoA) signaling pathway in the hypothalamus. A decreased fat volume in the body (or weight) induces the reduction of the peripheral leptin concentration and increases food intake [6]. Lu et al described subjects with both chronic social defeat stress and chronic mild stress that had decreased plasma leptin concentrations but did not have a change in body weight; they reported that leptin had an antidepressant-like activity [12,13]
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