Activations of c-fos/c-jun signaling are involved in the modulation of hypothalamic superoxide dismutase (SOD) and neuropeptide Y (NPY) gene expression in amphetamine-mediated appetite suppression

Hsieh, Yih‐Shou; Yang, Shun‐Fa; Chiou, Hui‐Ling; Kuo, Dong‐Yih

doi:10.1016/j.taap.2005.07.006

Cited by 22 publications

(34 citation statements)

References 57 publications

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“…These results show that Y1R play a functional role in regulating AP-1–mediated appetite control in AMPH-treated rats. These results expand our previous findings [26] and suggest that hypothalamic CA/NPY/Y1R/AP-1 signal pathway participates in the regulation of AMPH-induced anorexia.…”

Section: Discussionsupporting

confidence: 92%

“…The cascade of c-Jun and c-Fos signaling can be activated by AMPH [24-26]. The activator protein-1 (AP-1) binding protein, which is formed as a Fos/Jun heterodimer or a Jun/Jun homodimer of IEG, is a representative transcriptional factor that is activated in response to signal transduction cascades [27].…”

Section: Introductionmentioning

confidence: 99%

“…Thus, AP-1 activity is increased in several brain regions after methAMPH treatment [28], and AP-1 DNA binding activity is associated with enhanced motor behavior in AMPH-treated rats [29]. Previously, we reported that c-Fos/c-Jun participated in NPY-mediated appetite regulation in AMPH-treated rats [26]. However, it is still unclear whether Y1R and AP-1 signaling participated in the regulation of the NPY-mediated feeding.…”

Section: Introductionmentioning

confidence: 99%

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The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats

Hsieh

Chen

et al. 2013

Mol Brain

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BackgroundHypothalamic neuropeptide Y (NPY) and two immediate early genes, c-fos and c-jun, have been found to be involved in regulating the appetite-suppressing effect of amphetamine (AMPH). The present study investigated whether cerebral catecholamine (CA) might regulate NPY and POMC expression and whether NPY Y1 receptor (Y1R) participated in activator protein-1 (AP-1)–mediated feeding.MethodsRats were given AMPH daily for 4 days. Changes in the expression of NPY, Y1R, c-Fos, c-Jun, and AP-1 were assessed and compared.ResultsDecreased CA could modulate NPY and melanocortin receptor 4 (MC4R) expressions. NPY and food intake decreased the most on Day 2, but Y1R, c-Fos, and c-Jun increased by approximately 350%, 280%, and 300%, respectively, on Day 2. Similarly, AP-1/DNA binding activity was increased by about 180% on Day 2. The expression patterns in Y1R, c-Fos, c-Jun, and AP-1/DNA binding were opposite to those in NPY during AMPH treatment. Y1R knockdown was found to modulate the opposite regulation between NPY and AP-1, revealing an involvement of Y1R in regulating NPY/AP-1–mediated feeding.ConclusionsThese results point to a molecular mechanism of CA/NPY/Y1R/AP-1 signaling in the control of AMPH-mediated anorexia and may advance the medical research of anorectic and anti-obesity drugs.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats

Hsieh

Chen

et al. 2013

Mol Brain

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“…Liver samples from fructose-fed rats had a higher triglyceride content (1.6-fold) and lower fatty acid ␤-oxidation activity (0.8-fold) than liver samples from control rats. Livers from fructose-fed rats had higher expression of ChREBP and genes related to fatty acid synthesis and glycolysis than livers from control rats, and showed impaired phos- 44 phorylation at Ser 727 of STAT-3 and no significant changes in the expression of leptin-regulated genes (Supporting Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

Suppressor of cytokine signaling-3 (SOCS-3) and a deficit of serine/threonine (Ser/Thr) phosphoproteins involved in leptin transduction mediate the effect of fructose on rat liver lipid metabolism

et al. 2008

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There is controversy regarding whether fructose in liquid beverages constitutes another dietary ingredient of high caloric density or introduces qualitative changes in energy metabolism that further facilitate the appearance of metabolic diseases. Central to this issue is the elucidation of the molecular mechanism responsible for the metabolic alterations induced by fructose ingestion. Fructose administration (10% wt/vol) in the drinking water of Sprague-Dawley male rats for 14 days induced hyperleptinemia and hepatic leptin resistance. This was caused by impairment of the leptin-signal transduction mediated by both janus-activated kinase-2 and the mitogen-activated protein kinase pathway. The subsequent increase in activity in the liver of the unphosphorylated and active form of the forkhead box O1 nuclear factor, which transrepresses peroxisome proliferator-activated receptor ␣ activity, and a lack of activation of the adenosine monophosphate-activated protein kinase, led to hypertriglyceridemia and hepatic steatosis. These alterations are attributable to two key events: (1) F ructose makes up a significant proportion of energy in westernized diets, mainly due to the high intake of fructose-containing beverages. This situation has coincided with the growing prevalence of obesity and metabolic syndrome, recognized risk factors for cardiovascular diseases, over the past two decades. 1,2 Fructose in liquid diets induces hypertriglyceridemia to a greater extent than in solid diets. 3 A 10% dietary energy increase in

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“…One reason for these discrepancies may be fact the basal activities of various antioxidant enzymes, such as SOD, CAT, glutathione reductase, glutathione peroxidase, and glutathione-S-transferase are highly variable across brain regions [21]. It has been recently demonstrated that amphetamine regulates the expression of SOD mRNA via c-fos/c-jun activation in the hypothalamus [28]. Although speculative, it is possible that the regulation of antioxidant's gene expression by amphetamine in other brain regions may be relevant to the differences observed.…”

Section: Ae)mentioning

confidence: 99%

Changes in Antioxidant Defense Enzymes after d-amphetamine Exposure: Implications as an Animal Model of Mania

et al. 2006

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Studies have demonstrated that oxidative stress is associated with amphetamine-induced neurotoxicity, but little is known about the adaptations of antioxidant enzymes in the brain after amphetamine exposure. We studied the effects of acute and chronic amphetamine administration on superoxide dismutase (SOD) and catalase (CAT) activity, in a rodent model of mania. Male Wistar rats received either a single IP injection of D-: amphetamine (1 mg/kg, 2 mg/kg, or 4 mg/kg) or vehicle (acute treatment). In the chronic treatment rats received a daily IP injection of either D-: amphetamine (1 mg/kg, 2 mg/kg, or 4 mg/kg) or vehicle for 7 days. Locomotor behavior was assessed using the open field test. SOD and CAT activities were measured in the prefrontal cortex, hippocampus, and striatum. Acute and to a greater extent chronic amphetamine treatment increased locomotor behavior and affected SOD and CAT activities in the prefrontal cortex, hippocampus and striatum. Our findings suggest that amphetamine exposure is associated with an imbalance between SOD and CAT activity in the prefrontal cortex, hippocampus and striatum.

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Activations of c-fos/c-jun signaling are involved in the modulation of hypothalamic superoxide dismutase (SOD) and neuropeptide Y (NPY) gene expression in amphetamine-mediated appetite suppression

Cited by 22 publications

References 57 publications

The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats

The neuropeptide Y Y1 receptor knockdown modulates activator protein 1-involved feeding behavior in amphetamine-treated rats

Suppressor of cytokine signaling-3 (SOCS-3) and a deficit of serine/threonine (Ser/Thr) phosphoproteins involved in leptin transduction mediate the effect of fructose on rat liver lipid metabolism

Changes in Antioxidant Defense Enzymes after d-amphetamine Exposure: Implications as an Animal Model of Mania

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