Publications by authors named "Victoria F Turek"

In rodents, ovariectomy (OVX) elicits weight gain and diminished responsiveness to homeostatic signals. Here we characterized the response of obese OVX rats to peripheral amylin. Rats received sham surgery (SHAM), OVX, or OVX with hormonal replacement (17β-estradiol, 2 μg per 4 d; OVX+E) and were infused with vehicle or amylin (50 μg/kg · d) for 28 d.

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Circulating amylin inhibits food intake via activation of the area postrema (AP). The aim of this study was to identify the neurochemical phenotype of the neurons mediating amylin's hypophagic action by immunohistochemical and feeding studies in rats. Expression of c-Fos protein was used as a marker for neuronal activation and dopamine-beta-hydroxylase (DBH), the enzyme-catalyzing noradrenaline synthesis, as a marker for noradrenergic neurons.

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Cholecystokinin (CCK) acutely synergizes with amylin to suppress food intake in lean mice. To extend on these findings, the present studies sought to identify neural correlates for the interaction of amylin and CCK, as well as further understand the therapeutic potential of CCK-based combinations in obesity. First, c-Fos activation was assessed in various brain nuclei after a single intraperitoneal injection of amylin (5microg/kg) and/or CCK (5microg/kg).

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Active weight loss and the maintenance of a weight-reduced state elicit potent counter-regulatory responses in multiple neurochemical pathways rendering monotherapy-based anti-obesity agents relatively ineffective. Herein, we highlight potential strategies for overcoming counter-regulatory responses to states of negative energy balance using combinatorial approaches. We discuss methodological and practical considerations for preclinical modeling of additive/synergistic weight loss combinations that have emerged in our translational research program aimed at identifying naturally occurring neurohormonal synergies.

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The present studies aimed to identify mechanisms contributing to amylin/leptin synergy in reducing body weight and adiposity. We reasoned that if amylin/leptin harnessed complementary neuronal pathways, then in the leptin-sensitive state, amylin should augment leptin signaling/binding and that in the absence of endogenous amylin, leptin signaling should be diminished. Amylin (50 microg/kg, ip) amplified low-dose leptin-stimulated (15 microg/kg, ip) phosphorylated signal transducer and activator of transcription-3 signaling within the arcuate nucleus (ARC) in lean rats.

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An involvement of the transient receptor potential vanilloid (TRPV) 1 channel in the regulation of body temperature (T(b)) has not been established decisively. To provide decisive evidence for such an involvement and determine its mechanisms were the aims of the present study. We synthesized a new TRPV1 antagonist, AMG0347 [(E)-N-(7-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl)-3-(2-(piperidin-1-yl)-6-(trifluoromethyl)pyridin-3-yl)acrylamide], and characterized it in vitro.

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There is evidence that the peptide urocortin 1 (Ucn1) may be involved in mediating some of the effects of ethanol. The purpose of the present study was to characterize Ucn1 immunoreactivity in mice selectively bred for either high or low sensitivity to ethanol-induced sedation, with additional differences in their response to ethanol-induced hypothermia. The brains of naïve male mice of the inbred long sleep/short sleep (ILS/ISS) selected lines were analyzed by immunohistochemistry.

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Restraint stress, lipopolysaccharide (LPS), and ethanol (EtOH) administration have all been found to induce c-Fos in the brain, and to cause hypothermia. The present study was designed to assess whether the c-Fos expression that occurs in the Edinger-Westphal nucleus (EW) after EtOH administration is independent of the hypothermia or any stress effects that occur. To test this, we used restraint stress and LPS in addition to EtOH, and also examined two control areas, the dorsal raphe nucleus (DRN) and the periaqueductal gray (PAG), in addition to EW.

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Systemic inflammation is accompanied by changes in body temperature, either fever or hypothermia. Over the past decade, the rat and mouse have become the predominant animal models, and new species-specific tools (recombinant antibodies and other proteins) and genetic manipulations have been applied to study fever and hypothermia. Remarkable progress has been achieved.

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An oft-overlooked consequence of fever is the occurrence of thermoregulatory heat-seeking/producing behaviors. Subdiaphragmatic vagotomy attenuates fever resulting from low dose, peripherally administered pyrogens, suggesting that the vagus is involved in generating the pathogen-induced rise in core body temperature (T(c)). This study was designed to confirm that rats utilize behavioral thermoregulation to augment fever following systemic administration of lipopolysaccharide (LPS), and to test the hypothesis that, in febrile animals, vagotomy would block the preference for a higher ambient temperature (T(a)) as T(c) is rising.

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