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  • American Physiological Society  (7)
  • Grace, Martha K.  (7)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 5 ( 2001-11-01), p. R1605-R1612
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 5 ( 2001-11-01), p. R1605-R1612
    Abstract: The opioid receptor antagonist naloxone decreases consumption of high-sucrose diets but does not reduce cornstarch diet intake in energy-restricted rats. Sucrose-fed rats eat at a much higher rate, consuming more food than cornstarch-fed rats. We examined meal microstructure using an automated weighing system in food-restricted rats eating either a high-sucrose or high-cornstarch diet. Sucrose-fed rats exhibited a higher rate of eating during their first meal compared with cornstarch-fed rats (0.34 vs. 0.20 g/min, respectively). However, naloxone did not reduce eating rate in either group. Naloxone decreased the size of the first meal in both diet groups by shortening the length of the meal. Naloxone's anorectic effect was more potent in the sucrose-fed rats. These results indicate that naloxone's heightened anorectic effect on sucrose diet consumption is not “rate dependent.” Naloxone's anorectic actions may be modulated by two conditions, the sensory properties of food and the energy state of the animal. Thus the elevated anorectic potency of naloxone in energy-restricted sucrose-fed rats may reflect actions on neural systems that mediate orosensory and/or postingestive signals.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 281, No. 2 ( 2001-08-01), p. R673-R680
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 281, No. 2 ( 2001-08-01), p. R673-R680
    Abstract: Central injection of α-melanocyte-stimulating hormone (α-MSH) decreases food intake, suggesting a role for this peptide in the mediation of satiety. Inasmuch as α-MSH also supports the development of taste aversions under certain conditions, the nature of its influence on ingestive behavior, i.e., whether it is related to satiety or aversion, remains unclear. In the present studies, we used immunostaining, including that for c-Fos as a marker of neuronal activation, to further substantiate the physiological role for α-MSH in the regulation of consummatory behavior. We found that an increase in activation of α-MSH neurons in the arcuate nucleus coincided with meal termination. Administration of powerful aversive agents, LiCl and CuSO 4 , did not stimulate α-MSH cells but did induce pronounced activation of oxytocin (OT) and vasopressin (VP) neurons, the final components of circuitry mediating aversion. We observed fewer Fos-positive OT/VP neurons after α-MSH injection into the lateral ventricle or into the hypothalamic paraventricular nucleus, treatments that cause mild or no aversion, respectively. The degree of activation of OT/VP neurons paralleled the magnitude of aversive response to a given treatment. Our data support the hypothesis that, in the arcuate nucleus, α-MSH acts as a satiety mediator independent from aversion-related mechanisms.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 293, No. 1 ( 2007-07), p. R99-R105
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 293, No. 1 ( 2007-07), p. R99-R105
    Abstract: Previous work from our laboratory indicates that when rats are given a choice between a high-fat and a high-sucrose diet, opioid blockade with naltrexone (NTX) in a reward-related site (central amygdala) inhibits intake of the preferred diet only, whereas NTX injected into a homeostasis-related site, such as the hypothalamic paraventricular nucleus (PVN), inhibits intake of both diets. However, other work suggests that opioids increase intake of fat specifically. The present study further investigates the role of PVN opioids in food choices made by calorically-replete animals. We used a binge model with chow-maintained rats given 3-h access to a choice of a high-fat or high-sucrose diet 3 days a week. We hypothesized that intra-PVN injection of the μ-opioid agonist, DAMGO (0, 0.025, 0.25, and 2.5 nmol) would enhance, and NTX (0, 10, 30, and 100 nmol) would inhibit intake of both diets to an equal extent. We found that when animals were divided into groups according to sucrose or fat preference, DAMGO increased fat intake in fat-consuming animals, while having no effect on intake of either diet in sucrose-consuming animals. NTX, however, inhibited fat intake in both groups. Intra-PVN NTX did not inhibit intake of sucrose when presented in the absence of a fat choice, but did so when injected peripherally. Furthermore, intra-PVN and systemic NTX inhibited intake of chow by 24-h-food-deprived animals. These results indicate a complex role for PVN opioids in food intake with preference, nutrient type, and energy state affecting the ability of these compounds to change behavior.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 283, No. 5 ( 2002-11-01), p. R1149-R1154
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 283, No. 5 ( 2002-11-01), p. R1149-R1154
    Abstract: We hypothesized that the opioid antagonist naltrexone would inhibit the redevelopment of a preference for a high-sucrose diet after an abstention period from this diet. Rats that chose between a starch or sucrose diet for 10 days preferred the sucrose diet. Rats were then given access to the starch diet alone for another 10-day period. A miniosmotic pump containing saline or naltrexone was then implanted (70 μg/h; 1.7 mg/day) for ∼10 days. During the saline infusion, 77% of the total energy came from the sucrose diet, whereas during the naltrexone infusion, 33% of the total energy came from the sucrose diet. We repeated this study in another group of rats but did not restrict the sucrose diet. In this case naltrexone failed to decrease preference for the sucrose diet. Thus naltrexone infusion inhibited redevelopment of a preference for a sucrose diet after a period of restriction to a starch diet for 10 days but had no effect on preference if both diets were present throughout the study.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 276, No. 5 ( 1999-05-01), p. R1320-R1326
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 276, No. 5 ( 1999-05-01), p. R1320-R1326
    Abstract: Effects of streptozotocin (STZ)-induced diabetes and insulin on opioid peptide gene expression were examined in rats. In experiment 1, three groups were administered STZ (75 mg/kg ip single injection). Two groups were killed at either 2 or 4 wk. In the third group, insulin treatment (7.0 IU/kg × 1 day for 3 wk) was initiated 1 wk after STZ injection. STZ induced hyperphagia and reduced weight gain. Insulin decreased food intake and increased body weight relative to diabetes. Proopiomelanocortin (POMC) mRNA in arcuate nucleus (Arc) and pituitary decreased in diabetes and normalized after insulin treatment. Prodynorphin (proDyn) mRNA increased in diabetes and normalized in the pituitary after insulin but not in the Arc. Diabetes did not alter proenkephalin (proEnk) expression in the Arc or pituitary, nor dynorphin A 1–17 or β-endorphin in paraventricular nucleus (PVN). α-Melanocyte-stimulating hormone (α-MSH) peptide levels were decreased in the PVN and normalized following insulin treatment. Diabetes increased Arc neuropeptide Y mRNA, and insulin suppressed this increase. In experiment 2, insulin (2.5 IU/kg sc) daily for 1 wk in normal rats increased Arc POMC mRNA, but not proDyn and proEnk mRNA. These results suggest that Arc POMC expression and PVN α-MSH peptide levels decrease in diabetes. Also, insulin may influence Arc and pituitary POMC activity in neurons that regulate energy metabolism.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 275, No. 2 ( 1998-08-01), p. R478-R484
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 275, No. 2 ( 1998-08-01), p. R478-R484
    Abstract: Inhibition of a signal that produces positive energy balance involving neuropeptide Y (NPY) projection from arcuate nucleus (Arc; site of NPY synthesis) to paraventricular nucleus (PVN; site of NPY release) is one potential mechanism of leptin action. NPY in the PVN increases feeding and decreases uncoupling protein (UCP) activity in brown fat, whereas leptin decreases NPY biosynthesis in the Arc, which presumably decreases PVN NPY. It is hypothesized that decreased NPY activity is necessary for the satiety and thermogenic effects of leptin. To test this, we first determined the effect of leptin on feeding in two paradigms: satiated rats and food-deprived rats. Leptin was effective in decreasing feeding in the satiated rats but ineffective in the food-deprived rats. Next, we determined that leptin decreases NPY and increases UCP gene expression. Finally, we injected leptin intracerebroventricularly before specific PVN NPY microinjection. We found that repletion of NPY in PVN by specific NPY microinjection reverses the feeding-inhibitory and thermogenic effects of centrally administered leptin, the first functional evidence indicating that leptin acts on the Arc-PVN feeding-regulatory pathway.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 275, No. 2 ( 1998-08-01), p. R471-R477
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 275, No. 2 ( 1998-08-01), p. R471-R477
    Abstract: Neuropeptide Y (NPY) injected into the paraventricular nucleus (PVN) increases feeding and decreases brown adipose tissue (BAT) uncoupling protein (UCP) and lipoprotein lipase (LPL) mRNA. Previously we reported that the feeding and BAT effects induced by NPY in the PVN are blocked by 50 μg naltrexone (NTX) in the rostral nucleus of the solitary tract (rNTS). We sought to determine whether the effect of rNTS NTX on PVN NPY-induced alterations in energy metabolism occurred at lower doses of NTX. Male Sprague-Dawley rats were fitted with cannulas into two sites: PVN and rNTS. Feeding response, BAT UCP, and LPL mRNA were measured after injection of 0, 5, 10, and 25 μg NTX in the rNTS ± 1 μg NPY in the PVN. One-hour feeding response to PVN NPY was significantly and dose dependently decreased by 10 and 25 μg rNTS NTX (−23 and −31%, respectively). However, rNTS NTX did not block the PVN NPY-induced decrease in BAT UCP or LPL mRNA. BAT β-actin mRNA (as a measure of overall changes in gene expression) was unchanged among treatment groups. These results indicate a possible divergence in the PVN NPY feeding-stimulatory/BAT-inhibitory pathway, such that PVN NPY feeding effects may be routed through the rNTS whereas BAT effects may be due to alterations at another neural site.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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