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  • American Physiological Society  (5)
  • Kotz, C. M.  (5)
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  • American Physiological Society  (5)
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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1994
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 266, No. 5 ( 1994-05-01), p. R1578-R1583
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 266, No. 5 ( 1994-05-01), p. R1578-R1583
    Abstract: We measured the influence of diet composition on hypothalamic neuropeptide Y (NPY) message and brown fat uncoupling protein (UCP) mRNA using different diets. Sprague-Dawley rats ate ad libitum either chow, a high-carbohydrate (HC), an intermediate-carbohydrate (IHC), a high-fat (HF), or an intermediate-fat (IHF) diet, all with equal protein content (g/kcal). The HF and IHF groups ate less food mass and, except for HC, all groups consumed similar kilocalories during the study. After 1 wk, we killed the animals and extracted total RNA from arcuate nucleus, cortex, and brown adipose tissue (BAT). Arcuate NPY mRNA in the HF group was significantly (P 〈 0.001) lower than in the HC and chow group. There were no differences between groups in NPY message in cortex or NPY protein in the paraventricular nucleus. BAT UCP message levels were significantly higher (P = 0.001) in the HF group. Thus HF compared with HC and chow diet reduces expression of NPY mRNA in hypothalamic nuclei and increases expression of BAT UCP message.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 278, No. 2 ( 2000-02-01), p. R494-R498
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 278, No. 2 ( 2000-02-01), p. R494-R498
    Abstract: Neuropeptide Y (NPY) injected into the hypothalamic paraventricular nucleus (PVN) stimulates feeding and decreases uncoupling protein (UCP)-1 mRNA in brown adipose tissue (BAT). The present studies were undertaken to determine whether UCP-2 in white adipose tissue (WAT) and UCP-3 in muscle are regulated by NPY in the PVN. PVN-cannulated male Sprague-Dawley rats were injected with either saline or NPY (PVN, 117 pmol, 0.5 μl) every 6 h for 24 h. NPY in the PVN stimulated feeding and decreased UCP-1 mRNA in BAT independent of NPY-induced feeding. UCP-2 mRNA in WAT was unchanged by NPY. In acromiotrapezius muscle, NPY decreased UCP-3 mRNA, but this was reversed by restricting food intake to control levels. In biceps femoris muscle, NPY alone had no effect on UCP-3 mRNA, but UCP-3 mRNA was significantly increased in the NPY-treated rats that were restricted to control levels of intake. These results suggest that UCP-2 in WAT and UCP-3 in muscle are not subject to specific regulation by NPY in the PVN.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1996
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 271, No. 1 ( 1996-07-01), p. R289-R294
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 271, No. 1 ( 1996-07-01), p. R289-R294
    Abstract: Neuropeptide Y (NPY) has potent effects on several components of energy metabolism, including increased feeding and decreased brown fat thermogenesis. Negative energy balance, such as food deprivation, increases NPY mRNA in hypothalamic arcuate nucleus (ARC). Naltrexone (NLTX), an opioid receptor antagonist, decreases NPY-induced feeding. We hypothesized that NLTX would alter ARC NPY mRNA and change NPY effects on brown fat. Osmotic minipumps prefilled with either saline or NLTX (70 micrograms/h) were implanted subcutaneously in 32 male Sprague-Dawley rats. One-half of the rats were food deprived and one-half were allowed food ad libitum for 48 h. Food intake was measured at 24 and 48 h. At 48 h, ARC NPY mRNA and brown fat uncoupling protein (UCP) mRNA levels were determined using cDNA probes. Forty-eight-hour food intake was significantly decreased by 24% after NLTX infusion. Food deprivation and NLTX treatment significantly and independently increased ARC NPY mRNA and decreased UCP mRNA levels in brown fat, suggesting a complex interaction between hypothalamic NPY and endogenous opioids in the regulation of energy balance.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1996
    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 ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 278, No. 2 ( 2000-02-01), p. R499-R503
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 278, No. 2 ( 2000-02-01), p. R499-R503
    Abstract: Naltrexone (NLTX) in the nucleus of the solitary tract (NTS) decreases feeding induced by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). We sought to determine the NTS region most sensitive to NLTX blockade of PVN NPY-induced feeding. Male Sprague-Dawley rats were fitted with two cannulas; one in the PVN and one in a hindbrain region: caudal, medial, or rostral NTS or 1 mm outside the NTS. Animals received NLTX (0, 1, 3, 10, and 30 μg in 0.3 μl) into the hindbrain region just prior to PVN NPY (0.5 μg, 0.3 μl) or artificial cerebrospinal fluid (0.3 μl). Food intake was measured at 2 h following injection. PVN NPY stimulated feeding, and NLTX in the medial NTS significantly decreased NPY-induced feeding at 2 h, whereas administration of NLTX in the other hindbrain regions did not significantly influence PVN NPY induced feeding. These data suggest that opioid receptors in the medial NTS are most responsive to feeding signals originating in the PVN after NPY stimulation.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    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 ; 1997
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 272, No. 4 ( 1997-04-01), p. R1028-R1032
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 272, No. 4 ( 1997-04-01), p. R1028-R1032
    Abstract: We evaluated the effect of selective opioid peptides and naltrexone on feeding when injected into the nucleus of the solitary tract (NTS). Doses of 0, 1, 2, 4, and 8 nmol of [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAMGO, mu-agonist), dynorphin A-(1-17) (DynA-(1-17), kappa-agonist), and [D-Ser2] leucine enkephalin-thr, (delta-agonist) were injected into the NTS in satiated male rats, and food intake was measured at 1, 2, and 4 h. Only DAMGO significantly increased feeding above control levels at doses of 2, 4, and 8 nmol. Doses of 10 and 50 microg naltrexone in the NTS significantly decreased 18-h deprivation-induced feeding. These data suggest that NTS opioid receptors (primarily mu) may be involved in the regulation of feeding.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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