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Your search keyword '"Billington, C.J."' showing total 82 results
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82 results on '"Billington, C.J."'

1. Pathway analysis identifies novel non-synonymous variants contributing to extreme vascular outcomes in Williams-Beuren syndrome

Author

Liu, D., primary, Billington, C.J., additional, Raja, N., additional, Wong, Z.C., additional, Levin, M.D., additional, Resch, W., additional, Alba, C., additional, Hupalo, D.N., additional, Biamino, E., additional, Bedeschi, M.F., additional, Digilio, M.C., additional, Squeo, G.M., additional, Villa, R., additional, Parrish, P.C.R., additional, Knutsen, R.H., additional, Osgood, S., additional, Freeman, J.A., additional, Dalgard, C.L., additional, Merla, G., additional, Pober, B.R., additional, Mervis, C.B., additional, Roberts, A.E., additional, Morris, C.A., additional, Osborne, L.R., additional, and Kozel, B.A., additional

Published
2022
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2. Opioids in the nucleus of the solitary tract are involved in feeding in the rat

Author

Kotz, C.M., Billington, C.J., and Levine, A.S.

Subjects
Brain stem -- Physiological aspects, Opioids -- Receptors, Ingestion -- Physiological aspects, Animal behavior -- Physiological aspects, Biological sciences
Abstract

The feeding behavior of rats treated with selective opioids and naltroxenone was analyzed to determine the role of opioid receptors in the nucleus of the solitary tract (NTS) on feeding. Satiated rats injected with [D-Ala2, N-Me-Phe4,Gly5-o]enkephalin, dynorphin A-(1-17) and [D-Ser2]leucine enkephalin-thr exhibited increased feeding. On the other hand, deprivation-induced feeding was inhibited by naltroxenone by blocking the activity of NTS opioid receptors.

Published
1997

3. Naltrexone induces arcuate nucleus neuropeptide Y gene expression in the rat

Author

Kotz, C.M., Grace, M.K., Briggs, J.E., Billington, C.J., and Levine, A.S.

Subjects
Naltrexone -- Physiological aspects, Neuropeptide Y -- Physiological aspects, Rats -- Physiological aspects, Biological sciences
Abstract

Interaction between neuropeptide Y (NPY) and opioids has been demonstrated to influence certain aspects of energy metabolism. Naltrexone (NLTX) is an opioid receptor antagonist which is suggested to reduce NPY-induced feeding by altering the NPY mRNA in the hypothalamic arcuate nucleus. To test this hypothesis, food intake in the rat was measured in response to NLTX. The results showed that NLTX treatment increased NPY mRNA in food-deprived rats, suggesting the interaction between NPY and opioids.

Published
1996

4. Naloxone blocks that portion of feeding driven by sweet taste in food-restricted rats

Author

Levine, A.S., Weldon, D.T., Grace, M., Cleary, J.P., and Billington, C.J.

Subjects
Naloxone -- Physiological aspects, Animal feeding and feeds -- Physiological aspects, Biological sciences
Abstract

A study of the effect of naloxone on normal and sweet chow intake in schedule-fed and food-deprived rats reveals that sweet chow intake is more effectively lowered by naloxone than normal chow intake in rats subject to chronic food-deprivation. The potency of naloxone to inhibit feeding reduces with the magnitude of energy deficit in the rats. Palatability and deficit have a synergistic effect in determining food intake level.

Published
1995

5. Neuropeptide Y in hypothalamic paraventricular nucleus: a center coordinating energy metabolism

Author

Billington, C.J., Briggs, J.E., Harker, S., Grace, M., and Levine, A.S.

Subjects
Neuropeptide Y -- Physiological aspects, Brown adipose tissue -- Physiological aspects, Lipoprotein lipase -- Physiological aspects, Biological sciences
Abstract

Paraventricular nucleus (PVN) regulates decrease in brown fat thermogenesis and increases white fat lipoprotein lipase (LPC) enzymatic activity. The neuropeptide Y (NPY) stimulation at PVN suppresses gene expression for the brown fat protein, uncoupling protein, and accentuates gene expression for LPC. Administration of NPY into the cerebroventricular system reduces the sympathetic nerve response to brown adipose tissue.

Published
1994

8. Effect of NPY in the hypothalamic paraventricular nucleus on uncoupling proteins 1, 2, and 3 in the rat

Author

KOTZ, C. M., WANG, C. F., BRIGGS, J. E., LEVINE, A. S., and BILLINGTON, C.J.

Subjects
Adipose tissues -- Physiological aspects, Thermogenesis -- Physiological aspects, Brown adipose tissue -- Physiological aspects, Muscles -- Physiological aspects, Biological sciences
Abstract

Kotz, C. M., C. F. Wang, J. E. Briggs, A. S. Levine, and C. J. Billington. Effect of NPY in the hypothalamic paraventricular nucleus on uncoupling proteins 1, 2, and 3 in the rat. Am. J. Physiol. Regulatory Integrative Comp. Physiol. 278: R494-R498, 2000.--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 [micro]l) 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. thermogenesis; brown adipose tissue; white adipose tissue; muscle

Published
2000

10. WNT5A mutations in patients with autosomal dominant Robinow syndrome.

Author

Person, A.D., Beiraghi, S., Sieben, C.M., Hermanson, S., Neumann, A.N., Robu, M.E., Schleiffarth, J.R., Billington, C.J., Bokhoven, J.H.L.M. van, Hoogeboom, J.M., Mazzeu, J.F., Petryk, A., Schimmenti, L.A., Brunner, H.G., Ekker, S.C., Lohr, J.L., Person, A.D., Beiraghi, S., Sieben, C.M., Hermanson, S., Neumann, A.N., Robu, M.E., Schleiffarth, J.R., Billington, C.J., Bokhoven, J.H.L.M. van, Hoogeboom, J.M., Mazzeu, J.F., Petryk, A., Schimmenti, L.A., Brunner, H.G., Ekker, S.C., and Lohr, J.L.

Abstract

1 januari 2010, Contains fulltext : 87463.pdf (publisher's version ) (Closed access), Robinow syndrome is a skeletal dysplasia with both autosomal dominant and autosomal recessive inheritance patterns. It is characterized by short stature, limb shortening, genital hypoplasia, and craniofacial abnormalities. The etiology of dominant Robinow syndrome is unknown; however, the phenotypically more severe autosomal recessive form of Robinow syndrome has been associated with mutations in the orphan tyrosine kinase receptor, ROR2, which has recently been identified as a putative WNT5A receptor. Here, we show that two different missense mutations in WNT5A, which result in amino acid substitutions of highly conserved cysteines, are associated with autosomal dominant Robinow syndrome. One mutation has been found in all living affected members of the original family described by Meinhard Robinow and another in a second unrelated patient. These missense mutations result in decreased WNT5A activity in functional assays of zebrafish and Xenopus development. This work suggests that a WNT5A/ROR2 signal transduction pathway is important in human craniofacial and skeletal development and that proper formation and growth of these structures is sensitive to variations in WNT5A function.

Published
2010

11. WNT5A mutations in patients with autosomal dominant Robinow syndrome

Author

Person, A.D. (Anthony), Beiraghi, S. (Soraya), Sieben, C.M. (Christine), Hermanson, S. (Spencer), Neumann, A.N. (Ann), Robu, M.E. (Mara), Schleiffarth, J.R. (Robert), Billington, C.J. (Charles), Bokhoven, H. (Hans) van, Hoogeboom, A.J.M. (Jeannette), Mazzeu, J.F. (Juliana), Petryk, A. (Anna), Schimmenti, L.A. (Lisa), Brunner, H. (Han), Ekker, S.C. (Stephen), Lohr, J.L. (Jamie), Person, A.D. (Anthony), Beiraghi, S. (Soraya), Sieben, C.M. (Christine), Hermanson, S. (Spencer), Neumann, A.N. (Ann), Robu, M.E. (Mara), Schleiffarth, J.R. (Robert), Billington, C.J. (Charles), Bokhoven, H. (Hans) van, Hoogeboom, A.J.M. (Jeannette), Mazzeu, J.F. (Juliana), Petryk, A. (Anna), Schimmenti, L.A. (Lisa), Brunner, H. (Han), Ekker, S.C. (Stephen), and Lohr, J.L. (Jamie)

Abstract

Robinow syndrome is a skeletal dysplasia with both autosomal dominant and autosomal recessive inheritance patterns. It is characterized by short stature, limb shortening, genital hypoplasia, and craniofacial abnormalities. The etiology of dominant Robinow syndrome is unknown; however, the phenotypically more severe autosomal recessive form of Robinow syndrome has been associated with mutations in the orphan tyrosine kinase receptor, ROR2, which has recently been identified as a putative WNT5A receptor. Here, we show that two different missense mutations in WNT5A, which result in amino acid substitutions of highly conserved cysteines, are associated with autosomal dominant Robinow syndrome. One mutation has been found in all living affected members of the original family described by Meinhard Robinow and another in a second unrelated patient. These missense mutations result in decreased WNT5A activity in functional assays of zebrafish and Xenopus development. This work suggests that a WNT5A/ROR2 signal transduction pathway is important in human craniofacial and skeletal development and that proper formation and growth of these structures is sensitive to variations in WNT5A function.

Published
2010
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16. PL-316: Vagal blocking improves glycemic control and blood pressure in subjects with type 2 diabetes and hypertension

Author

Herrera, Miguel, primary, Pantoja, J.P., additional, Brancatisano, R., additional, Brancatisano, A., additional, Zulewski, H., additional, Frey, D.M., additional, Kulseng, B., additional, Johnsen, G., additional, Toouli, J., additional, Kow, L., additional, Tweden, K.S., additional, Vollmer, M.C., additional, Wilson, R.R., additional, and Billington, C.J., additional

Published
2010
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19. Intra-abdominal vagal blocking (VBLOC therapy): Clinical results with a new implantable medical device

Author

Camilleri, M., primary, Toouli, J., additional, Herrera, M.F., additional, Kulseng, B., additional, Kow, L., additional, Pantoja, J.P., additional, Marvik, R., additional, Johnsen, G., additional, Billington, C.J., additional, Moody, F.G., additional, Knudson, M.B., additional, Tweden, K.S., additional, Vollmer, M., additional, Wilson, R.R., additional, and Anvari, M., additional

Published
2008
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21. P195

Author

Whitson, B.A., primary, Leslie, D.B., additional, Kellogg, T.A., additional, Maddaus, M.A., additional, Buchwald, H., additional, Billington, C.J., additional, and Ikramuddin, S., additional

Published
2007
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41. Neuropeptides as Regulators of Consummatory Behaviors

Author

Levine, A.S., Morley, J.E., Gosnell, B.A., Billington, C.J., and Krahn, D.D.

Abstract

The control of ingestive behavior involves a variety of neurotransmitters, including monoamines, peptides and amino acids. For the past decade many investigators have focused their research on the role that regulatory peptides play in eating behavior. Many peptides, including cholecystokinin, bombesin, calcitonin, corticotropin-releasing factor, neurotensin and somatostatin, have been reported to decrease the amount of food ingested by laboratory animals. In contrast, a relatively small number of peptides increase food intake. The present review describes the effects of these peptides on consummatory behaviors in various species and their sites of action.

Published
1986
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