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1. Control of Food Intake

Author

Levine, Allen S., primary, Olszewski, Pawel K., additional, Billington, Charles J., additional, and Kotz, Catherine M., additional

Published
2024
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2. Obesogens and Obesity: State-of-the-Science and Future Directions Summary from a Healthy Environment and Endocrine Disruptors Strategies Workshop

Author

Heindel, Jerrold J., Alvarez, Jessica A., Atlas, Ella, Cave, Matthew C., Chatzi, Vaia Lida, Collier, David, Corkey, Barbara, Fischer, Douglas, Goran, Michael I., Howard, Sarah, Kahan, Scott, Kayhoe, Matthias, Koliwad, Suneil, Kotz, Catherine M., La Merrill, Michele, Lobstein, Tim, Lumeng, Carey, Ludwig, David S., Lustig, Robert H., Myers, Pete, Nadal, Angel, Trasande, Leonardo, Redman, Leanne M., Rodeheffer, Matthew S., Sargis, Robert M., Stephens, Jacqueline M., Ziegler, Thomas R., and Blumberg, Bruce

Published
2023
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3. Increasing diversity, equity, and inclusion in the fields of nutrition and obesity: A roadmap to equity in academia

Author

Rojas-Rodriguez, Raziel, Toribio, Mabel, Page-Wilson, Gabrielle, White, Ursula, Rowe, Glenn, Saint-Cyr, Marine, Brookheart, Rita, Fowler, Lauren Adele, Twillman, Gwen, Price, Felicia, Stull, April, Vega-Lopez, Sonia, Comuzzie, Tony, Kotz, Catherine M., Kazimierczuk, Francoise Knox, Baskin, Monica L., Newton, Robert, Greenberg, Andrew, Powe, Camile E., Gallagher, Dympna, Burk, David H., Epel, Elissa S., MacLean, Paul S., Truesdale, Kimberly P., Reeds, Dominic N., Schur, Ellen A., Redmond, Nicole, Cushion, Minor L., Martin, Samantha L., Cardel, Michelle I., Carson, Tiffany L., Hill, James O., Stanley, Takara, Grinspoon, Steven, Steger, Felicia, Blackman Carr, Loneke T., Ashby-Thompson, Maxine, Stewart, Delisha, Ard, Jamy, and Stanford, Fatima Cody

Published
2023
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8. Contributors

Author

Agca, Yuksel, primary, Alejandro, Emilyn U., additional, Allen, Portia S., additional, Allen, Kenneth P., additional, Allen–Worthington, Krystal, additional, Arndt, Tara P., additional, Baker, Henry J., additional, Bergin, Ingrid L., additional, Boone, Laura I., additional, Booth, Jennifer, additional, Borjeson, Tiffany Marie, additional, Boschen, Suelen Lucio, additional, Browne, Kevin D., additional, Budelsky, Carl L., additional, Cadillac, Joan M., additional, Carter, Philip B., additional, Compton, Susan R., additional, Conte, Marisa L., additional, Crisler, Robin, additional, Cullen, D. Kacy, additional, De la Vega, Rodolfo E., additional, Dell’Italia, Louis J., additional, Drake, Michael T., additional, Duke Boynton, Felicia, additional, Dunbar, Misha, additional, Dwinell, Melinda R., additional, El-Ayache, Nadine, additional, Esvelt, Marian, additional, Evans, Christopher H., additional, Faith, Robert E., additional, Foley, Patricia L., additional, Galligan, James J., additional, Geurts, Aron M., additional, Golledge, Huw DR., additional, Hanson, Marina M., additional, Hashway, Sara A., additional, Hedrich, Hans J., additional, Herbert, Ronald A., additional, Herfel, Tina Marie, additional, Hessler, Jack R., additional, Hickey, Raymond D., additional, Jaber, Samer M., additional, Janardhan, Kyathanahalli S., additional, Johnston, Nancy A., additional, King-Herbert, Angela P., additional, King-Herbert, Angela, additional, King, William W., additional, Koewler, Nathan, additional, Kohn, Dennis F., additional, Kolb, Bryan, additional, Kotz, Catherine M., additional, Lockridge, Amber D., additional, Lofgren, Jennifer LS., additional, Lohmiller, Jeffrey J., additional, Macy, James D., additional, Makidon, Paul E., additional, Meade, Theresa M., additional, Mexas, Angela M., additional, Mickelson, Barbara, additional, Wilson, Jolaine M., additional, Myers, Daniel D., additional, Myles, Matthew H., additional, Norin, Elisabeth, additional, Otto, Glen M., additional, Patil, Karuna, additional, Perez-Leighton, Claudio E., additional, Philips, Blythe H., additional, Ramos, Carlos Cuellar, additional, Scholz, Jodi A., additional, Sebastian, Manu M., additional, Shoulson, Rivka L., additional, Sivula, Christine, additional, Slate, Andrea R., additional, Suckow, Mark A., additional, Swennes, Alton G., additional, Swing, Sonya P., additional, Teske, Jennifer A., additional, Tunstall, Brendan J., additional, VanLith, Caitlin J., additional, Vasbinder, Mary Ann, additional, Vendruscolo, Leandro F., additional, Watson, Julie, additional, Weisbroth, Steven H., additional, Whishaw, Ian Q., additional, Wilding, Laura A., additional, and Wilson, Ronald P., additional

Published
2020
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10. Obesogens and Obesity: State-of-the-Science and Future Directions Summary from a HEEDS Workshop

Author

Heindel, Jerrold J., primary, Alvarez, Jessica A., additional, Atlas, Ella, additional, Cave, Matthew C., additional, Chatzi, Vaia Lida, additional, Collier, David, additional, Corkey, Barbara, additional, Fischer, Douglas, additional, Goran, Michael I., additional, Howard, Sarah, additional, Kahan, Scott, additional, Kayhoe, Matthias, additional, Koliwad, Suneil, additional, Kotz, Catherine M., additional, La Merrill, Michele, additional, Lobstein, Tim, additional, Lumeng, Carey, additional, Ludwig, David S., additional, Lustig, Robert H., additional, Myers, Pete, additional, Nadal, Angel, additional, Trasande, Leonardo, additional, Redman, Leanne M., additional, Rodeheffer, Matthew S., additional, Sargis, Robert M., additional, Stephens, Jacqueline M., additional, Ziegler, Thomas R., additional, and Blumberg, Bruce, additional

Published
2023
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12. Contributors

Author

Berrendero, Fernando, primary, Black, Emily M., additional, Blumenthal, Sarah A., additional, Burk, Joshua A., additional, de Lecea, Luis, additional, España, Rodrigo A., additional, Fadel, Jim R., additional, Flores, África, additional, Jennings, Kimberly J., additional, Kotz, Catherine M., additional, Kukkonen, Jyrki P., additional, Maness, Eden B., additional, Martin-Fardon, Rémi, additional, Matzeu, Alessandra, additional, Perez-Leighton, Claudio, additional, Petrovich, Gorica D., additional, Shaw, Jessica K., additional, Teske, Jennifer A., additional, and Zhang, Yanan, additional

Published
2019
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15. Increasing diversity, equity, and inclusion in the fields of nutrition and obesity: A roadmap to equity in academia

Author

Martin, Samantha L., primary, Cardel, Michelle I., additional, Carson, Tiffany L., additional, Hill, James O., additional, Stanley, Takara, additional, Grinspoon, Steven, additional, Steger, Felicia, additional, Blackman Carr, Loneke T., additional, Ashby-Thompson, Maxine, additional, Stewart, Delisha, additional, Ard, Jamy, additional, Rojas-Rodriguez, Raziel, additional, Toribio, Mabel, additional, Page-Wilson, Gabrielle, additional, White, Ursula, additional, Rowe, Glenn, additional, Saint-Cyr, Marine, additional, Brookheart, Rita, additional, Fowler, Lauren Adele, additional, Twillman, Gwen, additional, Price, Felicia, additional, Stull, April, additional, Vega-Lopez, Sonia, additional, Comuzzie, Tony, additional, Kotz, Catherine M., additional, Kazimierczuk, Francoise Knox, additional, Baskin, Monica L., additional, Newton, Robert, additional, Greenberg, Andrew, additional, Powe, Camile E., additional, Gallagher, Dympna, additional, Burk, David H., additional, Epel, Elissa S., additional, MacLean, Paul S., additional, Truesdale, Kimberly P., additional, Reeds, Dominic N., additional, Schur, Ellen A., additional, Redmond, Nicole, additional, Cushion, Minor L., additional, and Stanford, Fatima Cody, additional

Published
2023
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33. Chronic administration of brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus reverses obesity induced by high-fat diet

Author

Wang, ChuanFeng, Godar, Rebecca J., Billington, Charles J., and Kotz, Catherine M.

Subjects
Adipose tissues -- Health aspects, Brain-derived neurotrophic factor -- Health aspects, Obesity -- Care and treatment, Obesity -- Research, Biological sciences
Abstract

An acute injection of brain-derived neurotrophic factor (BDNF) in the hypothalamic paraventricular nucleus (PVN) reduces body weight by decreasing feeding and increasing energy expenditure (EE), in animals on standard laboratory chow. Animals have divergent responses to a high-fat diet (HFD) exposure, with some developing obesity and others remaining lean. In the current study, we tested two hypotheses: 1) BDNF in the PVN reverses HFD-induced obesity, and 2) animals with higher body fat have a greater physiological response to BDNF than those with less body fat. Eighty-four 10-wk old rats were allowed HFD ad libitum for 9 wk and then prepared with bilateral PVN cannulas. Animals were then divided into tertiles based on their body fat rank: high, intermediate, and low (H, I, and L). Each group was further divided into 2 subgroups and then PVN injected with BDNF or control (artificial cerebrospinal fluid, aCSF) every other day for 3 wk. Energy intake (EI), body weight, and body composition were measured. At study's end, rats were killed to allow measurement of other metabolic indices. In parallel, another 12 rats were fed control diet (CD), PVN-cannulated and injected with aCSF. HFD exposure induced obesity, particularly in the H body fat group, with a significant increase in El, body weight, fat mass, liver size, and serum glucose, triglycerides, insulin, and leptin. BDNF significantly reduced El, body weight, body fat, lean mass, and serum metabolic indices. These BDNF effects were greatest in the H body fat group. These data indicate that BDNF reduced HFD-induced obesity and metabolic syndrome-like measures, and the animals with the most body fat had the most significant response to BDNF. energy intake; body fat; metabolic syndrome doi: 10.1152/ajpregu.00844.2009.

Published
2010

35. Neuroregulation of nonexercise activity thermogenesis and obesity resistance

Author

Kotz, Catherine M., Teske, Jennifer A., and Billington, Charles J.

Subjects
Exercise -- Health aspects, Obesity -- Prevention, Thermogenesis -- Health aspects, Biological sciences
Abstract

High levels of spontaneous physical activity in lean people and the nonexercise activity thermogenesis (NEAT) derived from that activity appear to protect lean people from obesity during caloric challenge, while obesity in humans is characterized by dramatically reduced spontaneous physical activity. We have similarly demonstrated that obesity-resistant rats have significantly greater spontaneous physical activity than obesity-prone rats, and that spontaneous physical activity predicts body weight gain. Although the energetic cost of activity varies between types of activity and may be regulated, individual level of spontaneous physical activity is important in determining propensity for obesity. We review the current status of knowledge about the brain mechanisms involved in controlling the level of spontaneous physical activity and the NEAT so generated. Focus is on potential neural mediators of spontaneous physical activity and NEAT, including orexin A (also known as hypocretin 1), agouti-related protein, ghrelin, and neuromedin U, in addition to brief mention of neuropeptide Y, corticotrophin releasing hormone, cholecystokinin, estrogen, leptin, and dopamine effects on spontaneous physical activity. We further review evidence that strain differences in orexin stimulation pathways for spontaneous physical activity and NEAT appear to track with the body weight phenotype, thus providing a potential mechanistic explanation for reduced activity and weight gain. spontaneous physical activity; energy expenditure; orexin; neuromedin U; ghrelin; agouti-related protein

Published
2008

36. Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

Author

Wang, ChuanFeng, Bomberg, Eric, Levine, Allen, Billington, Charles, and Kotz, Catherine M.

Subjects
Bioenergetics -- Research, Energy metabolism -- Research, Obesity -- Research, Hypothalamus -- Research, Neurotrophic functions -- Research, Physiological research, Biological sciences
Abstract

Recent studies show that brainderived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor TrkB, are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF, given into the ventromedial nucleus of the hypothalamus (VMH), on normal and deprivation- and neuropeptide Y (NPY)-induced feeding behavior and body weight. BDNF injected unilaterally or bilaterally into the VMH of food-deprived and nondeprived rats significantly decreased feeding and body weight gain within the 0- to 24-h and the 24- to 48-h postinjection intervals. Doses effectively producing inhibition of feeding behavior did not establish a conditioned taste aversion. BDNF-induced feeding inhibition was attenuated by pretreatment of the TrkB-Fc fusion protein that blocks binding between BDNF and its receptor TrkB. VMH-injected BDNF significantly decreased VMH NPY-induced feeding at 1, 2, and 4 h after injection. In summary, BDNF in the VMH significantly decreases food intake and body weight gain, by TrkB receptor-mediated actions. Furthermore, the anorectic effects of BDNF in this site appear to be mediated by NPY. These data suggest that the VMH is an important site of action for BDNF in its effects on energy metabolism. food intake; body weight

Published
2007

37. Orexin-induced feeding requires NMDA receptor activation in the perifornical region of the lateral hypothalamus

Author

Doane, Dolores F., Lawson, Marcus A., Meade, Jonathan R., Kotz, Catherine M., and Beverly, J. Lee

Subjects
Obesity -- Research, Bioenergetics -- Research, Energy metabolism -- Research, Fat metabolism -- Research, Hypothalamus -- Research, Physiological research, Biological sciences
Abstract

Food intake is stimulated following administration of orexin-A into the perifornical region of the lateral hypothalamus (LH/PFA). Orexin neurons originating in the LH/PFA interact with a number of hypothalamic systems known to influence food intake, including glutamatergic neurons. Glutamatergic systems in the LH/PFA were demonstrated to initiate feeding through N-methyl-D-aspartic acid (NMDA) receptors. Male SpragueDawley rats fitted with brain guide cannulas to the LH/PFA were used in two experiments. In the first experiment, a combination microdialysis/microinjection probe was used to deliver artificial cerebrospinal fluid (aCSF) or 500 pmol of orexin-A into the LH/PFA. Orexin-A increased interstitial glutamate to 143 [+ or -] 12% of baseline (P < 0.05), which remained elevated over the 120-rain collection period. In the second experiment, the NMDA receptor antagonist D-2-amino-5phosphonopentanoic acid (D-AP5; 10 nmol) was administered before orexin-A. The orexin-induced increase in food intake (from 1.1 [+ or -] 0.4 to 3.2 [+ or -] 0.5 g, P < 0.05) during the first hour was absent in rats receiving D-AP5 + orexin-A (1.2 [+ or -] 0.5 g). There was no effect of D-AP5 alone on food intake. These data support glutamatergic systems in the LH/PFA mediating the feeding response to orexin-A through NMDA receptors. food intake regulation; hypocretin; microdialysis

Published
2007

38. Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus reduces energy intake

Author

Wang, ChuanFeng, Bomberg, Eric, Billington, Charles, Levine, Allen, and Kotz, Catherine M.

Subjects
Metabolic diseases -- Research, Obesity -- Research, Bioenergetics -- Research, Energy metabolism -- Research, Hypothalamus -- Research, Physiological research, Biological sciences
Abstract

Recent studies show that brain-derived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor tyrosine kinase B (TrkB) are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF in the hypothalamic paraventricular nucleus (PVN) on feeding. BDNF injected unilaterally or bilaterally into the PVN of food-deprived and nondeprived rats significantly decreased feeding and body weight gain within the 0- to 24-h and 24-to 48-h postinjection intervals. Effective doses producing inhibition of feeding behavior did not establish a conditioned taste aversion. PVN BDNF significantly decreased PVN neuropeptide Y (NPY)-induced feeding at 1, 2, and 4 h following injection. BDNF administration in the PVN abolished food-restriction-induced NPY gene expression in the hypothalamic arcuate nucleus. In conclusion, BDNF in the PVN significantly decreases food intake and body weight gain, suggesting that the PVN is an important site of action for BDNF in its effects on energy metabolism. Furthermore, BDNF appears to interact with NPY in its anorectic actions, although a direct effect on NPY remains to be established. food intake; hypothalamus; body weight

Published
2007

39. Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus increases energy expenditure by elevating metabolic rate

Author

Wang, ChuanFeng, Bomberg, Eric, Billington, Charles, Levine, Allen, and Kotz, Catherine M.

Subjects
Bioenergetics -- Research, Energy metabolism -- Research, Obesity -- Research, Metabolic diseases -- Research, Thermogenesis -- Research, Physiological research, Biological sciences
Abstract

Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified. The hypothalamic paraventricular nucleus (PVN) is important in energy metabolism regulation, and expresses both BDNF and its receptor. We tested three hypotheses: I) PVN BDNF reduces feeding and increases energy expenditure (EE), 2) PVN BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR), and 3) PVN BDNF thermogenic effects are mediated, in part, by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 [micro]g) was injected into the PVN of Sprague-Dawley rats; and oxygen consumption, carbon dioxide production, food intake, and SPA were measured for 24 h in an indirect calorimeter. SPA was also measured in open-field activity chambers for 48 h after BDNF injection. Animals were killed 6 or 24 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time PCR. BDNF significantly decreased food intake and body weight gain 24 h after injection. Heat production and RMR were significantly elevated for 7 h immediately after BDNF injection. BDNF had no effect on SPA, but increased UCP1 gene expression in BAT at 6 h, but not 24 h after injection. In conclusion, PVN BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased RMR, which may be due, in part, to BAT UCP1 activity. These data suggest that the PVN is an important site of BDNF action to influence energy balance. thermogenesis; resting metabolic rate; spontaneous physical activity

Published
2007

40. Central orexin sensitivity, physical activity, and obesity in diet-induced obese and diet-resistant rats

Author

Novak, Colleen M., Kotz, Catherine M., and Levine, James A.

Subjects
Thermogenesis -- Research, Ketogenic diet -- Health aspects, Rats -- Health aspects, Rats -- Food and nutrition, Rattus -- Health aspects, Rattus -- Food and nutrition, Biological sciences
Abstract

Nonexercise activity thermogenesis (NEAT), the most variable component of energy expenditure, can account for differential capacities for human weight gain. Also highly variable, spontaneous physical activity (SPA) may similarly affect weight balance in animals. In the following study, we utilized the rat model of obesity, the diet-induced obese (DIO) rat, as well as the diet-resistant (DR) rat strain, to investigate how access to a high-fat diet alters SPA and the associated energy expenditure (i.e., NEAT). DIO and DR rats showed no differences in the amount of SPA before access to the high-fat diet. After 29 days on a high-fat diet, the DIO rats showed significant decreases in SPA, whereas the DR rats did not. Next, we wanted to determine whether the DIO and DR rats showed differential sensitivity to microinjections of orexin into the paraventricular nucleus of the hypothalamus (PVN). Unilateral guide cannulae were implanted, aimed at the PVN. Orexin A (0, 0.125, 0.25, and 1.0 nmol in 500 nl) was microinjected through the guide cannula into the PVN, then SPA and energy expenditure were measured for 2 h. Using the response to vehicle as a baseline, the DR rats showed significantly greater increase in NEAT compared with the DIO rats. These data indicate that diet-induced obesity is associated with decreases in SPA and a lack of increase in NEAT. A putative mechanism for changes in NEAT that accompany obesity is a decreased sensitivity to the NEAT-activating effects of neuropeptides such as orexin. nonexercise activity thermogenesis; paraventricular nucleus of the hypothalamus; high-fat diet; hypocretin

Published
2006

42. Opioids

Author

Gosnell, Blake A., primary, Kotz, Catherine M., additional, Billington, Charles J., additional, and Levine, Allen S., additional

Published
2013
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43. Contributors

Author

Aalen, Reidunn B., primary, Abdel-Wahab, Yasser H.A., additional, Adams, Michael E., additional, Adan, Roger A.H., additional, Ahima, Rexford S., additional, Ahmed, Naima, additional, Al-Massadi, Omar, additional, Altstein, Miriam, additional, Anouar, Youssef, additional, Anselmi, Laura, additional, Ansorge, Siegfried, additional, Antcheva, Nikolinka, additional, Antonova-Koch, Yevgeniya, additional, Appel, Jon R., additional, Arik, Anam J., additional, Arter, Alison L., additional, Arvan, Peter, additional, Ashkenazi, Avraham, additional, Baas, P.W., additional, Bado, André, additional, Baird, Andrew, additional, Baiula, Monica, additional, Bakaletz, Lauren O., additional, Bakken, Earl E., additional, Balaskó, Márta, additional, Baldwin, Graham S., additional, Banks, William A., additional, Barra, Donatella, additional, Barson, Jessica R., additional, Basille, Magali, additional, Bauer, Natalie N., additional, Bedini, Andrea, additional, Beeton, Christine, additional, Begley, David J., additional, Beinfeld, Margery C., additional, Bendena, William G., additional, Benoit, Stephen C., additional, Bentov, Itay, additional, Bern, Howard, additional, Bierbaum, Gabriele, additional, Billington, Charles J., additional, Blasiak, Anna, additional, Block, Norman L., additional, Bloom, Stephen. R., additional, Bonney, Iwona, additional, Bowie, John H., additional, Boyd, Sunny K., additional, Brain, Susan D., additional, Brede, Dag A., additional, Broeck, Jozef Vanden, additional, Brown, Kelly L., additional, Brown, Mark R., additional, Bugni, James M., additional, Bundgaard, Jens R., additional, Burel, Delphine, additional, Butenko, Melinka A., additional, Call, Melissa J., additional, Calò, Girolamo, additional, Campbell, Duncan John, additional, Carlsson, Anna, additional, Carr, Daniel B., additional, Carraway, Robert E., additional, Carreira, Marcos C., additional, Casanueva, Felipe F., additional, Cassella, Sarah N., additional, Casson, Stuart A., additional, Castaño, Justo P., additional, Cebrat, Marek, additional, Chappe, Valerie, additional, Chatenet, David, additional, Chen, Keqiang, additional, Chen, Chen, additional, Chen, Longchuan, additional, Chen, Duan, additional, Cheng, Carrie Y.Y., additional, Cho, Sung Ki, additional, Chow, Billy K.C., additional, Christopoulos, Arthur, additional, Chu, Shijian, additional, Clarke, Iain J., additional, Coast, Geoffrey M., additional, Compere, Vincent, additional, Concepcion, Gisela P., additional, Cone, Roger D., additional, Conlon, J. Michael, additional, Cornélissen, Germaine, additional, Courel, Maité, additional, Couture, Réjean, additional, Cramer, W.A., additional, Croft, Nathan P., additional, Crujeiras, Ana B., additional, Cuttitta, Frank, additional, Cynis, Holger, additional, D’Acquisto, F., additional, Davis, Jon F., additional, Davis, Thomas P., additional, de La Serre, Claire Barbier, additional, de Lartigue, Guillaume, additional, de Lecea, Luis, additional, de Oliveira Santos, Marcelo, additional, De Waard, Michel, additional, Bolette Hartmann, Carolyn F. Deacon, additional, Delestre, Charlène, additional, Delgado, Mario, additional, Demuth, Hans-Ulrich, additional, Deng, Xiaoming, additional, Dharmawardhana, Palitha, additional, Di Cosmo, Anna, additional, Dias, Simoni Campos, additional, Dickerson, Jonathan W., additional, Diep, Dzung B., additional, Dircksen, H., additional, Dischinger, Jasmin, additional, do Rego, Jean-Claude, additional, Dobner, Paul R., additional, Dockray, Graham J., additional, Dores, Robert M., additional, Ducroc, Robert, additional, Dudek, Nadine L., additional, Dumont, Yvan, additional, Duraffourd, Celine, additional, Duterte-Boucher, Dominique, additional, Eberlé, Alex N., additional, Egleton, Richard D., additional, Eipper, Betty A., additional, Engel, Jorg B., additional, Englander, Ella W., additional, Epelbaum, Jacques, additional, Erlanson-Albertsson, Charlotte, additional, Evangelista, S., additional, Fagan, Karen A., additional, Farber, Joshua M., additional, Farkasfalvi, Klára, additional, Fekete, Csaba, additional, Flatt, Peter R., additional, Flower, R.J., additional, Forssmann, Wolf-Georg, additional, Fournier, Alain, additional, Foy, Kevin Chu, additional, Franco, Octávio Luiz, additional, Frenkel, Dan, additional, Fricker, Lloyd D., additional, de la Fuente-Núñez, César, additional, Fukuda, Hiroo, additional, Gäde, Gerd, additional, Galas, Ludovic, additional, Gallagher, Patricia E., additional, Gandolfo, Pierrick, additional, Garcia-Espinosa, Maria A., additional, García-Sanmartín, Josune, additional, Geary, Nori, additional, Geng, Hua, additional, Germano, Patrizia M., additional, Goetze, Jens P., additional, Gonzalez, Alexis A., additional, Gonzalez, Ana, additional, Gosnell, Blake A., additional, Goto, Katsutoshi, additional, Gourcerol, Guillaume, additional, Gozes, I., additional, Gracia-Navarro, Francisco, additional, Grayson, Bernadette E., additional, Greeley, George H., additional, Greenwald-Yarnell, Megan, additional, Gressens, Pierre, additional, Grider, John R., additional, Grünewald, Jan, additional, Guerreiro, Juliano R., additional, Guerrini, Remo, additional, Guida, Filomena, additional, Guilhaudis, Laure, additional, Guilmeau, Sandra, additional, Gundlach, Andrew L., additional, Gutkowska, Jolanta, additional, Hackbarth, Clifton, additional, Haim Ohana, Y., additional, Halberg, Franz, additional, Hallberg, Mathias, additional, Hamidi, Sayyed A., additional, Han, Song, additional, Han, Ji-Sheng, additional, Hancock, Robert E.W., additional, Haque, Samer-ul, additional, Hara-Nishimura, Ikuko, additional, Hariton, Aliza, additional, Hartsock, Wendy J., additional, Harvey, Alan L., additional, Hasunuma, Itaru, additional, Henning, Robert J., additional, Heppner, Kristy M., additional, Hertweck, Kate L., additional, Herzog, Herbert, additional, Higashiyama, Tetsuya, additional, Hinuma, Shuji, additional, Hippenstiel, Stefan, additional, Hirakawa, Yuki, additional, Hirose, Shuichi, additional, Hirsch, Jochen R., additional, Hocke, Andreas C., additional, Hodges, Robert S., additional, Hoffmann, Werner, additional, Hökfelt, Tomas, additional, Holst, Jens Juul, additional, Holzer, Peter, additional, Horodyski, Frank M., additional, Hosoda, Hiroshi, additional, Hou, Xiaowen, additional, Huffaker, Alisa, additional, Iijima, Norio, additional, Ikeuchi, Momoko, additional, Imperial, Julita S., additional, Improta, Giovanna, additional, Inui, Akio, additional, Irwin, Nigel, additional, Ishii, Munehiro, additional, Iturrioz, Xavier, additional, Ivanisevic, Ljubica, additional, Iwao, Hiroshi, additional, Iwata, Takeo, additional, Izumi, Yasukatsu, additional, Izumiyama, Hajime, additional, Jankowski, Marek, additional, Janssen, Tom, additional, Jégou, Sylvie, additional, Jensen, Robert T., additional, Jethwa, Preeti H., additional, Johannessen, Helene, additional, Johanson, Conrad, additional, Judkowski, Valeria, additional, Kaczmarek, Przemyslaw, additional, Kageyama, Haruaki, additional, Kakimoto, Tatsuo, additional, Kang, Ki Sung, additional, Kangawa, Kenji, additional, Kastin, Abba J., additional, Kato, Johji, additional, Kaumaya, Pravin T.P., additional, Keep, Richard F., additional, Kem, William R., additional, Khomenko, Tetyana, additional, Kikuyama, Sakae, additional, Kim, Young-Joon, additional, Kimura, Sadao, additional, King, Ross, additional, Kiptoo, Paul, additional, Kishimoto, Ichiro, additional, Kitamura, Kazuo, additional, Kluczyk, Alicja, additional, Kobori, Hiroyuki, additional, Kodama, Yosuke, additional, Kojima, Masayasu, additional, Kondo, Yuki, additional, Körner, Meike, additional, Kosson, Piotr, additional, Kotz, Catherine M., additional, Krishnan, Bhavani, additional, Kulseng, Bård, additional, Kumpf, Robert, additional, Laburthe, Marc, additional, Lacaille, Hélène, additional, Ladenheim, Ellen E., additional, Ladram, Ali, additional, Laksitorini, Marlyn D., additional, Lambert, David G., additional, Lange, Angela B., additional, Langhans, Wolfgang, additional, Larauche, Muriel, additional, Larhammar, Dan, additional, Larráyoz, Ignacio M., additional, Lattanzi, Roberta, additional, Lechan, Ronald M., additional, Lefranc, Benjamin, additional, Leibowitz, Sarah F., additional, Lelièvre, Vincent, additional, Leprince, Jérôme, additional, Levine, Allen S., additional, Li, Qun, additional, Lifshitz, Veronica, additional, Lihrmann, Isabelle, additional, Chi-Jen Lin, James, additional, Lindberg, Iris, additional, Lindsey, Keith, additional, Lipkowski, Andrzej W., additional, Liron, T., additional, Liu, Junli, additional, Liu, Ying, additional, Liu, Min, additional, Llorens-Cortes, Catherine, additional, Loizidou, Marilena, additional, Lopez, C., additional, Lovejoy, David A., additional, Luca, Vincenzo, additional, Lutz, Thomas A., additional, Ma, Sherie, additional, Mains, Richard E., additional, Malagon, Maria M., additional, Malendowicz, Ludwik K., additional, Wan, Jennifer Man-Fan, additional, Mangoni, Maria Luisa, additional, Manigrasso, Michaele B, additional, 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Published
2013
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44. Diminished feeding responsiveness to orexin A (hypocretin 1) in aged rats is accompanied by decreased neuronal activation

Author

Kotz, Catherine M., Mullett, Mary A., and Wang, ChuanFeng

Subjects
Biological sciences
Abstract

Orexin A is produced in caudal lateral, posterior, perifornical, and dorsomedial hypothalamic areas. Orexin A in the rostro-dorsal lateral hypothalamic area (rLHa) stimulates feeding and activates several feeding-regulatory brain areas. We hypothesized that aging diminishes feeding and c-Fos-immunoreactivity (c-Fos-ir; marker of neuronal activation) response to orexin A. Young (3 mo), middle-aged (12 mo), and old (24 mo) male Fischer 344 rLHa-cannulated rats were injected with orexin A (0.5, 1, and 2 nmol). Food intake was measured at 1, 2, and 4 h. c-Fos-ir in hypothalamic, limbic, and hindbrain regions was measured in two additional sets of rLHa-orexin A injected rats. In a separate study, orexin A effects on feeding and c-Fos-ir were measured in 6-mo-old rats. Orexin A significantly elevated feeding in rats aged 3, 6, and 12 mo in the 0-1 and 1-2- h time intervals, whereas in old rats this was significant in the 1-2 h time interval only. At 1 h, 6-8 (of 14) brain areas showed elevated c-Fos-ir in response to orexin A in 3- and 6-mo-old rats, but 24-mo-old rats exhibited attenuated or absent c-Fos-ir response in all brain regions except the hypothalamic paraventricular nucleus (PVN) and rostral nucleus of the solitary tract (rNTS). Orexin A did not elevate c-Fos-ir in 3-mo-old rats at 2 h after injection, whereas the PVN and mediodorsal thalamic nucleus (MD) showed elevated c-Fos-ir at 2 h in 24-mo-old rats. These data suggest that delayed and diminished feeding responses in old animals may be due to ineffective neural signaling and implicate the orexin A network as one feeding system affected by aging. feeding behavior; sleep; lateral hypothalamus; aging; c-Fos-immunoreactivity

Published
2005

46. Orexin A (hypocretin 1) injected into hypothalamic paraventricular nucleus and spontaneous physical activity in rats

Author

Kiwaki, Kohji, Kotz, Catherine M., Wang, Chuanfeng, Lanningham-Foster, Lorraine, and Levine, James A.

Subjects
Obesity -- Research, Biological sciences
Abstract

Kiwaki, Kohji, Catherine M. Kotz, Chuanfeng Wang, Lorraine Lanningham-Foster, and James A. Levine. Orexin A (hypocretin 1) injected into hypothalamic paraventricular nucleus and spontaneous physical activity in rats. Am J Physiol Endocrinol Metab 286: E551-E559, 2004. First published December 2, 2003; 10.1152/ ajpendo.00126.2003.--In humans, nonexercise activity thermogenesis (NEAT) increases with positive energy balance. The mediator of the interaction between positive energy balance and physical activity is unknown. In this study, we address the hypothesis that orexin A acts in the hypothalamic paraventricular nucleus (PVN) to increase non-feeding-associated physical activity. PVN-cannulated rats were injected with either orexin A or vehicle during the light and dark cycle. Spontaneous physical activity (SPA) was measured using arrays of infrared activity sensors and night vision videotaped recording (VTR). [O.sub.2] consumption and C[O.sub.2] production were measured by indirect calorimetry. Feeding behavior was assessed by VTR. Regardless of the time point of injection, orexin A (1 nmol) was associated with dramatic increases in SPA for 2 h after injection (orexin A: 6.27 [+ or -] 1.95 x [10.sub.3] beam break count, n = 24; vehicle: 1.85 [+ or -] 1.13 X [10.sup.3], n = 38). This increase in SPA was accompanied by compatible increase in [O.sub.2] consumption. Duration of feeding was increased only when orexin A was injected in the early light phase and accounted for only 3.5 [+ or -] 2.5% of the increased physical activity. In a dose-response experiment, increases in SPA were correlated with dose of orexin A linearly up to 2 nmol. PVN injections of orexin receptor antagonist SB-334867 were associated with decreases in SPA and attenuated the effects of PVN-injected orexin A. Thus orexin A can act in PVN to increase nonfeeding-associated physical activity, suggesting that this neuropeptide might be a mediator of NEAT. energy expenditure; hypothaiamus; obesity; nonexercise activity thermogenesls

Published
2004

48. Regional, metabolic, and circadian specificity of lateral hypothalamic orexin A feeding stimulation

Author

Thorpe, Andrew J., Mullett, Mary A., Wang, Chuanfeng, and Kotz, Catherine M.

Subjects
Human physiology -- Research, Hypothalamus -- Physiological aspects, Biological sciences
Abstract

Orexin A (OX-A) administered in the lateral hypothalamus (LH) increases feeding in a dose-dependent manner. The LH is a relatively large neural structure with a heterogeneous profile of neural inputs, efferent projections, and orexin receptor distribution. We sought to determine the LH region most sensitive to the feeding stimulatory effect of OX-A injection. Fifty-six male Sprague-Dawley rats were fitted with cannulas 1 mm above four separate LH regions ~1 mm apart in the rostral-caudal direction. There were 14-16 animals/LH region. After recovery, animals received either artificial cerebrospinal fluid or OX-A (250, 500, or 1,000 pmol). To determine whether there is a circadian effect of LH OX-A on the feeding response, we performed injections at 0200, 0900, 1400, and 2100. Food intake was measured at 1, 2, and 4 h after injection. The most rostral extent of the LH was the only region in which injection of OX-A significantly stimulated feeding. Within this region, feeding was increased at all times of the day, although the most robust and only significant feeding response occurred after the afternoon injection (1400) of OX-A. To determine the extent to which the metabolic status of the rat contributed to the circadian specificity of orexin-induced feeding, animals were placed on a restricted diet and injected with OX-A in the most rostral region of the LH. Under these conditions, OX-A significantly increased feeding and more robustly when compared with animals on a nonrestricted diet. These data suggest that the rostral LH is the only region of the LH sensitive to the injection of OX-A, and the metabolic status of the animal at the time of injection may influence the feeding response to OX-A. melanin-concentrating hormone; hypothalamus; hypocretin; restricted diet

Published
2003

49. Sugars and fats: the neurobiology of preference

Author

Levine, Allen S., Kotz, Catherine M., and Gosnell, Blake A.

Subjects
Sugar -- Physiological aspects, Sugar -- Health aspects, Dietary fat -- Physiological aspects, Dietary fat -- Health aspects, Opioids -- Physiological aspects, Neuropeptides -- Physiological aspects, Neurobiology, Dopamine -- Physiological aspects, Food/cooking/nutrition
Abstract

The appetite for specific foods and nutrients may be under neuroregulatory control. In animal studies, fat intake is increased by both opioids and galanin and reduced by enterostatin, whereas carbohydrate intake is increased by neuropeptide Y (NPY). However, what may be affected is the consumption of preferred foods rather than macronutrients. Fat and sugars are highly preferred whether consumed separately or as mixtures in foods. Studies suggest that sustained consumption of sugars and fats may have additional metabolic consequences; among these are neurochemical changes in brain sites involved in feeding and reward, some of which are also affected by drugs of abuse. Furthermore, the consumption of fats and sugars alters tissue expression of uncoupling proteins, which are also influenced by neuroregulatory peptides and may be markers of energy expenditure. These data suggest that these palatable nutrients may influence energy expenditure through changes in central neuropeptide activity. Fats and sugars could affect central reward systems, thereby increasing food intake, and might have an additional effect on energy expenditure. Such palatable substances may contribute to the observed increase in the body weight of populations from affluent societies during the past few decades. KEY WORDS: * sucrose * sugar * fat * opiods * neuropeptides * dopamine * energy expenditure

Published
2003

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