| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1
* Metabolic Research Laboratory, University of Navarra; and
Department of Endocrinology, Clínica Universitaria de Navarra, 31008-Pamplona, Spain
1Correspondence: Deptartment of Endocrinology, Clínica Universitaria de Navarra, 31008-Pamplona, Spain. E-mail: gfruhbeck{at}unav.es
Parabiosis studies with obese rodents demonstrated that circulating factors are involved in the long-term control of food intake and energy balance. More than 40 years ago it was hypothesized that rats made obese by hypothalamic or dietary means, as well as genetically obese fa/fa rats and db/db mice, produce a circulating factor that either inhibits food intake or acts metabolically to reduce the fat content of non-obese ad libitum-fed partners. However, none of these obese rodents showed a significant change in weight when parabiosed to a normal animal. It was therefore postulated that these obese rodents produced a circulating lipostatic factor but were unable to respond to it. In contrast, genetically obese ob/ob mice were thought to be deficient in the circulating signal, as they lost weight when parabiosed to lean or obese db/db mice. The discovery of leptin suggested that the circulating lipostatic signal had been identified. However, a closer look at the outcome of the parabiotic studies reveals that leptin alone does not explain all of the findings of the parabiotic experiments. Another (or more than one) as yet unidentified factor(s) may be involved in energy balance regulation. The evidence for the existence of further leptin-like hormones comes from observations in which the direct effect of leptin has been eliminated or can be excluded.—Frühbeck, G., Gómez-Ambrosi, J. Rationale for the existence of additional adipostatic hormones.
Key Words: leptin • parabiosis • lipostatic factor • obesity • energy balance
This article has been cited by other articles:
|
|
 |
|
  S. Miyamoto, Y. Yasui, T. Tanaka, H. Ohigashi, and A. Murakami Suppressive effects of nobiletin on hyperleptinemia and colitis-related colon carcinogenesis in male ICR mice Carcinogenesis, May 1, 2008; 29(5): 1057 - 1063. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Collinson, S. Moore, M. O'Connell, C. Charalambos, and A. Prentice Developmental changes in leptin as a measure of energy status in human infants in a natural ecologic setting Am. J. Clinical Nutrition, February 1, 2005; 81(2): 488 - 494. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Hirose, K. Hata, T. Kuno, K. Yoshida, K. Sakata, Y. Yamada, T. Tanaka, B. S. Reddy, and H. Mori Enhancement of development of azoxymethane-induced colonic premalignant lesions in C57BL/KsJ-db/db mice Carcinogenesis, May 1, 2004; 25(5): 821 - 825. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
