Skip to main content Accessibility help
×
Hostname: page-component-cd9895bd7-mkpzs Total loading time: 0 Render date: 2024-12-18T23:49:26.903Z Has data issue: false hasContentIssue false

2 - Regulation of food intake and body weight

from Part II - Scientific underpinnings

Published online by Cambridge University Press:  02 December 2009

Brett McDermott
Affiliation:
University of Queensland
Julian G. Mercer
Affiliation:
The Rowett Research Institute, Aberdeen, UK
Tony Jaffa
Affiliation:
Phoenix Centre, Cambridge
Get access

Summary

Introduction

To thrive, all mammals need to satisfy requirements for energy and nutrients. In order to maintain a stable body weight over an extended period, energy intake as solid or liquid food must be matched with energy expended in metabolism and physical activity with a remarkable degree of accuracy. For example, it has been calculated that the typical change in weight and body composition over a decade by an adult human would require energy supply and demand to be matched to a precision of around 0.2% (Weigle, 1994). This level of accuracy is achieved despite longitudinal variability in availability of, and requirement for, energy. For almost all mammals, other than those maintained under strictly controlled laboratory conditions, the composition, quality and quantity of food that is available for consumption will vary considerably between meals and from day to day, requiring the selection of a suitable combination of food types and quantities over longish periods to smooth out any temporary imbalances, such as a discontinuous supply. Similarly, energy demands will vary widely, being heavily influenced by factors such as developmental state (e.g. growing, reproducing), behaviour (e.g. social influences, migration) and environment (e.g. climate, season). Although the source of food may be discontinuous or irregular, a continuous supply of accessible energy is required for survival, necessitating storage of energy and nutrients, to ensure that supply always meets demand.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2006

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Ahima, R. S. & Flier, J. S. (2000). Leptin. Annual Review of Physiology, 25, 413–27.Google Scholar
Batterham, R. L., Cowley, M. A., Small, C. J.et al. (2002). Gut hormone PYY3-36 physiologically inhibits food intake. Nature, 418, 650–4.Google Scholar
Batterham, R. L., Cohen, M. A., Ellis, S. M.et al. (2003). Inhibition of food intake in obese subjects by peptide YY3-36. New England Journal of Medicine, 349, 941–8.Google Scholar
Bernardis, L. L. & Bellinger, L. L. (1998). The dorsomedial hypothalamic nucleus revisited: 1998 update. Proceedings of the Society for Experimental Biology and Medicine, 218, 284–306.Google Scholar
Clement, K., Vaisse, C., Lahlou, N.et al. (1998). A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature, 392, 398–401.Google Scholar
Cummings, D. E., Purnell, J. Q., Frayo, R. S., Schmidova, K., Wisse, B. E. & Weigle, D. S. (2001). A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes, 50, 1714–19.Google Scholar
Farooqi, I. S., Jebb, S. A., Langmack, G.et al. (1999). Effects of recombinant leptin therapy in a child with congenital leptin deficiency. New England Journal of Medicine, 341, 879–84.Google Scholar
Friedman, J. M. & Halaas, J. L. (1998). Leptin and the regulation of body weight in mammals. Nature, 395, 763–70.Google Scholar
Grill, H. J. & Smith, G. P. (1988). Cholecystokinin decreases sucrose intake in chronic decerebrate rats. American Journal of Physiology, 254, R853–6.Google Scholar
Hebebrand, J., Friedel, S., Schauble, N., Geller, F. & Hinney, A. (2003). Perspectives: molecular genetic research in human obesity. Obesity Reviews, 4, 139–46.Google Scholar
Heymsfield, S. B., Greenberg, A. S., Fujioka, K.et al. (1999). Recombinant leptin for weight loss in obese and lean adults – a randomized, controlled, dose-escalation trial. Journal of the American Medical Association, 282, 1568–75.Google Scholar
Kalra, S. P., Dube, M. G., Pu, S., Xu, B., Horvath, T. L. & Kalra, P. S. (1999). Interacting appetite-regulating pathways in the hypothalamic regulation of body weight. Endocrine Reviews, 20, 68–100.Google Scholar
Kristensen, P., Judge, M. E., Thim, L.et al. (1998). Hypothalamic CART is a new anorectic peptide regulated by leptin. Nature, 393, 72–6.Google Scholar
Krude, H., Biebermann, H., Luck, W., Horn, R., Brabant, G. & Gruters, A. (1998). Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans. Nature Genetics, 19, 155–7.Google Scholar
Larsen, P. J., Vrang, N. & Tang-Christensen, M. (2003). Central pre-proglucagon derived peptides: opportunities for treatment of obesity. Current Pharmaceutical Design, 9, 1373–82.Google Scholar
Leibowitz, S. F. & Wortley, K. E. (2004). Hypothalamic control of energy balance: different peptides, different functions. Peptides, 25, 473–504.Google Scholar
Mercer, J. G. & Lawrence, C. B. (1992). Selectivity of cholecystokinin (CCK) receptor antagonists, MK-329 and L-365,260, for axonally-transported CCK binding sites on the rat vagus nerve. Neuroscience Letters, 137, 229–31.Google Scholar
Mercer, J. G., Hoggard, N., Williams, L. M., Lawrence, C. B., Hannah, L. T. & Trayhurn, P. (1996). Localization of leptin receptor mRNA and the long form splice variant (Ob-Rb) in mouse hypothalamus and adjacent brain regions by in situ hybridization. FEBS Letters, 387, 113–16.Google Scholar
Montague, C. T., Farooqi, I. S., Whitehead, J. P.et al. (1997). Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature, 387, 903–8.Google Scholar
Ollmann, M. M., Wilson, B. D., Yang, Y. K.et al. (1997). Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein. Science, 278, 135–8.Google Scholar
Saper, C. B., Chou, T. C. & Elmquist, J. K. (2002). The need to feed: homeostatic and hedonic control of eating. Neuron, 36, 199–211.Google Scholar
Schwartz, G. J. (2004). Biology of eating behavior in obesity. Obesity Research, 12, 102S–6S.Google Scholar
Schwartz, M. W. & Niswender, K. D. (2004). Adiposity signalling and biological defense against weight gain: absence of protection or central hormone resistance?Journal of Clinical Endocrinology and Metabolism, 89, 5889–97.Google Scholar
Schwartz, M. W., Woods, S. C., Porte, D. Jr, Seeley, R. J. & Baskin, D. G. (2000). Central nervous system control of food intake. Nature, 404, 661–71.Google Scholar
Stellar, E. (1954). The physiology of motivation. Psychological Reviews, 61, 5–22.Google Scholar
Strader, A. D. & Woods, S. C. (2005). Gastrointestinal hormones and food intake. Gastroenterology, 128, 175–91.Google Scholar
Tartaglia, L. A., Dembski, M., Weng, X.et al. (1995). Identification and expression cloning of a leptin receptor, OB-R. Cell, 83, 1263–71.Google Scholar
Tschöp, M., Smiley, D. L. & Heiman, M. L. (2000). Ghrelin induces adiposity in rodents. Nature, 407, 908–13.Google Scholar
Weigle, D. S. (1994). Appetite and the regulation of body composition. FASEB Journal, 8, 302–10.Google Scholar
Williams, G., Cai, X. J., Elliott, J. C. & Harrold, J. A. (2004). Anabolic neuropeptides. Physiology and Behavior, 81, 211–22.Google Scholar
Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L. & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372, 425–32.Google Scholar
Zigman, J. M. & Elmquist, J. K. (2003). Minireview: from anorexia to obesity – the yin and yang of body weight control. Endocrinology, 144, 3749–56.Google Scholar

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×