Downloaded from

https://www.cambridge.org/core

British Journal of Nutrition (2003), 89, 1–2 DOI: 10.1079/BJN2002780 q The Author 2003

Editorial

. IP address:

Nutritional – “Nutrigenomics” 170.106.40.219

, on

27 Sep 2021 at 01:18:16

I have commented previously on what is perceived to have of biological systems at different levels of organisation and been the slowness, indeed reluctance, of nutritional science how these systems are integrated. The words of Eliot are, to incorporate concepts and technologies from the cutting perhaps, in practice especially apposite here. edge of genomics and of molecular and cellular biology The extent to which nutritional science has now aligned

(Trayhurn, 1998). In the last 2–3 years it is apparent that itself with is illustrated by the very , subject to the Cambridge Core terms of use, available at this situation has changed. Indeed, the gap between nutri- recent emergence of the new area of ‘nutritional geno- tional science and the frontiers of biology have, in my mics’, or ‘nutrigenomics’ as it is also termed. Indeed, view, been closing rapidly. This is partly because the over the last year or so there have been major develop- importance of nutrition has been increasingly recognised ments in Europe such as the establishment of a ‘Network by those in other fields such that they have begun to for ’ under the auspices of INSERM apply their expertise to nutritional issues. But in addition, in France and a similar initiative ‘The Centre for Human those in nutrition have also come to appreciate the need Nutrigenomics’ in the Netherlands. Parallel initiatives to harness the developments that are taking place have been taking place elsewhere, both on a national and elsewhere. a local level (e.g. the ‘Nutrigenomic Network Potsdam- The publication in February 2001 of the draft sequence of Berlin’). My own University has recently established the the human through the Project, ‘Liverpool Centre for Nutritional Genomics’, bringing with parallel papers in Nature and Science (Lander et al. together a group of senior scientists involved in functional 2001; Venter et al. 2001), is in many ways a major mile- genomics in relation to a range of nutritional issues. stone for nutrition as for other sciences. It has been followed Nutritional genomics covers a broad canvas. It encom- by a draft of the mouse genome sequence (http://www. passes the interaction between nutrients and the expression https://www.cambridge.org/core/terms ensembl.org/Mus_musculus/; see Marshall, 2002), aiding of genes, harnessing techniques such as DNA microarrays the identification of the function of unknown human genes and real-time PCR. It involves the characterisation of gene and their putative involvement in disease processes. products and the physiological function and interactions The human genome sequence is very much a beginning of these products; the latter includes how nutrients and not an end, a point emphasised by the publically- impact on the production and action of specific gene pro- funded International Consortium (Lander et al. 2001). ducts and how these proteins in turn affect the response Their paper is not only a landmark publication scientifi- to nutrients. As noted in a previous Editorial, cally, but also a model of scholarship, beginning as it is a key technology for the determination of the totality does with a reference to Gregor Mendel and ending with of gene products and their post-translational modification

a quotation from T.S. Eliot: “We shall not cease from (Trayhurn, 2000). .

https://doi.org/10.1079/BJN2002780 exploration. And the end of all our exploring will be to One of the key opportunities for nutritional genomics is arrive where we started, and to know the place for the the exploration of the link between specific gene poly- first time.” morphisms and the individual response to nutrients. Activity The sequencing of the human genome is a beginning in this area is now developing and there is a long-term goal since it provides a blueprint of biological potential, but of providing personalised dietary advice based on the pre- does not tell us what actually takes place – in other dicted response to nutrients derived from the genetic profil- words, what genes are expressed and what encoded pro- ing of an individual. With the growing focus on the teins are synthesised in which tissues and under what cir- identification of SNPs (single gene polymorphisms) in cumstances. Additionally, the genome tells us nothing of humans, this is an increasingly realistic long-term target. functionally critical post-translational changes in proteins There will, of course, be the issue of whether individuals such as glycosylation or phosphorylation. It is, of course, will respond more to personal nutritional advice tailored de rigeur to talk of being in the ‘post-genomic’ era with to their own genetic profile, than when advised generally the central task of biology now being ‘functional geno- on the basis of the population as a whole. mics’ – unravelling how genes and gene products operate. Obesity is one area where the application of both geno- The more cynical have regarded functional genomics mic and nutritional genomic approaches has already been essentially as a form of repackaging of what biologists highly successful, and as such it provides an exemplar have always sought to do – to understand the full complexity for nutrition as a whole. The most potent example comes Downloaded from

https://www.cambridge.org/core

2 P. Trayhurn from the identification by positional cloning of the gene References which in mutated form results in the obesity of the ob/ob mouse (Zhang et al. 1994). This in turn led to the discovery of a previously unknown hormone - leptin (and its recep- Arner P (2000) Obesity – a genetic disease of adipose tissue? tors) – which provides a direct signal from adipose British Journal of Nutrition 83, Suppl 1, S9–S16. . IP address: tissue to the brain, influencing food intake. It also resulted Cle´ment K, Vaisse C, Lahlou N, Cabrol S, Pelloux V, Cassuto D, in a radical change in perspective on the physiological role Gourmelen M, Dina C, Chambaz J, Lacorte JM, et al. (1998) A mutation in the human leptin receptor gene causes obesity and of white adipose tissue – as an endocrine organ, and not pituitary dysfunction. Nature 392, 398–401. 170.106.40.219 just a site of lipid storage (see Trayhurn & Beattie, Lander ES, Linton LM, Birren B, et al. (2001) Initial sequencing 2001). Mutations in the leptin and leptin receptor genes and analysis of the human genome. Nature 409, 860–921. have subsequently been shown to be associated with obes- Marshall E (2002) Public group completes draft of the mouse. ity in humans (Montague et al. 1997; Cle´ment et al. 1998; Science 296, 1005. , on

Strobel et al. 1998), while polymorphisms in several unre- Montague CT, Farooqi IS, Whitehead JP, Soos MA, Rau H, 27 Sep 2021 at 01:18:16 lated genes have been linked to increased body fatness Wareham NJ, Sewter CP, Digby JE, Mohammed SN, Hurst (Arner, 2000). JA, et al. (1997) Congenital leptin deficiency is associated Nutritional genomics/nutrigenomics will be a key area of with severe early-onset obesity in humans. Nature 387, nutritional science over the next decade. The significance 903–908. Strobel A, Issad T, Camoin L, Ozata M & Strosberg AD (1998) of its rapid development lies not only in the problems A leptin missense mutation associated with hypogonadism that can now be addressed, but also as a reflection of the and morbid obesity. Nature Genetics 18, 213–215. , subject to the Cambridge Core terms of use, available at closing of the cultural gap between nutrition and the Trayhurn P (1998) Molecular biology and nutrition: the quest for front-line of modern biology. integration. British Journal of Nutrition 80, 305–306. Trayhurn P (2000) Proteomics and Nutrition – A science for the Paul Trayhurn first decade of the new Millennium. British Journal of Nutrition Editor-in-Chief 83, 1–2. Liverpool Centre for Nutritional Genomics Trayhurn P & Beattie JH (2001) Physiological role of adipose Department of Medicine tissue: white adipose tissue as an endocrine and secretory University of Liverpool organ. Proceedings of the Nutrition Society 60, 329–339. Venter JC, Adams MD, Myers EW, et al. (2001) The sequence of Liverpool L69 3GA the human genome. Science 291, 1304–1351. U.K. Zhang YY, Proenca R, Maffei M, Barone M, Leopold L & Friedman JM (1994) Positional cloning of the mouse obese [email protected] gene and its human homolog. Nature 372, 425–432.

https://www.cambridge.org/core/terms

.

https://doi.org/10.1079/BJN2002780