Nutrigenomics: From Molecular Nutrition to Prevention of Disease

Until recently, nutrition research concentrated on nutrient deficiencies and impairment of health. The advent of genomics—interpreted broadly as a suite of high throughput technologies for the generation, processing, and application of scientific information about the composition and functions of genomes—has created unprecedented opportunities for increasing our understanding of how nutrients modulate gene and protein expression and ultimately influence cellular and organismal metabolism. Nutritional genomics (nutrigenomics), the junction between health, diet, and genomics, can be seen as the combination of molecular nutrition and genomics. The diverse tissue and organ-specific effects of bioactive dietary components include gene-expression patterns (transcriptome); organization of the chromatin (epigenome); protein-expression patterns, including posttranslational modifications (proteome); as well as metabolite profiles (metabolome). Nutrigenomics will promote an increased understanding of how nutrition influences metabolic pathways and homeostatic control, how this regulation is disturbed in the early phases of diet-related disease, and the extent to which individual sensitizing genotypes contribute to such diseases. Eventually, nutrigenomics will lead to evidence-based dietary intervention strategies for restoring health and fitness and for preventing diet-related disease. In this review, we provide a brief overview of nutrigenomics from our point of view by describing current strategies, future opportunities, and challenges. [1]

Nutrigenomics: the Rubicon of molecular nutrition

The success of the Human Genome Project and the powerful tools of molecular biology have ushered in a new era of medicine and nutrition. The pharmaceutical industry expects to leverage data from the Human Genome Project to develop new drugs based on the genetic constitution of the patient; likewise, the food industry has an opportunity to position food and nutritional bioactives to promote health and prevent disease based on the genetic constitution of the consumer. This new era of molecular nutrition—that is, nutrient-gene interaction—can unfold in dichotomous directions. One could focus on the effects of nutrients or food bioactives on the regulation of gene expression (ie, nutrigenomics) or on the impact of variations in gene structure on one’s response to nutrients or food bioactives (ie, nutrigenetics). The challenge of the public health nutritionist will be to balance the needs of the community with those of the individual. In this regard, the excitement and promise of molecular nutrition should be tempered by the need to validate the scientific data emerging from the disciplines of nutrigenomics and nutrigenetics and the need to educate practitioners and communicate the value to consumers—and to do it all within a socially responsible bioethical framework. [2]

Peroxisome proliferator-activated receptors: Bridging metabolic syndrome with molecular nutrition

Over recent years, obesity rates and the onset of obesity-induced chronic diseases have risen dramatically. The more we learn about the physiological and morphological changes that occur during obesity, the more it is becoming clear that obesity-related disorders can be traced back to adipocyte hypertrophy and inflammation at white adipose tissue (WAT). To combat this problem, the body has developed a regulatory system specifically designed at mediating the systemic response to obesity, utilizing free fatty acids (FFAs) and their metabolites as nutrient messengers to signal adaptations from peripheral tissues. These messages are predominantly interceded through the peroxisome proliferator-activated receptors (PPARs), a family of ligand-induced transcription factors that serve as a net of lipid sensors throughout the body. Understanding how and why nutrients, nutrient derivatives and metabolites exert their physiological effects are the key goals in the study of molecular nutrition. By learning about the mechanisms and tissue-specific effects of endogenous PPAR ligands and expanding our knowledge of the body’s integrated homeostatic system, we will significantly increase our odds of designing safe and effective preventive and therapeutic interventions that keep us one step ahead of obesity-related diseases. [3]

Nutritional and Molecular Analysis of Wild Edible Gelam Mushroom (Boletus sp.) from Kelantan, Malaysia

Aims: To conduct nutritional and molecular analysis of Gelam mushroom which is believed to have contained medicinal properties.

Place and Duration of Study: School of Biosciences and Biotechnology, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, between 2012 and 2014.

Methodology: The fruiting body of Gelam mushroom was collected from Bachok, Kelantan. Proximate composition and mineral content of the fruiting body of this mushroom was analyzed according to the guidelines of Association of Official Analytical Chemists and Alam et al. respectively. Fungal specific primers pairs ITS1-F and ITS4 were used in molecular analysis.

Results: Every 100 g of fruiting body containing 0.13 g fat, 4.53 g protein, 3.13 g fiber, 0.87 g ash, 5.1 g carbohydrate, 4.4 mg Ca, 297.13 mg K, 7.27 mg Mg and 24.4 mg Na. Molecular analysis using internal transcribed spacer (ITS) region of nuclear ribosomal deoxyribonucleic acid (DNA) on Gelam mushrooms collected from the state of Kelantan, Malaysia were identified to be from Boletus genus.

Conclusion: Present study demonstrated that Gelam mushroom could be a new Boletus species and is a potential source of food rich in minerals. [4]

Cancer, Molecular Basis and Nutrition: A Review

This article reports some eating habits that should be avoided and those to be encouraged in order to preventing the development of cancers. Cancers are multifactorial in origin but the likelihood of their development are predisposed by some such risk factors as tobacco smoking, high salt intake, excessive consumption of saturated fats, refined foods and sugar, alcohol, red meat and processed red meat, prolong exposure to ultraviolet radiation, such chemicals as lead, benzene, and to infections of human papillomavirus and hepatitis virus. There are more than 100 types of cancer which vary in occurrence by sex, region, socio-economy and race. Mutation of DNA that results in cancer is a multistep involving oncogenes, mutated tumour suppressor genes, genes that regulate apoptosis, inappropriately-activated telomerase and epigenetic perturbations. Cancerous cells experience increased replication, transcription and glycolysis, reduced requirement for growth factors and other changes. About 30-40 per cent of cancer cases are preventable by such good dietary means as regular consumption of fruits including apple, berries, grapes; vegetable including carrots, tomatoes, cruciferous vegetables and garlics; unprocessed or whole grains and flax seeds because they contain vitamins, minerals, phytochemicals and antioxidants that serve as anti-cancers and protection against DNA damage. These can also be complemented with enzyme supplements. Understanding the molecular basis of cancer can give an insight into the protocol for aggregate prevention, treatment or/and curing of cancer. It is inter-alia recommended that about 5-6 or more serving a day of such vegetables as cruciferous, carrots, tomatoes, dark green vegetables, spinach etc., five or more serving a day of such fruits as apple, berries, grape etc. should be eaten; legumes such as beans, soya beans, peas, etc. and whole grain such as millet, sorghum, wheat, oats etc. should be regularly consumed; daily consumption of red meat and processed red meat should not be more than 40 g and be spiced up with a regular drinking of green tea. [5]

Reference

[1] Afman, L. and Müller, M., 2006. Nutrigenomics: from molecular nutrition to prevention of disease. Journal of the American Dietetic Association, 106(4), pp.569-576.

[2] Gillies, P.J., 2003. Nutrigenomics: the Rubicon of molecular nutrition. Journal of the American Dietetic Association, 103(12), pp.50-55.

[3] Guri, A.J., Hontecillas, R. and Bassaganya-Riera, J., 2006. Peroxisome proliferator-activated receptors: bridging metabolic syndrome with molecular nutrition. Clinical nutrition, 25(6), pp.871-885.

[4] Hafis Yuswan, M., On, Y.-Y., Tan, Y.-J., Lai, W.-H., Zainal, Z., Sz, J.-X. and Daud, F. (2017) “Nutritional and Molecular Analysis of Wild Edible Gelam Mushroom (Boletus sp.) from Kelantan, Malaysia”, Journal of Advances in Biology & Biotechnology, 13(3), pp. 1-7. doi: 10.9734/JABB/2017/33701.

[5] Sheriff, A. (2015) “Cancer, Molecular Basis and Nutrition: A Review”, Journal of Scientific Research and Reports, 8(1), pp. 1-14. doi: 10.9734/JSRR/2015/15564.