**Abstract**

Healthy diet and proper nutrition are basic necessity of life and play a key role in preventing diseases. Nutrigenomics (NG) is an emerging approach in nutritional research which deals with the gene-diet interactions. The concept of nutrigenomics is not new and it is commonly associated with "inborn errors of metabolism", the rare genetic (inherited) disorders in which the body cannot properly turn food into energy. These disorders are related to insufficient availability of metabolic enzymes or cofactors due to alteration of gene. Usually cure of these diseases lies in restricted diet. Presently non communicable diseases (NCDs) like cardiovascular diseases, obesity, diabetes and cancers are outnumbering the other health ailments among the different human populations of world. The main reason behind the occurrence of these NCDs is the abruptly changing life style and food habits after industrial revolution. With the advent of industrial revolution and economical concerns, the life style of people across the world has changed so much so that it resulted in approximately millions of death cases due to these NCDs. Study related to NG is one step forward in nutritional research involving the techniques of nutrition, molecular biology, genomics, bioinformatics, molecular medicine and epidemiology together to understand the role of food as an epigenetic factor which unravel its role in the occurrence of these diseases. Hence, under the prevailing scenario of world health, it has become an urgency to boost NG research to find cure for dreaded diseases caused due to lack of healthy food and improper nutrition. Thus, such type of research findings ensures the effective benefit of genomic revolution for mankind near future.

**Keywords:** nutrigenomics, non communicable diseases, personalized nutrition, human health, genomic study

## **1. Introduction**

Life, as a single-cell embryo, which is literally an envelope of the human diploid genome primed for replication. Almost every cell of a multicellular organism contains the same type of genetic material—its genome. Chromosomes, nucleic acid molecules that are the repository of an organism's genetic information, are the largest molecules in a cell and may contain thousands of genes as well as considerable tracts of intergenic DNA. This genome has to be replicated with high fidelity millions of times during development to a fetal and adult stage and millions of times thereafter simply to replenish dead cells and cells lost as a result of exfoliation. Many cofactors and substrates are required for DNA replication and DNA repair. Any error during proof reading of DNA may lead to faulty

replication, accumulation of such errors may further trigger cell death by apoptosis. Consequently, there is an accumulation of mutations at the base sequence or chromosomal level as a result of genotoxic insults due to endogenous and exogenous factors is now recognized as a fundamental underlying cause of developmental defects and accelerated aging as well as of an increased risk of degenerative conditions such as infertility, immune dysfunction, cancer, and cardiovascular and neurodegenerative diseases [1–5].

Dietary reference values (DRVs) provide us a guide for the appropriate intake of nutrients for prevention of diseases caused by deficiency (e.g., scurvy in the case of vitamin C deficiency) or excess (e.g., iron-overload disease, which may be fatal in excess iron in the cell system) [6]. It is important to determine these extreme conditions associated with nutritional disorders now-a-days and the biggest challenge lies in the prevention of these type of developmental and degenerative disease in populations which are not short of food, fortified food, or supplements but needs intervention through appropriate intake of micronutrients individually or in combination (nutriomes) to optimize cellular and organism performance on both a personal and a genetic subgroup level at different life stages. Optimization of cellular function ultimately depends on the prevention of damage to the nuclear and mitochondrial genome [7–9].

### **1.1 Nutrigenomics**

Nutrigenomics, an globally emerging high-throughput science which depicts the effect of genetic variation in response to diet. The term "nutrigenomics" was first given by Peregrin [10] and after one year it was reviewed by Van Ommen and Stierum, [11]. In a molecular era, Wellen and Hotamisligil, [12], considered nutrients as "signalling molecules" which transmit and translate the dietary signals into the cell and within the cellular system it changes the expression of genes in nucleus leads to changes in protein and metabolite expression. Now the big question arises that what is happening within the cell system when we are having our meals in less or excess amount? So to get the answer of this question we have to study in detail of food-gene interlinking signaling mechanism which is the science behind nutrigenomics.

The sciences of nutrigenetic and nutrigenomic are based on three central factors i.e. firstly, there is a great inherited genomic diversity between the ethnic groups and individuals affected by nutrient bioavailability and its metabolism. Secondly, people may differ greatly in their food habit/nutrient availability and choices depending on cultural, geographical, economical, and taste perception differences. Thirdly, malnutrition (deficiency or excess) itself can affect gene expression and genome stability [13].

The field, nutrigenomics involves multiple disciplines under one umbrella to the study the designing of individual's diet that leads to stability of genomes by minimizing the DNA damage, epigenome alterations (DNA methylation), transcriptomics (i.e. RNA and micro-RNA expression), proteomics (protein expression) and finally metabolomics i.e. controlled metabolite changes. Study of all the field individually and interlinking of all is very important.

Within nutrigenomics, the studies related to nutrient-gene interaction and its potential for both intra- and transgenerational effects is epigenetics [14, 15]. In genetics, epigenetics is the processes which control the expression of certain genes by up/ down regulating without altering the DNA sequence, whereas the reversible changes of gene expression in epigenetics is due to DNA methylation, histone modification and chromatin-associated proteins which controls the expression of house-keeping genes and suppress the expression of parasitic DNA such as transposons. However,

**11**

*Nutrigenomics: An Interface of Gene-Diet-Disease Interaction*

human population from such non-communicable diseases?

**2. Dietary signals and nutrient sensors**

epigenomics is the study which deals with the analytical part of complete epigenetic changes takes place on a genome in a cell/entire organism. Epigenetic processes strongly influenced the normal growth and development of an organism. The epigenomic changes can be inherited upto 2 to 3 generation, which is modified by diet. In a nutshell, the study of nutrigenomics requires a collaborative effort to protect

the human population from endangered diseases by maintaining the balance in genetics and the industries of public health, food science and culinary. It's very easy task to make a tasty food by putting some lard or butter in it, and it's going to be tasty and yummy. But the whole population have to accept the challenge that how to prepare good tasty healthy food without using much oil or butter or ghee or any kind of unhealthy food product which is not good for health. By observing the present trend of increasing lifestyle disease, personalised nutrition diet chart should be prescribed based on individuals genomic construction by the nutritionist and this will be the future aspect of nutrigenomics. This chapter has emphasized on the nutrigenomics approach based on gene-diet interaction in relevance to existing advance studies to understand its present and future prospect, and how to protect

Dealing with the complex human genome, nutrigenomics has the ability to decipher variability of genome in terms of wide range of nutrient concentration and a variety of food nutrition by identification of specific dietary signal, signal sensing or perceiving receptors. Ruden et al., [16] did an nutrigenomics research, an experiment with Drosophila which is model organism and depicted that each and every nutrient have numerous targets sites with various affinities and specificities. It was found that, drosophila has adipose-like tissues and a lipid transport system, which has a similarity with humans in respect to obesity and associated diseases than any other model organisms. In addition, Müller and Kersten [17] recognized specialized cellular-sensing mechanisms and considered nutrients and dietary metabolitesas signaling elements. The molecular structure of the nutrients are naturally designed in such a way that it carries the information that how to activate a specific signaling pathways to hit the target site. Minor changes in structure (e.g., saturated vs unsaturated fatty acids or cholesterol vs plant sterols) can have a profound influence on which sensor pathways are activated. Its a great challenge for the scientist to identify the molecular pathways and the up/downstream regulation by each nutrients. Study of nutrigenomics can allow the identification of molecular pathways by genomewide characterization of nutritional target genes. This type of information can help the researchers to understand the plan of action of individual nutrient and how it is linked with diet which has an important role in good health and diseases. Ultimately, nutrigenomics research will lead to development of evidence-based healthful food

and lifestyle advice and dietary interventions for contemporary humans. For instance, Patsouris et al., [18] revealed that though the role of PPARα towards obesity is unclear then also there is some clue where PPARα has some important function in obesity-linked pathophysiology of type 2 diabetes. Recently,

it has been demonstrated that PPARα directly regulates expression of genes involved in hepatic gluconeogenesis and glycerol metabolism [18, 19]. Visceral obesity is linked to increased free fatty acid levels [20], elevated levels of free fatty acids in the cytosol promote the plasma free fatty acids to binds with the PPARα, and these molecules may be recognized by the liver as "hunger" or "in need of glucose" signals resulting in increased gluconeogenesis in a PPARα-dependent manner,

particularly under conditions of hepatic insulin resistance.

*DOI: http://dx.doi.org/10.5772/intechopen.94602*

*Nutrigenomics: An Interface of Gene-Diet-Disease Interaction DOI: http://dx.doi.org/10.5772/intechopen.94602*

*Mineral Deficiencies - Electrolyte Disturbances, Genes, Diet and Disease Interface*

neurodegenerative diseases [1–5].

and mitochondrial genome [7–9].

**1.1 Nutrigenomics**

nutrigenomics.

genome stability [13].

replication, accumulation of such errors may further trigger cell death by apoptosis.

chromosomal level as a result of genotoxic insults due to endogenous and exogenous factors is now recognized as a fundamental underlying cause of developmental defects and accelerated aging as well as of an increased risk of degenerative conditions such as infertility, immune dysfunction, cancer, and cardiovascular and

Dietary reference values (DRVs) provide us a guide for the appropriate intake of nutrients for prevention of diseases caused by deficiency (e.g., scurvy in the case of vitamin C deficiency) or excess (e.g., iron-overload disease, which may be fatal in excess iron in the cell system) [6]. It is important to determine these extreme conditions associated with nutritional disorders now-a-days and the biggest challenge lies in the prevention of these type of developmental and degenerative disease in populations which are not short of food, fortified food, or supplements but needs intervention through appropriate intake of micronutrients individually or in combination (nutriomes) to optimize cellular and organism performance on both a personal and a genetic subgroup level at different life stages. Optimization of cellular function ultimately depends on the prevention of damage to the nuclear

Nutrigenomics, an globally emerging high-throughput science which depicts the effect of genetic variation in response to diet. The term "nutrigenomics" was first given by Peregrin [10] and after one year it was reviewed by Van Ommen and Stierum, [11]. In a molecular era, Wellen and Hotamisligil, [12], considered nutrients as "signalling molecules" which transmit and translate the dietary signals into the cell and within the cellular system it changes the expression of genes in nucleus leads to changes in protein and metabolite expression. Now the big question arises that what is happening within the cell system when we are having our meals in less or excess amount? So to get the answer of this question we have to study in detail of food-gene interlinking signaling mechanism which is the science behind

The sciences of nutrigenetic and nutrigenomic are based on three central factors i.e. firstly, there is a great inherited genomic diversity between the ethnic groups and individuals affected by nutrient bioavailability and its metabolism. Secondly, people may differ greatly in their food habit/nutrient availability and choices depending on cultural, geographical, economical, and taste perception differences. Thirdly, malnutrition (deficiency or excess) itself can affect gene expression and

The field, nutrigenomics involves multiple disciplines under one umbrella to the study the designing of individual's diet that leads to stability of genomes by minimizing the DNA damage, epigenome alterations (DNA methylation), transcriptomics (i.e. RNA and micro-RNA expression), proteomics (protein expression) and finally metabolomics i.e. controlled metabolite changes. Study of all the field

Within nutrigenomics, the studies related to nutrient-gene interaction and its potential for both intra- and transgenerational effects is epigenetics [14, 15]. In genetics, epigenetics is the processes which control the expression of certain genes by up/ down regulating without altering the DNA sequence, whereas the reversible changes of gene expression in epigenetics is due to DNA methylation, histone modification and chromatin-associated proteins which controls the expression of house-keeping genes and suppress the expression of parasitic DNA such as transposons. However,

individually and interlinking of all is very important.

Consequently, there is an accumulation of mutations at the base sequence or

**10**

epigenomics is the study which deals with the analytical part of complete epigenetic changes takes place on a genome in a cell/entire organism. Epigenetic processes strongly influenced the normal growth and development of an organism. The epigenomic changes can be inherited upto 2 to 3 generation, which is modified by diet.

In a nutshell, the study of nutrigenomics requires a collaborative effort to protect the human population from endangered diseases by maintaining the balance in genetics and the industries of public health, food science and culinary. It's very easy task to make a tasty food by putting some lard or butter in it, and it's going to be tasty and yummy. But the whole population have to accept the challenge that how to prepare good tasty healthy food without using much oil or butter or ghee or any kind of unhealthy food product which is not good for health. By observing the present trend of increasing lifestyle disease, personalised nutrition diet chart should be prescribed based on individuals genomic construction by the nutritionist and this will be the future aspect of nutrigenomics. This chapter has emphasized on the nutrigenomics approach based on gene-diet interaction in relevance to existing advance studies to understand its present and future prospect, and how to protect human population from such non-communicable diseases?

## **2. Dietary signals and nutrient sensors**

Dealing with the complex human genome, nutrigenomics has the ability to decipher variability of genome in terms of wide range of nutrient concentration and a variety of food nutrition by identification of specific dietary signal, signal sensing or perceiving receptors. Ruden et al., [16] did an nutrigenomics research, an experiment with Drosophila which is model organism and depicted that each and every nutrient have numerous targets sites with various affinities and specificities. It was found that, drosophila has adipose-like tissues and a lipid transport system, which has a similarity with humans in respect to obesity and associated diseases than any other model organisms. In addition, Müller and Kersten [17] recognized specialized cellular-sensing mechanisms and considered nutrients and dietary metabolitesas signaling elements. The molecular structure of the nutrients are naturally designed in such a way that it carries the information that how to activate a specific signaling pathways to hit the target site. Minor changes in structure (e.g., saturated vs unsaturated fatty acids or cholesterol vs plant sterols) can have a profound influence on which sensor pathways are activated. Its a great challenge for the scientist to identify the molecular pathways and the up/downstream regulation by each nutrients. Study of nutrigenomics can allow the identification of molecular pathways by genomewide characterization of nutritional target genes. This type of information can help the researchers to understand the plan of action of individual nutrient and how it is linked with diet which has an important role in good health and diseases. Ultimately, nutrigenomics research will lead to development of evidence-based healthful food and lifestyle advice and dietary interventions for contemporary humans.

For instance, Patsouris et al., [18] revealed that though the role of PPARα towards obesity is unclear then also there is some clue where PPARα has some important function in obesity-linked pathophysiology of type 2 diabetes. Recently, it has been demonstrated that PPARα directly regulates expression of genes involved in hepatic gluconeogenesis and glycerol metabolism [18, 19]. Visceral obesity is linked to increased free fatty acid levels [20], elevated levels of free fatty acids in the cytosol promote the plasma free fatty acids to binds with the PPARα, and these molecules may be recognized by the liver as "hunger" or "in need of glucose" signals resulting in increased gluconeogenesis in a PPARα-dependent manner, particularly under conditions of hepatic insulin resistance.

Mandard et al., [19], Kersten et al., [21] reported that fasted PPARα null mice mutant (lack of functional PPARα) suffers from a variety of metabolic defects, include hypothermia, hypoglycemia, hypoketonemia, and elevated plasma-free fatty acid levels.
