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Nutrigenomics and chronic diseases

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6. Nutrigenomics and chronic diseases

Nutrition is the act of providing various constituents to the organism. Nutrients play important functions carbohydrates and fats are the source of energy, for the structure of cell protein is the best sources, vitamins and minerals is good for the control of metabolism, allowing the organism to maintain its homeostasis. The com- bination of different factors, like social state, emotional, physical activity and genetic background, determines an individual’s nutritional status [20]. Diet plays an impor- tant role because the minerals and other bioactive chemicals found in food can either be healthy or cause a variety of disorders. Many chronic disease like phenylketonuria, cancer, diabetes, and dyslipidemias, are among the disorders linked to food consump- tion. In this approach, a person’s health will be determined by the interaction of their genes and their dietary habits. As a result, nutrigenomics, like other omic sciences, aims to better understand the relationship among genes and diet (nutrients) [21].

6.1 Obesity

Obesity is the common problem now days different factors are responsible like environmental, genetic factors, lifestyle and metabolic syndromes. Genetic variables

Nutrigenomics: Challenges and Opportunities DOI: http://dx.doi.org/10.5772/intechopen.104438

account for 80 percent of the variance in body mass index (BMI) between twins.

Because obesity generates a persistent inflammatory response, using Nutrigenomics to control it is extremely promising. In food bioactive compounds are present like in olive oils tyrosol present, in fruits and greeneries quercetin present and in tomatoes lycopene is present etc. [22].

Food-derived bioactive chemicals can also interfere with genes in different ways. One of the principal pathways for the expression of gene modification is during transcription, when inflammatory mediators are synthesized, which plays a key role in a variety of chronic diseases, including obesity. Interleukin-1 is one of these mediators, and it induces the creation of numerous other molecules during the inflammatory cascade after it is activated. Green tea bioactive ingredient tocopherol works as an anti-inflammatory [12].

6.2 Cancer

Different factors are responsible for cancer like age, genetic, lifestyle, physical activity, and diet. Due to deficiencies of nutrients like vitamins E, C, B12, as folic acid, vitamin B6, C, and as well as zinc, selenium and niacin, have previously been found to cause change in DNA similar to those seen after contact to radiation. These changes can result in double-strand DNA breakage and oxidative damage. They were also found to be closely linked to the growth of cancer. Contaminated food produce harmful metabolites that regulate the gene expression [13].

Mutation has the potential to cause serious liver problems such cancer, necrosis and cirrhosis. During metabolism of folate, folic acid in food is absorbed by the intestine and converted into 5-methyltetrahydrofolate by a series of chemical catabo- lism and synthesis processes. 5-methyltetrahydrofolate component is required for the production of methionine, which is employed in the DNA mutilation process.

Therefore, a low-folic acid diet can disrupt this process and also interfere with the replication of DNA, increasing the risk of cancer formation. Nonetheless, many minerals defend against the development of cancer [23]. Selenium stimulates the production of glutathione peroxidase, an enzyme that reduces hydrogen peroxide and maintains the integrity of cell membranes and zinc which also influences processes such as apoptosis genomic stability modulation and genetic expression [24].

6.3 Diabetes

Around 90% of people in world suffer from diabetes. Type 2 diabetes is a complex disease that is caused by a combination of hereditary and environmental factors.

There are Single-nucleotide polymorphism SNPs linked to the likelihood of acquiring type 2 diabetes. Tests for the detection of SNPs linked to Type II Diabetes became available to the general public as genome sequencing and decoding progressed.

During these tests, the patient might find out if he or she has a genetic predisposition to developing the condition. Due to low food income and insulin tolerance, some people got diabetes later in life. Patients who had a positive result for the existence of type II diabetes changed their lifestyles, particularly their eating habits, which later reduced the disease’s progression in this group [1].

6.4 Cardiovascular

CVD is defined by the creation of intimal lesions in the blood arteries as a result of fibrosis, lipid buildup, inflammatory response, and cell death. According to a

WHO report, cardiovascular disease is the leading cause of death. Global estimates put the death toll at 17.5 million in 2012, representing for 31% among all deaths. In the treatment and prevention of cardiovascular disease, diet is essential. Changes in diet can protect genes involved in lipid metabolism and synthesis, such as arachidonate 5-lipoxygenase (ALOX5), apolipoprotein E (APOE), fatty acid synthase (FASN), and peroxisome proliferator activated receptors (PPARs), lipoprotein lipase (LPL), and others. The 28.1-kDa protein apolipoprotein (APOA1) is important for bodily disposal and is a form of high lipoprotein (HDL). This gene is used as a biomarker to diagnose cardiovascular illnesses like myocardial infarction in the early stages. As a result, HDL clearance from plasma is necessary while eating a low-fat diet. PUFAs play a key func- tion in influencing the expression of factors involved in glucose and lipid metabolism [25]. Fatty acids helps individuals lower their LDL cholesterol levels. Lipoxygenase, also known as arachidonate 5-lipoxigenase (5-LOX), is an important enzyme that controls the production of leukotrienes, inflammatory cytokines, and chemokines. Its expression is increased in atherosclerotic lesions, causing more inflammatory cells to be mobilized. Endothelial nitric oxide synthase in blood arteries converts L-arginine to nitric oxide (NO). By activating the guanylyl cyclase receptor and boosting cGMP levels, NO migration into vascular smooth cells devalues blood cells. It also works as a leukotriene and platelet aggregation inhibitor, lowering the risk of white blood cell adhesion and atherosclerosis. Increased eNOS expression has been linked to the creation of H2O2 and has been linked to endothelial dysfunction, which leads to CVD.

In both animals and humans, L-arginine has been demonstrated to be useful in the treatment of hypercholesterolemia. Omega three polyunsaturated fatty acids increase eNOS expression, resulting in vasorelaxation, while lowering circulating indicators such as E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 (VCAMs- 11) [26].

6.5 Cholesterol

The endothelium and leukocytes interact through the vascular cell adhesion molecule-1 (VCAM-1). During the start of atherosclerosis VCAM-1 binds monocytes and T lymphocytes, resulting in plaque development. However, proinflammatory cytokines such as tumor necrosis factor- (TNF-) and interleukin-1 generate oxidized lipids necessary for VCAM-1 expression (IL-1) [19].

6.6 Inflammation

The inflammatory process is known to be influenced by the nutritional composition of diet systems resulting in immune response regulation, via altering gene expression as well as interfering with signaling cascade. Inflammation is the body’s biological response to any invasion or injury, and it can be acute (short-term self-healing) or chronic (long- term). Inflammation later in life might linger for many years, leading to a variety of disorders such as cancer, intestinal allergies, atherosclerosis, and so on [23]. The immune system regulates the inflammatory process, and numerous immunological mediators play a key role. The famous spice curcuma longa (turmeric) has long been used in Ayurvedic medicine to treat inflammation. It includes a variety of bioactive chemicals, but ‘curcumin’ is one of the most important metabolites, accounting for a wide range of pharmacological actions including antioxidant, antibacterial, and anti-inflammatory effects. There is evidence that curcumin is a greatly pleiotropic chemical having potential to interact with inflammatory molecular targets. This was discovered as promising

Nutrigenomics: Challenges and Opportunities DOI: http://dx.doi.org/10.5772/intechopen.104438

Nutrients Gene Diseases Reference

Curcumin H+, K + - ATPase Help in the treatment of gastric ulcers [27]

IL-6,TNF-_, COX2 Reduces inflammation [28]

SOCS1–3,p38MAPK Trans locates nuclear material in a different way.

TLRs & MyD88 Infection with Helicobacter pylori has an anti-inflammatory impact.

[29]

Retinoic Acid TLR4/NF-kappa B It helps to minimize mastitis irritation. [30]

Vitamin E CRP, IL-8, PAI_1 Arthrosclerosis [31]

Sesamol MCP-1, RANTES, IL-1_, IL-6, and CXCL-16

Reduce the number of lesions caused by arthrosclerosis.

[32]

ABCA1, ABCA2, APO2, LCAY, CYP7AI, APOE,

Help in cholesterol metabolism and transportation

[32]

Vitamin B6 TNF_,, COX-2, iNOS and IL-6, IFN-_

Help in the inflammatory bowel diseases

[33]

Grains, legumes and refined rice

APOA5 c.-1131CNT and triglyceride and APOA-V

Diabetes type 2 [34]

Polymorphisms APOA5 Uyghur [35]

polymorphism Triglycerides and the APOA5 c.-1131TNC,

Age-related association in mice [35]

APOC3 (rs5128) Metabolic syndrome [36]

1β (PGC-1β), a co-activator of PPARγ

It reacts to changes in the macronutrient content of the food.

[37]

Selenoproteins DIO1, SEPHS1, DIO2, GPX1, TXNRD2, GPX3 and SEPSECS

Crohn’s disease [38]

Zinc ZNF365 Low zinc levels [39]

Eicosapentaenoic acid

omega-3 (n − 3) fatty acids are docosahexaenoic acid (DHA) the long chain polyunsaturated

Inflammation [40]

Vitamin D NOD2 Crohn’s disease [41]

Flavonoids and carotenoids

ω − 3 fatty acids Gene expression and oxidative stress production of inflammatory mediators

[42]

Gluten HLA-DQ (DQ2 and/or

DQ8)

Coeliac disease [43]

SNPs. SNPs Obesity, diabetes, cancers,

cardiovascular disease and brain disorders

[44]

Avian responses to nutrition

IGF1 and lysine (K)-specific histone demethylase 5A (KDM5A)

Growth and epigenetic regulation of genes

[45]

Vitamin D Retinoic acid receptor (RAR) binds

Nutritional imbalances have been linked to aging, behavioral problems, chronic fatigue, cardiovascular disease (CVD), diabetes, neurological disorders, cancer, immunological diseases, stroke, multiple sclerosis, Parkinson’s disease.

[46]

helpful not just for inflammatory diseases, but also for some tumors. Curcumin play an important role in the activity of H+, K + -ATPase and it also decreased the histone H3 acetylation, which hindered the expression of gene (H+, K + -ATPase). It regulates the production of cytokine signaling-1 (SOCS-1 and 3) and p38 MAPK suppressors, which suppress the expression of LPS-induced inflammatory mediators such as IL-6, TNF-_, and COX-2 mRNAs in macrophages. LPS-induced SOCS-1 and -3 expression as well as p38 MAPK kinase activation are reduced when nuclear translocation is altered further.

TNF-_ activity and production are reduced in vitro, in vivo, and in people when cur- cumin (diferyloylmethane) is taken orally, according to bioavailability and safety stud- ies. Vitamin A supplementation has been shown to help with a variety of inflammatory illnesses, including skin disorders and precancerous and cancerous situations. Retinoid, a vitamin A derivative, has been shown to prevent tumors growth and boost the immune system (Table 1) [19].