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INTRODUCTION TO NUTRIGENOMICES
AND
ITS APPLICATIONS
DEPARTMENT OF PHARMACOLOGY
ISF COLLEGE OF PHARMACY, MOGA (PUNJAB)
1
Presented by : Sunpreet kaur
M.Pharm : Pharmacology (II nd sem)
Roll No: 160750015
Introduction
2
 Any nutrition can induce metabolic changes in muscles,
being reflected in tissue remodeling, increased protein turnover,
and muscle atrophy.
 Relationship of nutrition with health is well known.
 But how the components exert their effect is not known
completely till the date.
 Revolution in genomic field raise the question about how
genome get alters by nutrients.
Introduction
3
 Bioactive nutriental components are the key environment
factors regulating gene expression.
(Mead, 2007)
Advencements of molecular techniques and analysis systems
revealed the mechanism how nutrient status and their
metabolism acould alters genome.
With these knowledge a new area of study called
“NUTRIGENOMICS” has emerged.
(Roche et al 2006)
Why we need to study nutrigenomics…??
 Improper diets are risk factors for diseases.
 Dietary components alter gene expression and /or change
genome structure.
 Variation in genetic makeup could make a person prones
towards a disease.
 Some diet-regulated genes are likely to play a role in the
onset, incidence, progression and severity of chronic
diseases.
4
5
A time for New
Nutritional Strategies…!!!!
We need to make a change
what we take in diet
We need to change the way
we evaluate the diet
What are omics……????
 Omics is the term used to address the study of particular
field that includes all the events and techniques utilise to
understand that field.
 It explain us how genome work in genomics .
 Explains how any intraction causes alteration in genome
and how these alteration leads to specific disease
progression
6
Why to pay attention to omics…??
7
Some relevant omics to deal…..!!!
• Comparitive genomics
• Epigenomics
• Neurogenomics
• Toxicogenomics
• Personal genomics
• Neutrigenomics
• Cognitive genomics
• Metagenomics
8
Introduction to NUTRIGENOMICS
 Nutrigenomics is the branch of OMICS that utilises the
genomic tools and techniques to study the effect of dietery
components on genes.
 Nutrigenomics includes the interaction between nutrient
and gene.
 Nutrients modulate the expression and regulation of
coding genes for protein, metabolism, cellular
differentiation and growth.
9
Dual role of nutrigenomics
10
How diet affects our gene…????
11
How nutrients interacts to our gene..??
12
Common food gene ineractions
13
These are 5 basic principles of nutrigenomics (German,
2005):
 Substances contained in the food (micro- and macro-
nutrients) can directly or indirectly affect the human genome
through changes in its structure and gene expression.
Under certain circumstances and in some individuals the diet
can be an important risk factor for the development of the
number of diseases.
 Some genes regulated by active substances in the diet
probably play a crucial role in the onset, incidence, progression
and severity of the disease.
 The degree to which diet influences the balance between
health and disease may depend on individual’s genetic
makeup.
 Nutritional intervention is based on the knowledge of
individual’s nutritional status and needs as well as genotype
(individualized nutrition) and can be used for prevention,
mitigation or healing the chronic diseases.
15
Types of food gene ineraction
16
Direct interactions:
Nutrients interacts with a receptor behave as transcription
factors which can bind at the DNA level cause the acute
expression of a gene.
Epigenetic interactions:
Nutrients can alter the structure of DNA so that gene expression
is chronically altered.
Genetic variations:
Common genetic variations (single nucleotide polymorphism-
SNPs) can modify a expression or functionality of gene.
Food gene expression
17
DIRECT INTERACTIONS
Direct intertactions involves a short term trigger and causes the
acute modification of the transcription process.
This effect generally disappears once the exposure to the
specific nutrient has been stopped.
Examples of direct interactions are:
 Vitamin A interacts with retinoic acid receptor and the
resulted complex causes transcription activation or inhibition
of gene expression.
 Fatty acids can interact with PPAR (peroxisome proliferator-
activated receptors) which can modify genes expression by
attaching at DNA level
 Interaction between vitamin D and its receptor
18
EPIGENETIC INTERACTIONS
 Epigenetic mechanisms are mediated either by DNA
methylation or by histone methylation or acetylation.
 Such epigenetic modifications can lead to gene expression
changes which can last the whole life and can be transmitted
to the coming generations.
 EXAMPLES includes:
 High dietry fats can raise the chances of diabetes even in
offspring.
 High dietry cocaine, morphine etc can cause impairment in
mesolimbic pathway hereditically decrease addiction
threshold even in offsprings.
19
20
EPIGENETIC INTERACTIONS
21
Genetic variations at SNPs
Example of variation at SNPs level
 Human dietry intake for choline if not normal can cause
organ dysfunction.
 Occurs due to alteration of specific nucleotide region, a
region involved in metabolism of choline.
 As it cause limitance to export of trigylcerides from liver ,
induces apoptosis and leakage of enzymes from liver or
muscle.
 In pregenancy women could got neural tube defect if have
defeciency of choline.
22
23
Application of Nutrigenomics
 Identification of biomarkers for diseases which may previously known as
idiopathic in nature. Eg: Cancer
 Nutrigenomics gives us new advancements as therapeutic potientials of
nutrients.
Eg: Vitamin B12 in AD
 Provide info regarding suspectibility of individuals genes towards the role
of ADME in diseases.
 Nutrients may upregulate or disregulate the genes leads to diseases.
Eg : SREBP role in cholestrol intake.
24
CVS Disorders
 Genetic variation in genes encoding for apolipoproteins, some enzymes
and hormones can alter individual sensitivity to develop the cardiovascular
diseases.
 Particular allels study shows that specific allels like Apo E2, E3, E4 shows
difference in cholestrol intake as serum TGs varied among the individuals.
 Specific polymorphism in genes encoding lipid transport proteins, their
receptors, and lipid-processing enzymes and inflammation related proteins
were shown to be associated with the characteristic changes in blood lipid
concentrations
 One polymorphism in the hepatic lipase gene is associated with an
increase in protective HDL levels compared with the specific genotype
25
Role in understanding DISEASES
OBESITY
 Obesity may regulates by expression of mRNA levels regulated by
specific genes for neuropeptides Y , AgRP, leptin etc.
•Make individuals genetic make up
make it prone to obesity
26
Hypertension
Arterial hypertension contributes by dietery factors and genetic factors
which characterizes essential (primary) hypertension.
Dietary SALT INTAKE a major cause behind hypertension. As only about
15% people have sodium-sensitive hypertension. Rest the 85%, eliminating
salt from the diet has no effect on their blood pressure.
Sodium transport/metabolism-related genes such as those encoding
epithelial sodium channel (ENaC) subunits, adducin, and 11B-hydroxysteroid
dehydrogenase have well-proven association between dietary salt intake
and hypertension .
 Polymorphic genes implicated in blood pressure regulation include renin-
angiotensin system genes including those encoding angiotensinogen (AGT),
angiotensin converting enzyme (ACE), and aldosterone synthetase
(CYP11B2).
27
Cancer
Deficiency in micronutrients required as cofactors or as components of
DNA repair enzymes and methylation of DNA can lead to epigenetic
mechanisms behind cancer.
Nutrients may considered as a source of either carcinogens (intrinsic or
cooking-generated) present in certain foods or constituents acting in a
protective manner (vitamins, antioxidants, detoxifying enzyme-activating
substances, etc.)
Carcinogen metabolism-affecting polymorphisms may modify probability
of contact between carcinogens and target cells, thus acting at the stage of
cancer initiation.
Influences of polymorphisms of gene encoding factors involved in
hormonal regulation are most strongly manifested in hormone dependent
tumors such as breast, prostate, ovarian and endometrial cancers.
28
Minerals
As similar to other nutrients, mostly minerals are involved in several gene
expressions
“Bivalent metals”; strong influence gene expression.
Both parenteral and oral zinc or cadmium application enhance the
transcription rate of the metallothionein (MT) gene in intestinal tissue.
(Ouellette et al., 1982)
 Others like copper, iron, selenium and phosphorus are among the many
minerals known to alter gene expression.
29
ALUMINIUM
 Aluminum when from any source enters in body then it makes bonds with
phosphates inside the cell, nucleus, neurons etc.
And adversly effect normal protein formation and cause impairment in
functioing like neurodegeneration as in AD.
 In body , aluminium replaces the divalent and trivalent ions ions
performing cellular functions in various cycles of body. Thus impairs
intracellular communication, growth and other functions of ce
30
Effect of imbalance of micronutrients on gene expression:
31
Deficiency of some micronutrients and their associated
health effects
Thank you !!!....
32

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nutrigenomics.ppt

  • 1. INTRODUCTION TO NUTRIGENOMICES AND ITS APPLICATIONS DEPARTMENT OF PHARMACOLOGY ISF COLLEGE OF PHARMACY, MOGA (PUNJAB) 1 Presented by : Sunpreet kaur M.Pharm : Pharmacology (II nd sem) Roll No: 160750015
  • 2. Introduction 2  Any nutrition can induce metabolic changes in muscles, being reflected in tissue remodeling, increased protein turnover, and muscle atrophy.  Relationship of nutrition with health is well known.  But how the components exert their effect is not known completely till the date.  Revolution in genomic field raise the question about how genome get alters by nutrients.
  • 3. Introduction 3  Bioactive nutriental components are the key environment factors regulating gene expression. (Mead, 2007) Advencements of molecular techniques and analysis systems revealed the mechanism how nutrient status and their metabolism acould alters genome. With these knowledge a new area of study called “NUTRIGENOMICS” has emerged. (Roche et al 2006)
  • 4. Why we need to study nutrigenomics…??  Improper diets are risk factors for diseases.  Dietary components alter gene expression and /or change genome structure.  Variation in genetic makeup could make a person prones towards a disease.  Some diet-regulated genes are likely to play a role in the onset, incidence, progression and severity of chronic diseases. 4
  • 5. 5 A time for New Nutritional Strategies…!!!! We need to make a change what we take in diet We need to change the way we evaluate the diet
  • 6. What are omics……????  Omics is the term used to address the study of particular field that includes all the events and techniques utilise to understand that field.  It explain us how genome work in genomics .  Explains how any intraction causes alteration in genome and how these alteration leads to specific disease progression 6
  • 7. Why to pay attention to omics…?? 7
  • 8. Some relevant omics to deal…..!!! • Comparitive genomics • Epigenomics • Neurogenomics • Toxicogenomics • Personal genomics • Neutrigenomics • Cognitive genomics • Metagenomics 8
  • 9. Introduction to NUTRIGENOMICS  Nutrigenomics is the branch of OMICS that utilises the genomic tools and techniques to study the effect of dietery components on genes.  Nutrigenomics includes the interaction between nutrient and gene.  Nutrients modulate the expression and regulation of coding genes for protein, metabolism, cellular differentiation and growth. 9
  • 10. Dual role of nutrigenomics 10
  • 11. How diet affects our gene…???? 11
  • 12. How nutrients interacts to our gene..?? 12
  • 13. Common food gene ineractions 13
  • 14. These are 5 basic principles of nutrigenomics (German, 2005):  Substances contained in the food (micro- and macro- nutrients) can directly or indirectly affect the human genome through changes in its structure and gene expression. Under certain circumstances and in some individuals the diet can be an important risk factor for the development of the number of diseases.  Some genes regulated by active substances in the diet probably play a crucial role in the onset, incidence, progression and severity of the disease.
  • 15.  The degree to which diet influences the balance between health and disease may depend on individual’s genetic makeup.  Nutritional intervention is based on the knowledge of individual’s nutritional status and needs as well as genotype (individualized nutrition) and can be used for prevention, mitigation or healing the chronic diseases. 15
  • 16. Types of food gene ineraction 16 Direct interactions: Nutrients interacts with a receptor behave as transcription factors which can bind at the DNA level cause the acute expression of a gene. Epigenetic interactions: Nutrients can alter the structure of DNA so that gene expression is chronically altered. Genetic variations: Common genetic variations (single nucleotide polymorphism- SNPs) can modify a expression or functionality of gene.
  • 18. DIRECT INTERACTIONS Direct intertactions involves a short term trigger and causes the acute modification of the transcription process. This effect generally disappears once the exposure to the specific nutrient has been stopped. Examples of direct interactions are:  Vitamin A interacts with retinoic acid receptor and the resulted complex causes transcription activation or inhibition of gene expression.  Fatty acids can interact with PPAR (peroxisome proliferator- activated receptors) which can modify genes expression by attaching at DNA level  Interaction between vitamin D and its receptor 18
  • 19. EPIGENETIC INTERACTIONS  Epigenetic mechanisms are mediated either by DNA methylation or by histone methylation or acetylation.  Such epigenetic modifications can lead to gene expression changes which can last the whole life and can be transmitted to the coming generations.  EXAMPLES includes:  High dietry fats can raise the chances of diabetes even in offspring.  High dietry cocaine, morphine etc can cause impairment in mesolimbic pathway hereditically decrease addiction threshold even in offsprings. 19
  • 22. Example of variation at SNPs level  Human dietry intake for choline if not normal can cause organ dysfunction.  Occurs due to alteration of specific nucleotide region, a region involved in metabolism of choline.  As it cause limitance to export of trigylcerides from liver , induces apoptosis and leakage of enzymes from liver or muscle.  In pregenancy women could got neural tube defect if have defeciency of choline. 22
  • 23. 23 Application of Nutrigenomics  Identification of biomarkers for diseases which may previously known as idiopathic in nature. Eg: Cancer  Nutrigenomics gives us new advancements as therapeutic potientials of nutrients. Eg: Vitamin B12 in AD  Provide info regarding suspectibility of individuals genes towards the role of ADME in diseases.  Nutrients may upregulate or disregulate the genes leads to diseases. Eg : SREBP role in cholestrol intake.
  • 24. 24 CVS Disorders  Genetic variation in genes encoding for apolipoproteins, some enzymes and hormones can alter individual sensitivity to develop the cardiovascular diseases.  Particular allels study shows that specific allels like Apo E2, E3, E4 shows difference in cholestrol intake as serum TGs varied among the individuals.  Specific polymorphism in genes encoding lipid transport proteins, their receptors, and lipid-processing enzymes and inflammation related proteins were shown to be associated with the characteristic changes in blood lipid concentrations  One polymorphism in the hepatic lipase gene is associated with an increase in protective HDL levels compared with the specific genotype
  • 25. 25 Role in understanding DISEASES OBESITY  Obesity may regulates by expression of mRNA levels regulated by specific genes for neuropeptides Y , AgRP, leptin etc. •Make individuals genetic make up make it prone to obesity
  • 26. 26 Hypertension Arterial hypertension contributes by dietery factors and genetic factors which characterizes essential (primary) hypertension. Dietary SALT INTAKE a major cause behind hypertension. As only about 15% people have sodium-sensitive hypertension. Rest the 85%, eliminating salt from the diet has no effect on their blood pressure. Sodium transport/metabolism-related genes such as those encoding epithelial sodium channel (ENaC) subunits, adducin, and 11B-hydroxysteroid dehydrogenase have well-proven association between dietary salt intake and hypertension .  Polymorphic genes implicated in blood pressure regulation include renin- angiotensin system genes including those encoding angiotensinogen (AGT), angiotensin converting enzyme (ACE), and aldosterone synthetase (CYP11B2).
  • 27. 27 Cancer Deficiency in micronutrients required as cofactors or as components of DNA repair enzymes and methylation of DNA can lead to epigenetic mechanisms behind cancer. Nutrients may considered as a source of either carcinogens (intrinsic or cooking-generated) present in certain foods or constituents acting in a protective manner (vitamins, antioxidants, detoxifying enzyme-activating substances, etc.) Carcinogen metabolism-affecting polymorphisms may modify probability of contact between carcinogens and target cells, thus acting at the stage of cancer initiation. Influences of polymorphisms of gene encoding factors involved in hormonal regulation are most strongly manifested in hormone dependent tumors such as breast, prostate, ovarian and endometrial cancers.
  • 28. 28 Minerals As similar to other nutrients, mostly minerals are involved in several gene expressions “Bivalent metals”; strong influence gene expression. Both parenteral and oral zinc or cadmium application enhance the transcription rate of the metallothionein (MT) gene in intestinal tissue. (Ouellette et al., 1982)  Others like copper, iron, selenium and phosphorus are among the many minerals known to alter gene expression.
  • 29. 29 ALUMINIUM  Aluminum when from any source enters in body then it makes bonds with phosphates inside the cell, nucleus, neurons etc. And adversly effect normal protein formation and cause impairment in functioing like neurodegeneration as in AD.  In body , aluminium replaces the divalent and trivalent ions ions performing cellular functions in various cycles of body. Thus impairs intracellular communication, growth and other functions of ce
  • 30. 30 Effect of imbalance of micronutrients on gene expression:
  • 31. 31 Deficiency of some micronutrients and their associated health effects

Editor's Notes

  1. When it comes to mechanism; inside every cell there is nucleus and there are chromosomes (X and Y) Each chromosomes is entirely packed in chromotin fiber.Chromotin fiber is made up DNA and proteins called histones. DNA is bound aroun 2 groups of 4 histones called Histone Octamer.Linking Histone H1 binds toDNA and keeps it in place so this forms the structure Nucleosome Alteration known a methylation occurs on DNA. Clusters of nucleotides Cystosine and Guanin called cpG island where areas methylation are concentrated. A similar process happens to the histone tails; acetylation, methylation and phosphorilation all factoring chromotin regulation and gene expression. Methylated histones interact with the methylated DNA and these two contract creating areas heterochromotins(tightly coiled) and euchromatins (loosely coiled) controlling what areas of DNA are available for the expression. Methylation is heritable through the generations and depending on which pair of markers come from identical methylation on the same bit of DNA can have dramatically give different results. Through this we can understand why identical twins dont stay the same throughout their lives, how one generations’ experience effect second generations and maybe some day we’ll even be able to switch cancer cells back into properly functionaing members of the body.