This document provides an introduction to nutrigenomics and its applications. It discusses how nutrigenomics is the study of how dietary components interact with genes and alter gene expression. There are different types of food-gene interactions, including direct interactions where nutrients directly bind to receptors and regulate genes, and epigenetic interactions where nutrients can alter DNA structure and chronically change gene expression. Nutrigenomics helps understand how an individual's genetic makeup can influence their susceptibility to diet-related diseases and how personalized diets based on genetics can be used for disease prevention and treatment. The document outlines several examples of how nutrigenomics provides insights into cardiovascular, cancer, obesity and hypertension by studying genetic factors and their interaction with diet.
Nutrigenomics is the science that examines the response of individuals to food compounds using post-genomic and related technologies (e.g. genomics, transcriptomics, proteomics, metabol/nomic etc.). The long-term aim of nutrigenomics is to understand how the whole body responds to real foods using an integrated approach termed 'systems biology'. The huge advantage in this approach is that the studies can examine people (i.e. populations, sub-populations - based on genes or disease - and individuals), food, life-stage and life-style without preconceived ideas.
the new emerging field of science that is nutrigenomics can deal with the issues of health and improve out health with the simple tools by understanding the risk and the baic genome of a person
Short intro epigenetics & nutrigenomics& the early impact of nutrition Norwich Research Park
Our “genes” are not fixed: “Plasticity” of the genotype by epigenetic mechanisms => important for the phenotypic impact of nutrition.
• Histone and DNA modifications have impact on gene transcription efficiency. Methylation (more stable) and acetylation (more flexible) have impact on chromatin
structures.
• Epigenetic modifications have impact on offspring, embryo development, ageing and disease development or prevention => example: Dutch Hunger Winter.
Health status of future parents are very important for the future health of children.
Early healthy nutrition & lifestyle essential for successful healthy life & “ageing”.
Nutrigenomics is the science that examines the response of individuals to food compounds using post-genomic and related technologies (e.g. genomics, transcriptomics, proteomics, metabol/nomic etc.). The long-term aim of nutrigenomics is to understand how the whole body responds to real foods using an integrated approach termed 'systems biology'. The huge advantage in this approach is that the studies can examine people (i.e. populations, sub-populations - based on genes or disease - and individuals), food, life-stage and life-style without preconceived ideas.
the new emerging field of science that is nutrigenomics can deal with the issues of health and improve out health with the simple tools by understanding the risk and the baic genome of a person
Short intro epigenetics & nutrigenomics& the early impact of nutrition Norwich Research Park
Our “genes” are not fixed: “Plasticity” of the genotype by epigenetic mechanisms => important for the phenotypic impact of nutrition.
• Histone and DNA modifications have impact on gene transcription efficiency. Methylation (more stable) and acetylation (more flexible) have impact on chromatin
structures.
• Epigenetic modifications have impact on offspring, embryo development, ageing and disease development or prevention => example: Dutch Hunger Winter.
Health status of future parents are very important for the future health of children.
Early healthy nutrition & lifestyle essential for successful healthy life & “ageing”.
Autophagy the housekeeper in every cellfathi neana
Autophagy is a catabolic process involving the degradation of a cell’s own components through the lysosomal machinery. It is a tightly regulated process that plays a normal part in cell growth, development, and homeostasis, helping to maintain a balance between the synthesis, degradation, and subsequent recycling of cellular products.
It is a major mechanism by which a starving cell reallocates nutrients from unnecessary processes to more-essential processes. Autophagy is an evolutionarily conserved mechanism of cellular self-digestion in which proteins and organelles are degraded through delivery to lysosomes. Defects in this process are implicated in numerous human diseases including cancer.
Genomics, Transcriptomics, Proteomics, Metabolomics - Basic concepts for clin...Prasenjit Mitra
This set of slides gives an overview regarding the various omics technologies available and how they can be used for improvement in clinical setting or research
Pharmacogenetics and pharmacogenomics is an upcoming branch in therapeutics. Various pharmacogenomic tests are currently available to aid in actual clinical practice. It has shown to have promising results in personalized medicine It is my attempt to compile the basic concepts from various books, articles, and online journals. Please feel free to comment.
Developmental Origins of Obesity: The Role of Epigeneticszferraro
This presentation will:
- Review the concept of ‘fetal programming’
- Demonstrate that early life nutritional events may serve as molecular memory of individual in utero experiences
- Show how changes persist following multiple rounds of cell division
- Highlight extrinsic (recapitulation) & Intrinsic (genetic) mechanisms that strongly suggest Intergenerational transmission of traits via epigenetics in humans
- Look at how to best move forward as a scientific and clinical community
A mitochondrion (singular of mitochondria) is part of every cell in the body that contains genetic material.
Mitochondria are responsible for processing oxygen and converting substances from the foods we eat into energy for essential cell functions.
The mitochondria of the zygote come from the oocyte, that is, from the mother and almost never from the sperm, form of transmission is called maternal inheritance
Which mitochondrial gene is mutated.
The extent of replicative segregation of the mutant mitochondrial genome during the early stages of embryonic development.
The abundance of the mutant mitochondrial gene in a particular tissue.
The threshold level of mutant mitochondrial DNA required in a tissue before an abnormality is evident clinically
Mitochondrial disease affects tissues most highly dependent on ATP production
*Nerves
*Muscles
Endocrine
Kidney
Low energy-requiring tissues are rarely directly affected, but may be secondarily
Lung
Connective tissue
Symptoms can be intermittent
Increased energy demand (illness, exercise)
Decreased energy supply (fasting)
Common feature
myoclonus epilepsy, deafness, blindness, anemia, diabetes, seizures and loss of cerebral blood supply (stroke).
Myoclonic epilepsy and ragged-red fiber disease (MERRF)
MERRF is a member of a group of disorders called mitochondrial encephalomyopathies that feature mitochondrial defects with altered brain and muscle functions.
The term “ragged red fibers” refers to large clumps of abnormal mitochondria that accumulate mostly in muscle cells and are stained red by a dye that is specific for complex II of the electron transport chain.
rare, maternally inherited, heteroplasmic, (point mutation in tRNA lysine gene)
Mutation is MTTK*MERRF8344G.
MT means mitochondrial gene is mutated
T means transfer RNA gene
K means the single-letter amino acid designation for lysine
MERRF means the clinical features
8344G means the mutant nucleotide is guanine (G) at nucleotide position 8344
If 90% of the mitochondria in nerve and muscle cells carry the MTTK*MERRF8344G mutation, then the defining symptoms of MERRF are present.
Maternally inherited mitochondrial disease
The MTTL1*MELAS3243G mutation accounts for more than 80% of the cases of MELAS.
This base substitution is in one of the two mitochondrial transfer RNALeu genes.
the A3243G mutation occurs in thetRNALeu(UUR) gene
When this mutation is present in ≥90% of the mitochondrial DNA of muscle tissue, there is an increased likelihood of recurrent strokes, dementia, epilepsy, and ataxia.
When heteroplasmy for the A3243G mutation
is ~40% to 50%, chronic progressive external ophthalmoplegia (CPEO), myopathy, and deafness are likely to occur.
Other MELAS mutations occur at sites 3252, 3271, and 3291 within the tRNALeu(UUR) gene and in the mitochondrial tRNAVal (MTTV) and COX III (MTCO3) genes.
Reduced activities in Complexes I and IV are established
Proteomics and its applications in phytopathologyAbhijeet Kashyap
Dear friends, I Abhijeet kashyap presenting the basics of proteomics to you all . Proteomics is the large-scale study of proteins, particularly their structures and functions.Proteomics helps in understanding the structure and function of different proteins as well as protein-protein interactions of an organism.
Autophagy the housekeeper in every cellfathi neana
Autophagy is a catabolic process involving the degradation of a cell’s own components through the lysosomal machinery. It is a tightly regulated process that plays a normal part in cell growth, development, and homeostasis, helping to maintain a balance between the synthesis, degradation, and subsequent recycling of cellular products.
It is a major mechanism by which a starving cell reallocates nutrients from unnecessary processes to more-essential processes. Autophagy is an evolutionarily conserved mechanism of cellular self-digestion in which proteins and organelles are degraded through delivery to lysosomes. Defects in this process are implicated in numerous human diseases including cancer.
Genomics, Transcriptomics, Proteomics, Metabolomics - Basic concepts for clin...Prasenjit Mitra
This set of slides gives an overview regarding the various omics technologies available and how they can be used for improvement in clinical setting or research
Pharmacogenetics and pharmacogenomics is an upcoming branch in therapeutics. Various pharmacogenomic tests are currently available to aid in actual clinical practice. It has shown to have promising results in personalized medicine It is my attempt to compile the basic concepts from various books, articles, and online journals. Please feel free to comment.
Developmental Origins of Obesity: The Role of Epigeneticszferraro
This presentation will:
- Review the concept of ‘fetal programming’
- Demonstrate that early life nutritional events may serve as molecular memory of individual in utero experiences
- Show how changes persist following multiple rounds of cell division
- Highlight extrinsic (recapitulation) & Intrinsic (genetic) mechanisms that strongly suggest Intergenerational transmission of traits via epigenetics in humans
- Look at how to best move forward as a scientific and clinical community
A mitochondrion (singular of mitochondria) is part of every cell in the body that contains genetic material.
Mitochondria are responsible for processing oxygen and converting substances from the foods we eat into energy for essential cell functions.
The mitochondria of the zygote come from the oocyte, that is, from the mother and almost never from the sperm, form of transmission is called maternal inheritance
Which mitochondrial gene is mutated.
The extent of replicative segregation of the mutant mitochondrial genome during the early stages of embryonic development.
The abundance of the mutant mitochondrial gene in a particular tissue.
The threshold level of mutant mitochondrial DNA required in a tissue before an abnormality is evident clinically
Mitochondrial disease affects tissues most highly dependent on ATP production
*Nerves
*Muscles
Endocrine
Kidney
Low energy-requiring tissues are rarely directly affected, but may be secondarily
Lung
Connective tissue
Symptoms can be intermittent
Increased energy demand (illness, exercise)
Decreased energy supply (fasting)
Common feature
myoclonus epilepsy, deafness, blindness, anemia, diabetes, seizures and loss of cerebral blood supply (stroke).
Myoclonic epilepsy and ragged-red fiber disease (MERRF)
MERRF is a member of a group of disorders called mitochondrial encephalomyopathies that feature mitochondrial defects with altered brain and muscle functions.
The term “ragged red fibers” refers to large clumps of abnormal mitochondria that accumulate mostly in muscle cells and are stained red by a dye that is specific for complex II of the electron transport chain.
rare, maternally inherited, heteroplasmic, (point mutation in tRNA lysine gene)
Mutation is MTTK*MERRF8344G.
MT means mitochondrial gene is mutated
T means transfer RNA gene
K means the single-letter amino acid designation for lysine
MERRF means the clinical features
8344G means the mutant nucleotide is guanine (G) at nucleotide position 8344
If 90% of the mitochondria in nerve and muscle cells carry the MTTK*MERRF8344G mutation, then the defining symptoms of MERRF are present.
Maternally inherited mitochondrial disease
The MTTL1*MELAS3243G mutation accounts for more than 80% of the cases of MELAS.
This base substitution is in one of the two mitochondrial transfer RNALeu genes.
the A3243G mutation occurs in thetRNALeu(UUR) gene
When this mutation is present in ≥90% of the mitochondrial DNA of muscle tissue, there is an increased likelihood of recurrent strokes, dementia, epilepsy, and ataxia.
When heteroplasmy for the A3243G mutation
is ~40% to 50%, chronic progressive external ophthalmoplegia (CPEO), myopathy, and deafness are likely to occur.
Other MELAS mutations occur at sites 3252, 3271, and 3291 within the tRNALeu(UUR) gene and in the mitochondrial tRNAVal (MTTV) and COX III (MTCO3) genes.
Reduced activities in Complexes I and IV are established
Proteomics and its applications in phytopathologyAbhijeet Kashyap
Dear friends, I Abhijeet kashyap presenting the basics of proteomics to you all . Proteomics is the large-scale study of proteins, particularly their structures and functions.Proteomics helps in understanding the structure and function of different proteins as well as protein-protein interactions of an organism.
The study of how genes and gene products interact with dietary chemicals to alter phenotype and, conversely, how genes and their products metabolize nutrients is called nutritional genomics or “Nutrigenomics”.
What is Epigenetic Changes? Understanding Their Role in Health and Disease | ...The Lifesciences Magazine
Epigenetic changes are garnering increasing attention in the field of genetics and medicine for their profound influence on gene expression and cellular function.
My recent introduction talk for the Nutrigenomics Masterclass 2011in Wageningen (The Netherlands):
How to use Nutrigenomics & molecular nutrition? From challenges to solutions
Richard's entangled aventures in wonderlandRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
Slide 1: Title Slide
Extrachromosomal Inheritance
Slide 2: Introduction to Extrachromosomal Inheritance
Definition: Extrachromosomal inheritance refers to the transmission of genetic material that is not found within the nucleus.
Key Components: Involves genes located in mitochondria, chloroplasts, and plasmids.
Slide 3: Mitochondrial Inheritance
Mitochondria: Organelles responsible for energy production.
Mitochondrial DNA (mtDNA): Circular DNA molecule found in mitochondria.
Inheritance Pattern: Maternally inherited, meaning it is passed from mothers to all their offspring.
Diseases: Examples include Leber’s hereditary optic neuropathy (LHON) and mitochondrial myopathy.
Slide 4: Chloroplast Inheritance
Chloroplasts: Organelles responsible for photosynthesis in plants.
Chloroplast DNA (cpDNA): Circular DNA molecule found in chloroplasts.
Inheritance Pattern: Often maternally inherited in most plants, but can vary in some species.
Examples: Variegation in plants, where leaf color patterns are determined by chloroplast DNA.
Slide 5: Plasmid Inheritance
Plasmids: Small, circular DNA molecules found in bacteria and some eukaryotes.
Features: Can carry antibiotic resistance genes and can be transferred between cells through processes like conjugation.
Significance: Important in biotechnology for gene cloning and genetic engineering.
Slide 6: Mechanisms of Extrachromosomal Inheritance
Non-Mendelian Patterns: Do not follow Mendel’s laws of inheritance.
Cytoplasmic Segregation: During cell division, organelles like mitochondria and chloroplasts are randomly distributed to daughter cells.
Heteroplasmy: Presence of more than one type of organellar genome within a cell, leading to variation in expression.
Slide 7: Examples of Extrachromosomal Inheritance
Four O’clock Plant (Mirabilis jalapa): Shows variegated leaves due to different cpDNA in leaf cells.
Petite Mutants in Yeast: Result from mutations in mitochondrial DNA affecting respiration.
Slide 8: Importance of Extrachromosomal Inheritance
Evolution: Provides insight into the evolution of eukaryotic cells.
Medicine: Understanding mitochondrial inheritance helps in diagnosing and treating mitochondrial diseases.
Agriculture: Chloroplast inheritance can be used in plant breeding and genetic modification.
Slide 9: Recent Research and Advances
Gene Editing: Techniques like CRISPR-Cas9 are being used to edit mitochondrial and chloroplast DNA.
Therapies: Development of mitochondrial replacement therapy (MRT) for preventing mitochondrial diseases.
Slide 10: Conclusion
Summary: Extrachromosomal inheritance involves the transmission of genetic material outside the nucleus and plays a crucial role in genetics, medicine, and biotechnology.
Future Directions: Continued research and technological advancements hold promise for new treatments and applications.
Slide 11: Questions and Discussion
Invite Audience: Open the floor for any questions or further discussion on the topic.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
Cancer cell metabolism: special Reference to Lactate PathwayAADYARAJPANDEY1
Normal Cell Metabolism:
Cellular respiration describes the series of steps that cells use to break down sugar and other chemicals to get the energy we need to function.
Energy is stored in the bonds of glucose and when glucose is broken down, much of that energy is released.
Cell utilize energy in the form of ATP.
The first step of respiration is called glycolysis. In a series of steps, glycolysis breaks glucose into two smaller molecules - a chemical called pyruvate. A small amount of ATP is formed during this process.
Most healthy cells continue the breakdown in a second process, called the Kreb's cycle. The Kreb's cycle allows cells to “burn” the pyruvates made in glycolysis to get more ATP.
The last step in the breakdown of glucose is called oxidative phosphorylation (Ox-Phos).
It takes place in specialized cell structures called mitochondria. This process produces a large amount of ATP. Importantly, cells need oxygen to complete oxidative phosphorylation.
If a cell completes only glycolysis, only 2 molecules of ATP are made per glucose. However, if the cell completes the entire respiration process (glycolysis - Kreb's - oxidative phosphorylation), about 36 molecules of ATP are created, giving it much more energy to use.
IN CANCER CELL:
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
Unlike healthy cells that "burn" the entire molecule of sugar to capture a large amount of energy as ATP, cancer cells are wasteful.
Cancer cells only partially break down sugar molecules. They overuse the first step of respiration, glycolysis. They frequently do not complete the second step, oxidative phosphorylation.
This results in only 2 molecules of ATP per each glucose molecule instead of the 36 or so ATPs healthy cells gain. As a result, cancer cells need to use a lot more sugar molecules to get enough energy to survive.
introduction to WARBERG PHENOMENA:
WARBURG EFFECT Usually, cancer cells are highly glycolytic (glucose addiction) and take up more glucose than do normal cells from outside.
Otto Heinrich Warburg (; 8 October 1883 – 1 August 1970) In 1931 was awarded the Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme.
WARNBURG EFFECT : cancer cells under aerobic (well-oxygenated) conditions to metabolize glucose to lactate (aerobic glycolysis) is known as the Warburg effect. Warburg made the observation that tumor slices consume glucose and secrete lactate at a higher rate than normal tissues.
Observation of Io’s Resurfacing via Plume Deposition Using Ground-based Adapt...Sérgio Sacani
Since volcanic activity was first discovered on Io from Voyager images in 1979, changes
on Io’s surface have been monitored from both spacecraft and ground-based telescopes.
Here, we present the highest spatial resolution images of Io ever obtained from a groundbased telescope. These images, acquired by the SHARK-VIS instrument on the Large
Binocular Telescope, show evidence of a major resurfacing event on Io’s trailing hemisphere. When compared to the most recent spacecraft images, the SHARK-VIS images
show that a plume deposit from a powerful eruption at Pillan Patera has covered part
of the long-lived Pele plume deposit. Although this type of resurfacing event may be common on Io, few have been detected due to the rarity of spacecraft visits and the previously low spatial resolution available from Earth-based telescopes. The SHARK-VIS instrument ushers in a new era of high resolution imaging of Io’s surface using adaptive
optics at visible wavelengths.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
In silico drugs analogue design: novobiocin analogues.pptx
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
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
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
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.