This fascinating field of epigenomics examines how genes are modified without changing the DNA sequence — that is, how
a gene for obesity, for instance, is modified by eating nonstarchy vegetables versus cupcakes.
Other accomplishments in this area include the mapping of variation in the FTO
gene for obesity, characterizing the role of interleukin (IL)-6, IL - 10, and IL - 1RA in obesity and insulin resistance in African Americans (AA), and determining the loci associated with CRP, IL - 10, IL - 1Ra, and IL - 6 levels in a GWAS of AA.
The effects of
the gene for obesity do not show up much in the starving Third World.
Don't blame gluttony or
genes for the obesity epidemic — it's our sedentary habits echoing down the generations, says obesity theorist Edward Archer
These genes are associated with these traits through SNPs, which may be located in intergenic regions, and they do not need to have functional evidence as causal
genes for obesity or T2D.
Several candidate
genes for obesity and T2D (e.g., IRS1 and VEGFA) were differentially expressed in discordant twins.
Moreover, 127 sites representing 65 candidate
genes for obesity were differentially methylated in case - control cohort 2 (q < 0.15, P = 0.5, χ2 test; Supplementary Table 15).
Not exact matches
«Together, our data strongly suggest that cutaneous
gene therapy with inducible expression of GLP1 can be used
for the treatment and prevention of diet - induced
obesity and pathologies,» the authors wrote.
Seven
genes for intelligence are also associated with schizophrenia; nine
genes also with body mass index, and four
genes were also associated with
obesity.
Until now, hundreds of labs searching
for a leptin defect or another
gene that might cause human
obesity had come up empty - handed.
We now know how to turn fat cells into ones that burn calories as heat rather than store them — raising the prospect of a
gene therapy
for obesity
For example, researchers reported in a much touted 2006 Science article that they had discovered a gene variant that seemed to confer a risk for obesity, and they replicated the results in four human populatio
For example, researchers reported in a much touted 2006 Science article that they had discovered a
gene variant that seemed to confer a risk
for obesity, and they replicated the results in four human populatio
for obesity, and they replicated the results in four human populations.
For the first time, Whitehead Institute scientists have documented a direct link between deletions in two
genes — fam57ba and doc2a — in zebrafish and certain brain and body traits, such as seizures, hyperactivity, enlarged head size, and
obesity.
The revolution in
obesity research began less than five years ago with the landmark discovery of a
gene for leptin, the weight - regulating hormone found in both mice and people.
What does it mean
for a
gene to be associated with
obesity?
«The BDNF
gene has previously been linked to
obesity, and scientists have been working
for several years to understand how changes in this particular
gene may predispose people to
obesity,» said Jack A. Yanovski, M.D., Ph.D., one of the study authors and an investigator at NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
«We provide the first evidence that the PPARα - dependent
gene Fgf21 demethylation occurs in the postnatal mouse liver, and once established it persists into adulthood and exerts long - term effects on the magnitude of
gene expression response to environmental cues, which may account in part
for the attenuation of diet - induced
obesity (Figure).»
A single variation in the
gene for brain - derived neurotropic factor (BDNF) may influence
obesity in children and adults, according to a new study funded by the National Institutes of Health.
«The large number of
genes makes it less likely that one solution to beat
obesity will work
for everyone and opens the door to possible ways we could use genetic clues to help defeat
obesity,» she says.
«Finding the
genes that increase risk of
obesity is only the end of the beginning,» says senior author Ruth Loos, Ph.D., professor of preventive medicine at Mt. Sinai Hospital, and director of the Genetics of Obesity and related Metabolic Traits Program in the Charles Bronfman Institute for Personalized Me
obesity is only the end of the beginning,» says senior author Ruth Loos, Ph.D., professor of preventive medicine at Mt. Sinai Hospital, and director of the Genetics of
Obesity and related Metabolic Traits Program in the Charles Bronfman Institute for Personalized Me
Obesity and related Metabolic Traits Program in the Charles Bronfman Institute
for Personalized Medicine.
By analyzing genetic samples
for over half a million individuals as part of the GIANT research project, which aims to identify
genes that regulate human body and size, researchers found more than 100 locations across the genome that play roles in various
obesity traits.
«A lot of diabetes in the elderly goes undiagnosed because they don't have the classical risk factors
for type 2 diabetes, such as
obesity,» says Evans, director of Salk's
Gene Expression Laboratory and senior author of the new paper, which was published November 18, 2015 in Nature.
«Our findings suggest that certain mutations in the BRCA1
gene may put people at increased risk
for metabolic diseases like
obesity and type 2 diabetes,» said Dr. Spangenburg.
«Lots of
genes have multiple roles, but the idea here is that this
gene may be involved in the coordination of roles in traits important
for feeding and
obesity.»
MEGENA (
for Multiscale Embedded
Gene Co-expression Network Analysis) projects gene expression data onto a three dimensional sphere, allowing scientists to study hierarchical organization patterns in complex networks that are characteristic of diseases such as cancer, obesity, and Alzheime
Gene Co-expression Network Analysis) projects
gene expression data onto a three dimensional sphere, allowing scientists to study hierarchical organization patterns in complex networks that are characteristic of diseases such as cancer, obesity, and Alzheime
gene expression data onto a three dimensional sphere, allowing scientists to study hierarchical organization patterns in complex networks that are characteristic of diseases such as cancer,
obesity, and Alzheimer's.
For example, higher chocolate intake and a larger waist size was associated with certain forms of the oxytocin receptor
gene, and an
obesity - associated
gene played a role in vegetable and fiber intake.
Animals with
gene mutations that significantly alter their circadian rhythms have shorter life spans, and circadian rhythm sleep disorders in humans can have profoundly negative effects, including increased risk
for obesity, depression, cardiovascular disease and cancer.
The relationship held: Of the 78
genes the researchers examined
for epigenetic marks, only the methylation of the RXRα
gene showed a strong relationship with
obesity.
Viewed this way, humans can be considered to have lost two
genes — one affecting uricase and the other affecting the ability to produce vitamin C — whose absence helped our ancestors during famine but, in today's world, may be increasing our risk
for obesity and diabetes.
The team identified multiple germline mutations in the human
genes responsible
for SNRK production that were directly associated with higher body mass index, higher waist circumference and risk of
obesity in a cohort of 12,000 women who participated in the Women's Health Initiative.
SNPs in the human IL15 and IL15RA
genes have been associated with muscle phenotypes (16), muscle responses to resistance training (17), metabolic syndrome (16), and
obesity (18 — 20), providing additional rationale to support a role
for these molecules in muscle.
These fruit flies in a lab at UNLV are good models
for studying how
genes affect human
obesity.
«Finding a SIRT3
gene mutation linked to metabolic syndrome is a big step towards developing treatments
for this increasingly common collection of
obesity - related illnesses,» said Dr. Verdin, who is also a UCSF professor of medicine.
Among differentially expressed
obesity and T2D candidate
genes (Supplementary Tables 4 and 5), there were significant associations between methylation and expression
for 65 sites corresponding to 17
genes (Supplementary Table 20).
«It's a timely reminder that when contemplating the scene of a crime, it is wise to look beyond those potential culprits standing nearest to the body, some of whom may well be innocent bystanders, and to look
for «motive» amongst those who may be standing a little distance away,» Mark McCarthy of the University of Oxford, a researcher who has worked on the connection between
obesity and the FTO
gene, told National Geographic's Not Exactly Rocket Science.
We also examined whether candidate
genes for T2D and / or
obesity, previously identified by GWAS (P < 1.0 × 10 − 5 [www.genome.gov/gwastudies]-RRB-, exhibit differential methylation in adipose tissue of unrelated patients with diabetes versus nondiabetic subjects.
Obesity increases the risk
for T2D, and, hence, it is possible that altered expression and / or methylation of these
genes may contribute to the development of T2D.
Common forms of these
genes confer significant predisposition to
obesity Reykjavik, ICELAND, December 11, 2003 — deCODE genetics (Nasdaq: DCGN) today announced that it has isolated two new
genes as part of its alliance with Merck & Co, Inc. to develop drugs
for the...
Prior to modern agriculture, it was very important
for the body to keep extra resources, but in today's environment, those
genes have been linked to
obesity.
A mutation in a single
gene has been linked to cases of severe
obesity, offering scientists new targets
for future
gene therapy drugs (Credit: < a href ="https://depositphotos.com/19154541/stock-photo-serious-doctor-examining-a-patient.html" rel="nofollow"> sunabesyou / Depositphotos )
A mutation in a single
gene has been linked to cases of severe
obesity, offering scientists new targets
for future
gene therapy drugs (Credit: sunabesyou / Depositphotos)
A mutation in a single
gene has been linked to cases of severe
obesity, offering scientists new targets
for future
gene therapy drugs
Reykjavik, ICELAND, December 11, 2003 — deCODE genetics (Nasdaq: DCGN) today announced that it has isolated two new
genes as part of its alliance with Merck & Co, Inc. to develop drugs
for the treatment of
obesity.
«Dark chocolate, a high source of polyphenols, and flavanols in particular, has lately received attention
for its possible role in modulating
obesity because of its potential effect on fat and carbohydrate metabolism, as well as on satiety... The research undertaken to date has shown promising results, with the possible implication of cocoa / dark chocolate in the modulation of
obesity and body weight through several mechanisms including decreasing the expression of
genes involved in fatty acid synthesis, reducing the digestion and absorption of fats and carbohydrates and increasing satiety.»
Dr. Tove Fall, lead study researcher at the Department of Medical Sciences and the Science
for Life Laboratory at Uppsala University commented, «We knew already that
obesity and cardiovascular disease often occur together... in this study we found that individuals with
gene variants that lead to increased body - mass index also had an increased risk of heart failure and diabetes.»
It is accepted that the regulation of adipocytokine secretion or the adipocyte specific
gene expression is one of the most important targets
for the prevention of
obesity and amelioration of insulin sensitivity.
It is accepted that the regulation of adipocytokine secretion or the adipocyte - specific
gene expression is one of the most important targets
for the prevention of
obesity and amelioration of insulin sensitivity.
Recent research into a field of science called nutrigenomics makes it safe and easy to use a simple home kit to examine your
genes for the presence of particular variants that predispose you to weakness in detoxification, Vitamin D metabolism, antioxidant processing, other nutrient imbalances and certain conditions, such as
obesity, hypertension, diabetes and cardiovascular disease.
An additional Harvard study concluded that regularly consuming drinks high in sugar interacts with the
genes that affect weight, dramatically increasing a person's risk
for obesity.
In the Diet,
Obesity, and
Gene (Diogenes) Project, increased protein consumption together with a modest reduction in glycemic index was beneficial
for weight control.49 Substituting protein
for carbohydrate also partly resulted in lower blood pressure, improved lipids levels, and concomitantly reduced cardiovascular risk.50 Higher vitamin D intake might have beneficial effects on the reduction of visceral adipose tissue51 and other cardiovascular risk factors52.