Interindividual variation in posture allocation: possible role
in human obesity.
This gene, which the companies believe is involved in regulating how the body stores and uses energy, implicates a novel pathway
in human obesity.
Elevated circulating levels of succinate
in human obesity are linked to specific gut microbiota — Carolina Serena — The ISME Journal
Reduced adipose tissue oxygenation
in human obesity.
Not exact matches
This has not been shown
in humans but may spark additional research
in the battle against
obesity.
This factor is being touted as having great potential towards reducing
obesity in humans.
In addition to reducing the chance of
obesity and improving mental health, gardening is relaxing and helps us engage with our
human roots.
Human milk is low
in protein compared to other milks and formula which appears to lead to decreased risk of
obesity.
I think that medicalized birth practices resulting
in inter-generational deprivation of our basic
human rights has been a major contributor epidemics of diabetes and
obesity and mental health problems.
Because
HUMAN Healthy Vending co-founders Sean Kelly and Andy Mackensen know that there is a link between low access to nutritious foods and childhood
obesity, they are on a mission to place these machines
in areas where people need access to healthful meals the most, including
in areas designated as food deserts.
We know there is so much more to do
in solving the problem of childhood
obesity and
in bringing healthy food to food deserts; so, we're just getting started,» said Andy,
HUMAN's managing partner.
Two are the Office of Minority Health
in the Department of Health and
Human Services, and HBO, which produced the Weight of the Nation
obesity documentary I discussed a few weeks ago.
Low levels of physical activity and inefficient sleep patterns intensify the effects of genetic risk factors for
obesity, according to results of a large - scale study presented at the American Society of
Human Genetics (ASHG) 2017 Annual Meeting
in Orlando, Fla..
«Alterations
in the gut microbiota are associated with
obesity and the metabolic syndrome
in both
humans and rodents,» Shulman noted.
Segal says that the global rise
in sweetener consumption — along with other major shifts
in human nutrition — coincided with the dramatic increase
in obesity and diabetes epidemics around the world.
Similarly, jet lag
in two
humans who had traveled from the United States to Israel changed the composition of gut microbes, favoring the growth of bacteria that have been linked to
obesity and metabolic disease.
«Our findings confirm
in humans what has been shown
in animal models — that maternal
obesity has a more significant impact on the body composition of boys than girls,» said Dr. Andres.
Obesity in animals, including
humans, is not dependent on the amount of body weight, but on the amount of body fat - specifically adipose tissue.
«We wanted to investigate whether
human adults had the ability to transform some white fat deposits into beige fat when they were exposed to cold,» said one of the study's authors, Philip A. Kern, MD, of the University of Kentucky School of Medicine
in Lexington, KY. «Browning fat tissue would be an excellent defense against
obesity.
With global increase
in obesity and diet - related metabolic diseases, interest has intensified
in ancestral or «Palaeolithic» diets, not least because — to a first order of approximation —
human physiology should be optimized for the nutritional profiles we have experienced during our evolution.
If it can be shown to work
in humans, it could decrease
obesity, lengthening life.
Mice without the leptin gene, called ob / ob, overeat, weigh
in at three to four times normal, and develop symptoms similar to the
obesity - related diabetes seen
in humans.
In humans, too much fructose puts the liver at risk for conditions such as fatty liver disease, and raises the overall risk of
obesity and type 2 diabetes (SN: 10/5/13, p. 18).
Similar alterations
in humans taking antibiotics, especially children, might be adding to the
obesity epidemic
If the therapy can be improved and shown to work well
in humans, it could be an entirely new way to help battle
obesity, diabetes and related conditions.
Regulatory issues must be addressed before moving to
human studies, Davies said, but the findings published
in the August issue of the Journal of Clinical Investigation suggest that it may be possible to manipulate the bacterial residents of the gut — the gut microbiota — to treat
obesity and other chronic diseases.
Comparative anatomy and
human evolution experts from the University's School of Medicine have been studying the correlation between meat consumption and
obesity rates
in 170 countries.
This pattern of weight gain and insulin resistance parallels the development of
obesity and Type 2 diabetes
in humans, Hinton said.
If acetate does the same
in humans, dietary fibre may hold the key to curbing appetites and perhaps help battle
obesity — although boosting our intake might not be the best way to see an effect.
In the study, the scientists examined the human serotonin receptor, which plays a role in learning, mood and sleep and is the target of drugs that combat obesity, depression and migraine
In the study, the scientists examined the
human serotonin receptor, which plays a role
in learning, mood and sleep and is the target of drugs that combat obesity, depression and migraine
in learning, mood and sleep and is the target of drugs that combat
obesity, depression and migraines.
«Knowing which microbes live
in various ecological niches
in healthy people allows us to better investigate what goes awry
in diseases thought to have a microbial link, like Crohn's disease and
obesity,» says George Weinstock, associate director of the Genome Institute at Washington University
in St Louis and one of the
Human Microbiome Project's principal investigators.
He explained that rimonabant, a drug which blocked endocannabinoid signaling at cannabinoid receptors, was on the market
in Europe for the treatment of
human obesity.
DiPatrizio and Argueta caution that further research is necessary to identify whether similar mechanisms drive
obesity in humans.
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 populations.
Kajimura is hopeful but cautious about the prospects for using these drugs to treat
human obesity in the near future.
It is exciting that there is now evidence that brown fat can be useful
in treating
obesity in adult
humans,...
«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).
Given the importance of this discovery, the researchers are confident they will obtain the funding needed to continue their work — says principle researcher Ahmad Agil — «and be able to achieve their final objective: to confirm these findings
in humans, by administering melatonin to help combat
obesity and diabetes.»
The results suggest that drugs capable of targeting similar molecular pathways
in human fat cells could one day become major tools for fighting the growing worldwide epidemics of
obesity and type 2 diabetes, according to senior investigator Shingo Kajimura, PhD, an assistant professor of cell and tissue biology
in UCSF's School of Dentistry.
Their analysis — which used DNA data from a Neandertal woman from the Altai Mountains
in Siberia (SN: 1/25/14, p. 17) and 112,338 present - day British people — confirmed some links between Neandertal heritage and
human diseases made by previous studies (SN: 3/5/16, p. 18), but didn't find evidence that Neandertal gene variants contribute to
obesity.
The researchers are now examining whether CK2 - inhibitors can effectively reduce
obesity as well as prevent it, and whether they can be used alongside next - generation drugs that mimic the effects of cold to trigger brown fat to burn energy
in humans.
From that perspective, it becomes clear that
humans are prone to
obesity because our bodies evolved
in an environment of scarcity, where consuming as much high - energy food as possible was a useful survival strategy.
The researchers note that while some genes involved
in obesity could already have been implicated
in other aspects of
human health, others could be part of pathways that are not yet understood.
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.
«Since BPA has also been linked to
obesity in humans, people need to be aware that environmental factors can lead to increased susceptibility to
obesity and cardio - metabolic disorders.»
But
in the past decade, researchers have come to appreciate that the bacteria living
in and on our bodies — collectively called the
human microbiome — play a role
in how our bodies work, affecting everything from allergies to
obesity.
«The addition of osteocalcin as a metabolic regulator may one day lead to novel therapies, but we need to understand much better how it works and how it fits into physiology before such therapies can be attempted
in humans,» says endocrinologist Mitch Lazar, director of the Institute for Diabetes,
Obesity, and Metabolism at the University of Pennsylvania.
Satellite studies of outdoor lighting have also found an increased risk of
obesity in humans who live
in highly lit areas.
Acute sleep loss
in humans is associated with increased appetite and insulin insensitivity, while chronically sleep - deprived individuals are more likely to develop
obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease.
A hormonal imbalance could lead to overeating; indeed,
obesity runs rampant
in certain
human families that have a genetic deficiency
in leptin.