Birmingham Researchers Granted Almost £140,000 To Investigate Obesity In Children, UK

Researchers in Birmingham have just been awarded a grant of almost £140,000 by Action Medical Research - the leading UK-wide medical research charity dedicated to helping babies and children.

The charity has been supporting significant medical breakthroughs for nearly 60 years, and today announced its latest round of funding to top research institutes at universities and hospitals investigating conditions affecting babies and children.

In this latest round of funding, the charity has given £138,762 to the Diabetes Centre, Heart of England NHS Foundation Trust, Birmingham Heartlands Hospital and Birmingham University, for a project looking at links between obesity in children and sleep patterns.

Obesity has become a major public health problem. The condition is now affecting children and we know that this will have serious consequences for their health and wellbeing.

An estimated 17 per cent of boys and 15 per cent of girls in the UK aged between two and 15 are classified as being obese. Around 30 per cent of children are either overweight or obese in the UK and many of these cases will continue into adulthood.

Obesity is associated with other conditions such as heart disease, diabetes, breathing disorders, some cancers, infertility, arthritis, depression and can seriously affect an individual's physical and mental wellbeing. There is a major need to understand factors that contribute to obesity so that this serious condition can be prevented and treated effectively.

Action Medical Research funds a total of approximately £3 million worth of research grants every year, with grant rounds in July and November, as well as awarding Research Training Fellowships in February.

None of our work would be possible without the generosity of people who make donations, raise funds and take part in events, as well as our trust and corporate partners. Action Medical Research receives no income from the government or any other statutory source.

Alexandra Dedman, Senior Research Evaluation Manager: said: "At Action Medical Research we are determined to stop the suffering of babies and children caused by disease and disability. We know that medical research can save and change children's lives. The charity finds and funds some of the best medical research in the world for the benefit of babies, children and young people.

 

 

Researchers Receive NIMH Brain Awards

Two Boston University School of Medicine (BUSM) faculty members, Pietro Cottone, PhD, an assistant professor of pharmacology and psychiatry and Michael Silverstein, MD, an associate professor of pediatrics, were each awarded the prestigious National Institute of Mental Health (NIMH) Biobehavioral Research Awards for Innovative New Scientisits (BRAINS) grant with ten other investigators from around the country. The BRAINS award called for innovative and groundbreaking research projects from early stage investigators to explore the complex mechanisms underlying mental disorders or novel treatments and prevention strategies.

The BRAINS initiative was created to support the research programs and career development of outstanding scientists who are in the early, formative stages of their careers and who plan to make a long term commitment to research most relevant to NIMH. This award seeks to assist these individuals in launching an innovative clinical, translational, or basic research program that holds the potential to profoundly transform the understanding, diagnosis, treatment, or prevention of mental disorders.

Cottone, whose research explores the neural mechanisms underlying addictive disorders summarizes his proposal. "We propose that a history of dieting and relapse represents a vicious circle between stress and compulsive eating. In other words, the next attempt to avoid junk food is going to be more painful and stressful than the previous one, and the likelihood of relapse will progressively increase. We propose that during dieting the endocannabinoids (chemicals of the brains that protect from stress and promote the consumption of our favorite foods) are released to try to fight this stressful condition but on the other side they also increase our craving for junk food. Therefore blockade of the endocannabinoid action on one hand reduces compulsive eating, but on the other hand it induces anxiety and depression. This proposal will clarify the mechanisms linking eating disorders and obesity to anxiety and mood disorders."

Silverstein is studying maternal depression and is exploring detection and treatment options in the community setting, using for example, programs like Head Start and Early Intervention. He is experimenting with motivational interviewing and cognitive behavior therapy. "Our project is a community-based maternal depression prevention trial that enrolls young mothers at risk for developing major depressive disorder. The project takes place in Head Start and aims to enroll 230 women over five years."

"While these awards fund specific projects, they are truly an investment in specific people," said NIMH director Thomas R. Insel, MD. Inspired by the success of the NIH Director's Pioneer Awards and New Innovator Awards, both of which are designed to provide support for innovative research that has the potential for unusually high impact on health science. "The hope is that BRAINS awards will give early stage investigators enough flexibility to take risks on tough problems that are central to neuroscience and to the understanding of mental illness, such as the nature and development of neural circuits and the genetic factors and environmental influences that both shape and disrupt them," he adds.

The BRAINS program awards up to $1.625 million over five years for early career scientists focusing on a gap area identified in the Institute's Strategic Plan.

Source:
Gina DiGravio
Boston University Medical Center

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Feast Or Famine; Researchers Identify Leptin Receptor's Sidekick As A Target For Appetite Regulation

A study by researchers at Mayo Clinic's campus in Florida and Washington University School of Medicine adds a new twist to the body of evidence suggesting human obesity is due in part to genetic factors. While studying hormone receptors in laboratory mice, neuroscientists identified a new molecular player responsible for the regulation of appetite and metabolism.

In the Jan. 11 online issue of PLoS Biology, the authors report that mice engineered not to express the lipoprotein receptor LRP1, in the brain's hypothalamus, began to eat uncontrollably, growing obese as well as lethargic. They found that LRP1, a major transporter of lipids and proteins into brain cells, is a "co-receptor" with the leptin receptor meaning that both the leptin and LRP1 receptors need to work together to transmit leptin signals.

Leptin decides whether fat should be stored or used, resulting in lethargy or energy. When working properly, the hormone, which is made when body cells take in fat from food, travels to the brain to tamp down appetite.

"If a person is born with too little gene expression in the leptin pathway, which includes its receptors, or the circuitry is not functioning well, then leptin will not work as well as it should," says the study's lead investigator, neuroscientist Guojun Bu, Ph.D., of Mayo Clinic. "Appetite will increase, and body fat will be stored."

Given these results, Dr. Bu says it may be possible to develop a treatment that increases gene expression in one or both of the protein receptors, which then increases the messages meant to decrease appetite sent to the brain.

The serendipitous findings were born out of Dr. Bu's primary research focus, Alzheimer's disease. He has been studying how cholesterol, essential to the smooth functioning of neurons, is carried from star-shaped astrocytes to the surface of neurons by apolipoprotein E (APOE). There are two major receptors for APOE on brain neurons, and LRP1 is one of them.

Inheriting one version of APOE APOE4 is a known risk factor for development of Alzheimer's disease, and Dr. Bu has found that APOE4 is less effective at transporting cholesterol. To understand what role LRP1 plays in bringing APOE4 into neurons, he created a knockout mouse model with no expression of LRP1 in its forebrain neurons; the rest of its body expressed the receptor normally.

He found neurons lacking LRP1 had even less ability to absorb cholesterol, and that they lost synaptic contact with other neurons, impairing their ability to retain memory.

But Dr. Bu was surprised to find the mice suddenly gained weight. "This is the opposite of what had been observed in mice who did not have the receptor in their body fat cells," he says. "Those animals became skinny because they couldn't absorb enough lipoproteins."

The knockout mice were indistinguishable from control mice for the first six months of life but then gained weight rapidly, a phenomenon that correlated with a decrease in LPR1 expression in the central nervous system. At 12 months old, the genetically engineered mice had twice as much body fat as control mice, lacked energy, and were insulin resistant. "Together, these results indicate that LRP1, which is critical in lipid metabolism, also regulates food intake and energy balance in the adult central nervous system," Dr. Bu says.

The study was funded by the National Institutes of Health and the Alzheimer's Association.

Source: Mayo Clinic

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Researchers Identify Site In Brain Where Leptin May Trigger Puberty

UT Southwestern Medical Center researchers have pinpointed a tiny site in the brain where the hormone leptin may help trigger the onset of puberty.

The findings in mice indicate that a site within the hypothalamus called the ventral premammillary nucleus, or PMV, is the target where the hormone leptin effectively kick starts puberty in females.

Researchers have known that puberty starts when individuals have enough energy stores or fat to meet the demands of reproduction, and that leptin - a hormone produced by fat cells - acts in the brain to mediate this process, but the precise locale in the brain where leptin exerts this effect remained unclear.

"We found that the PMV is a key site of leptin action on puberty. This may not be the only site, considering the importance of the reproductive function for species survival, but the role played by PMV neurons has not been recognized before," said Dr. Carol Elias, assistant professor of internal medicine at UT Southwestern and senior author of the article available online and in the Jan. 4, 2011, print issue of the Journal of Clinical Investigation. "Our findings show that leptin action only in the PMV is sufficient to induce puberty in female mice."

Prior research has shown that in mice and humans lacking leptin, puberty grinds to a screeching halt at the prepubescent level, and the animals are infertile. Studies also have shown that reintroducing leptin to leptin-deficient people causes puberty to resume. Partly because of this, some researchers speculate that obese children may begin puberty earlier due to the higher levels of leptin produced by their fat tissues.

"We are witnessing an alarming situation in which the increasing incidence of childhood obesity may be inducing an advance in the onset of puberty in girls," Dr. Elias said. "The main obstacle for researchers in the field has been identifying the cell population involved in this event."

In this study, the researchers wanted to determine where leptin plays its role. To do this, they developed transgenic mouse models in which the mice had functional leptin receptors only in the PMV. Because of the lack of leptin signaling everywhere else in the body, the mice were obese but showed pubertal development and were able to get pregnant.

"One result that surprised us was that leptin acting only in the PMV was sufficient to induce puberty and improve fertility in females, but not in males," Dr. Elias said. "We're now trying to understand what's going on with males and whether leptin acts in different brain sites to induce puberty and fertility in males."

The next step, Dr. Elias said, will be to determine the molecular mechanism behind leptin's effects on puberty and reproductive control.

Notes:

Other UT Southwestern researchers involved in the study included Drs. Jose Donato Jr. and Roberta Cravo, co-lead authors and postdoctoral researchers in internal medicine; Dr. Renata Frazão, postdoctoral researcher in internal medicine; Dr. Lisandra Margatho, former postdoctoral researcher in internal medicine; Drs. Laurent Gautron, Michael Scott and Syann Lee, instructors of internal medicine; Charlotte Lee, senior research scientist; Dr. James Richardson, professor of pathology, molecular biology and plastic surgery; Dr. Roberto Coppari, assistant professor of internal medicine; Dr. Jeffrey Zigman, assistant professor of internal medicine and psychiatry; and Dr. Joel Elmquist, professor of internal medicine, psychiatry and pharmacology.

Researchers from the University of São Paulo, Acceleron Pharma, Rockefeller University and the Albert Einstein College of Medicine also participated.

The study was supported by the National Institutes of Health, the Foundation for Research Support of the State of São Paulo, and the Brazilian Federal Agency for the Support and Evaluation of Graduate Education.

Source:
Kristen Holland Shear
UT Southwestern Medical Center

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