Sanford Burnham
  • Sanford Burnham
  • Twitter
  • Facebook
  • Youtube
  • Navigate Sanford-Burnham
    • Main Site
    • Our Mission
    • Research
    • Talent
    • Technology
    • Training & Education
    • Our Supporters
    • News

Beaker

Sanford-Burnham Science Blog

Subscribe

Top Stories - Metabolic Signaling & Disease

Obesity-waist_circumference
How belly fat differs from...

Researchers discover that the genes active in a person’s belly fat are significantly different...

Moscat_Diaz-Meco
Shifting the balance between...

Sanford-Burnham researchers show that protein p62 balances metabolism in fat tissue—making it an...

This calorimetry suite will be an important tool in the new Translational Research Institute facility, opening January 2012 (rendering by Flad Architects)
A different kind of dorm room

When the Florida Hospital/Sanford-Burnham Translational Research Institute for Metabolism and...

Dr. Steven Smith and Dr. Stephen Gardell leave their marks on the new TRI building.
Building translational...

The Translational Research Institute for Metabolism and Diabetes (TRI), a collaboration between...

White blood cell enzyme contributes to inflammation and obesity

by Heather Buschman, Ph.D. on April 2, 2013 at 12:02 pm | 1 comment
Full Article
Left: In fat tissue from a lean mouse, neutrophil elastase and a1-antitrypsin levels are balanced. Right: In fat tissue from an obese mouse, they are imbalanced—neutrophil elastase levels are high (dark staining) and a1-antitrypsin levels are low.

Left: In fat tissue from a lean mouse, neutrophil elastase and a1-antitrypsin levels are balanced. Right: In fat tissue from an obese mouse, they are imbalanced—neutrophil elastase levels are high (dark staining) and a1-antitrypsin levels are low.

Imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver in mice and humans—providing a new therapeutic target for these health conditions

Many recent studies have suggested that obesity is associated with chronic inflammation in fat tissues. In a new study, researchers discovered that an imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. This enzyme is produced by white blood cells called neutrophils, which play an important role in the body’s immune defense against bacteria.

Read More

Molecule’s structure reveals new therapeutic opportunities for rare diabetes

by Heather Buschman, Ph.D. on March 13, 2013 at 11:00 am | 1 comment
Full Article
3D structure of HNF-4α, a protein mutated in MODY1, a rare, inherited form of diabetes, reveals new pockets that could be targeted with therapeutic drugs

3D structure of HNF-4α, a protein mutated in MODY1, a rare, inherited form of diabetes, reveals new pockets that could be targeted with therapeutic drugs

Researchers have determined the complete three-dimensional structure of a protein called HNF-4α. HNF-4α controls gene expression in the liver and pancreas, switching genes on or off as needed. People with mature onset diabetes of the young (MODY1), a rare form of the disease, have inherited mutations in the HNF-4α protein. This first-ever look at HNF-4α’s full structure, published today in Nature, uncovers new information about how it functions. The study also reveals new pockets in the protein that could be targeted with therapeutic drugs aimed at alleviating MODY1.

Read More

Type 2 diabetes: a cellular metabolism problem

by Heather Buschman, Ph.D. on January 10, 2013 at 12:27 pm | 2 Comments
Full Article
Left: healthy beta cells.  Right: type 2 diabetic beta cells lose their glucose-sensing capability as glucose transporters (green) are internalized due to environmental disturbances brought about by fat and obesity.

Left: healthy beta cells. Right: type 2 diabetic beta cells lose their glucose-sensing capability as glucose transporters (green) are internalized due to environmental disturbances brought about by fat and obesity.

A new computational model of sugar transport in the pancreas reveals a metabolic “tipping point” in type 2 diabetes—a discovery that may form the basis for new efforts to prevent and treat the disease.

Changes in cellular metabolism play a bigger role in the development of type 2 diabetes than previously thought—perhaps an even larger part than genetic predisposition plays in the disease. That’s what Sanford-Burnham and UC Santa Barbara researchers concluded in a study published recently in the journal PLOS ONE. The team, including Jamey Marth, Ph.D., developed a computational model to better understand the underlying causes and progression of type 2 diabetes. The model revealed a metabolic “tipping point” that, when crossed, prevents the pancreas from adequately sensing blood sugar and secreting insulin. The team expects the discovery will form the basis for new efforts to prevent and treat type 2 diabetes.

Read More

How belly fat differs from thigh fat—and why it matters

by Heather Buschman, Ph.D. on January 9, 2013 at 6:20 am | 4 Comments
Full Article
Obesity-waist_circumference

Researchers discover that the genes active in a person’s belly fat are significantly different from those in his or her thigh fat, a finding that could shift the way we approach unwanted belly fat—from banishing it to relocating it.

Men tend to store fat in the abdominal area, but don’t usually have much in the way of hips or thighs. Women, on the other hand, are more often pear-shaped—storing more fat on their hips and thighs than in the belly.

Why are women and men shaped differently?

The answer still isn’t clear, but it’s an issue worth investigating, says Steven Smith, M.D., director of the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes. That’s because belly fat is associated with higher risks of heart disease and diabetes. On the other hand, hip and thigh fat don’t seem to play a special role in these conditions.

Read More

Shifting the balance between good fat and bad fat

by Bruce Lieberman on January 4, 2013 at 10:39 am | 3 Comments
Full Article
Moscat_Diaz-Meco

Sanford-Burnham Professors Jorge Moscat, Ph.D., and Maria Diaz-Meco, Ph.D. co-authored a study on p62's role in fat metabolism

Sanford-Burnham researchers show that protein p62 balances metabolism in fat tissue—making it an attractive target for anti-obesity therapies

In many cases, obesity is caused by more than just overeating and a lack of exercise. Something in the body goes haywire, causing it to store more fat and burn less energy. But what is it? Sanford-Burnham researchers have a new theory—a protein called p62. According to a study the team published December 21 in the Journal of Clinical Investigation, when p62 is missing in fat tissue, the body’s metabolic balance shifts—inhibiting “good” brown fat, while favoring “bad” white fat. These findings indicate that p62 might make a promising target for new therapies aimed at curbing obesity.

“Without p62 you’re making lots of fat but not burning energy, and the body thinks it needs to store energy,” said Jorge Moscat, Ph.D., Sanford-Burnham professor. “It’s a double whammy.” Moscat led the study with collaborators at Helmholtz Zentrum München in Germany and the University of Cincinnati.

Read More

Dr. Sheila Collins receives Novo Nordisk Diabetes Innovation Award

by Patrick Bartosch on November 2, 2012 at 7:58 am | 0 Comments
Full Article
The Novo Nordisk award will help fund Dr. Collins' (above) research into how hormones made in the heart act on fat cells.

The Novo Nordisk award will help fund Dr. Collins' (above) research into how hormones made in the heart act on fat cells.

Sheila Collins, Ph.D., professor in the Metabolic Signaling and Disease Program at Sanford-Burnham at Lake Nona, was awarded a Novo Nordisk Diabetes Innovation Award of $975,000 over two years. The program period will begin on January 1, 2013. The grant will help Collins and her team conduct research into how hormones made in the heart act on fat cells to regulate metabolic processes that can stimulate energy expenditure and weight loss.

The Novo Nordisk Diabetes Innovation Award Program was launched in 2011 and is very competitive, with more than 100  proposals submitted  for funding this year. The goal of the award program is to translate science into new therapies, helping diabetes and obesity patients receive better treatment and increase their chances of living more rewarding lives.

Read More

Meet Rebecca, Sanford-Burnham employee and obesity study participant

by Patrick Bartosch on August 3, 2012 at 5:57 am | 0 Comments
Full Article
Scientists at the TRI measure Rebecca Kaercher's oxygen levels, among other parameters

Scientists at the TRI measure Rebecca Kaercher's oxygen levels, among other parameters

Rebecca Kaercher has been struggling with her weight for years. “Losing weight has been a very frustrating endeavor for me. I go on diets, I work out, but I just don’t lose any weight,” she says. Rebecca has been working at Sanford-Burnham at Lake Nona for three years and, together with a few of her Institute coworkers, was thrilled to volunteer as a metabolism and weight loss study subject at the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes (TRI). “I am very proud to work at Sanford-Burnham and I want to be an active part of our research. Except for being overweight, I am a very healthy person. I don’t have high cholesterol, no high blood pressure, no diabetes. So it was hard for me to understand why I didn’t lose any weight.”

Rebecca is the kind of person scientists at the TRI are currently looking for as volunteers – people who have tried to lose weight by exercising and changing their diets but didn’t succeed. As with many other people who have the same problem, something in Rebecca’s body keeps her from losing weight and researchers at the TRI are trying to find out what that could be. The common perception is that overweight people only need to eat healthier and exercise more in order to lose weight. But this simple approach does not work for everyone. That is about to change with the research taking place at the TRI’s new facility in downtown Orlando.

Read More

A “twisted” grand opening ceremony

by Patrick Bartosch on March 29, 2012 at 3:35 pm | 0 Comments
Full Article
TRI grand opening speakers (from left to right): John Reed, Terry Owen, Dan Kelly, Steve Smith, Lars Houmann, Des Cummings, Don Jernigan

TRI grand opening speakers (from left to right): John Reed, Terry Owen, Dan Kelly, Steve Smith, Lars Houmann, Des Cummings, Don Jernigan

“My goal is to cure diabetes,” Steven Smith, M.D., scientific director of the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes (TRI), said boldly at the opening ceremony of the TRI’s new state-of-the-art facility in downtown Orlando on March 27. “We believe that personalized medicine is our best shot at discovering cures for our most serious health problems like diabetes.”

The ceremony’s highlight was the unveiling of a spectacular nine-foot double-helix DNA structure that will be placed at the main entrance of the building, symbolizing the fundamental research being conducted at the TRI, as well as the synergies and collaborations the TRI represents. Selected board members and presenters each added one illuminated “bar,” representing a nucleotide, to the double helix.

“This is one of those rare times when the reality far exceeds the dream,” said John Reed, M.D., Ph.D., CEO of Sanford-Burnham. “The TRI is a wonderful opportunity for our organization, which will bring more and more to life our slogan From Research, the Power to Cure. We’re very excited about this opportunity to take our relationship with Florida Hospital to the next level.”

Read More

Tasting fructose with the pancreas

by Heather Buschman, Ph.D. on February 6, 2012 at 12:01 pm | 1 comment
Full Article
Taste receptors (green) in pancreatic insulin-producing beta cells (red). Nuclei are shown in blue.

Taste receptors (green) in pancreatic insulin-producing beta cells (red). Nuclei are shown in blue.

Taste receptors on the tongue help us distinguish between safe food and food that’s spoiled or toxic. But taste receptors are now being found in other organs, too. In a study published online February 6 by the Proceedings of the National Academy of Sciences, Sanford-Burnham researchers discovered that beta cells in the pancreas use taste receptors to sense fructose, a type of sugar. According to the study, the beta cells respond to fructose by secreting insulin, a hormone that regulates the body’s response to dietary sugar.

“Before this study, fructose’s effect on insulin release was not appreciated. Fructose, and especially high-fructose corn syrup, is found in everything from sodas to cereals, but it remains to be seen whether dietary fructose is good or bad for beta cells and human metabolism,” said Björn Tyrberg, Ph.D., adjunct assistant professor in the Diabetes and Obesity Research Center at Sanford-Burnham’s Lake Nona campus in Orlando and senior author of the study.

Read More

Sanford-Burnham experts talk about why Americans are fat

by Deborah Robison on January 6, 2012 at 10:11 am | 0 Comments
Full Article
Fireworks over the Sydney Opera House

Fireworks over the Sydney Opera House

New Year’s resolutions and dieting seem to go hand-in-hand. Setting a personal goal to lose weight and exercise more may jump-start the New Year but “February frustration” can derail even the most determined. Scientists in Sanford-Burnham’s Diabetes and Obesity Research Center recently shared their expertise on the causes of weight gain and the metabolic challenges that make it so hard to keep off the extra pounds. Their insights on genetics, diet, metabolism and lifestyle were included in a four-part series called “What’s making Americans so fat?” that ran in the Orlando Sentinel beginning January 1. Medical reporter Marni Jameson spoke with national obesity experts to compile a list of 40 reasons for why 60 percent of U.S. adults are obese or overweight.

“It’s not gluttony, and it’s not lack of willpower,” says Dr. Steven Smith, scientific director of the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes. “No scientist in the field will say the problem is strictly one of willpower,” he says. “It’s a result of the way our genes are interacting with an environment that is stacked against them.”

Here’s an excerpt of how the experts weighed in:

Read More

All weight gain is not the same

by Deborah Robison on January 4, 2012 at 2:09 pm | 0 Comments
Full Article
Steven R. Smith, M.D.

Steven R. Smith, M.D.

Malnutrition in its many forms remains a world-wide epidemic. In the United States, more than 60 percent of adults are classified as overweight or obese, whereas third-world nations are struggling with under-nutrition and insufficient food supplies. A new study provides scientific insight that may benefit development of public health policy to influence healthy weight gain.

The study, published January 4 in the Journal of the American Medical Association (JAMA), examines the impact of diets containing varying amounts of protein on weight gain, body composition, and energy expenditure. The research, led by Sanford-Burnham’s Steven R. Smith, M.D. and George Bray, M.D., Pennington Biomedical Research Center, found that total calories account for increases in body fat, while increasing the percent of dietary protein during overfeeding led to more lean body mass storage. This work appears to be the first to analyze the impact of dietary protein during overfeeding and provides guidance on dietary composition for healthy weight gain.

Read More

How a few extra mice prompted a diabetes collaboration

by Heather Buschman, Ph.D. on December 5, 2011 at 8:59 am | 1 comment
Full Article
insulin-producing beta-cells in a mouse pancreas (Image courtesy of Edward Monosov)

insulin-producing beta-cells in a mouse pancreas (Image courtesy of Edward Monosov)

Dr. Barbara Ranscht and her lab are working to better understand how T-cadherin—a protein found on the surface of neurons, muscle, and other cells—regulates communication between cells during development and disease. The best way to go about this is to see what happens when the protein is missing. To do this, her lab developed a mouse model that lacks the protein altogether. Using these animals, Dr. Ranscht’s group has revealed that T-cadherin protects the stressed heart and is necessary for new blood vessel growth in injury models.

One day, Dr. Ranscht found herself discussing possible roles for T-cadherin in metabolism with Sanford-Burnham colleagues Dr. Björn Tyrberg and Dr. Fred Levine. The researchers especially wondered about T-cadherin’s role in the pancreas (Drs. Tyrberg’s and Levine’s organ of expertise).

Read More

Obesity is not one condition: an interview with Dr. Steven Smith

by Heather Buschman, Ph.D. on October 21, 2011 at 9:28 am | 0 Comments
Full Article
Dr. Steven Smith, scientific director of the Translational Research Institute for Metabolism and Diabetes

Dr. Steven Smith, scientific director of the Translational Research Institute for Metabolism and Diabetes

Dr. Steven Smith is the scientific director of the Translational Research Institute for Metabolism and Diabetes, a collaboration between Sanford-Burnham and Florida Hospital. In a special presentation at Obesity 2011: The Obesity Society 29th Annual Scientific Meeting, held October 1-5 in Orlando, Fla., Dr. Smith discussed some up-and-coming anti-obesity agents, how they work, and how physicians might be able to put them to use. In his talk, he emphasized the importance of better understanding the fundamental cellular mechanisms that fuel obesity. With a greater appreciation for human metabolism, Dr. Smith explained, scientists will be able to develop new medications that focus less on appetite suppression (the target of most current weight loss drugs) and more on peripheral targets such as muscle or fat.

Read More

Fighting fat with fat

by Heather Buschman, Ph.D. on October 4, 2011 at 9:00 am | 0 Comments
Full Article
Loss of orexin impairs brown fat function and promotes obesity in mice. The leaner mouse with functional brown fat (left) dissipates considerable amounts of energy as heat. The orexin-deficient mouse (right) lacks fat fuel and active mitochondria, thus storing energy as fat instead of burning it. (Image by Peter Allen, UCSB)

Loss of orexin impairs brown fat function and promotes obesity in mice. The leaner mouse with functional brown fat (left) dissipates considerable amounts of energy as heat. The orexin-deficient mouse (right) lacks fat fuel and active mitochondria, thus storing energy as fat instead of burning it. (Image by Peter Allen, UCSB)

The fat we typically think of as body fat is called white fat. But there’s another type—known as brown fat—that does more than just store fat. It burns fat. Scientists used to think that brown fat disappeared after infancy, but recent advances in imaging technology led to its rediscovery in adult humans. Because brown fat is so full of blood vessels and mitochondria—that’s what makes it brown—it’s very good at converting calories into energy, a process that malfunctions in obesity.

In a study published October 5 in Cell Metabolism, Sanford-Burnham researchers discovered that orexin, a hormone produced in the brain, activates calorie-burning brown fat in mice. Orexin deficiency is associated with obesity, suggesting that orexin supplementation could provide a new therapeutic approach for the treatment of obesity and other metabolic disorders. Most current weight loss drugs are aimed at reducing a person’s appetite. An orexin-based therapy would represent a new class of fat-fighting drugs—one that focuses on peripheral fat-burning tissue rather than the brain’s appetite control center.

“Our study provides a possible reason why some people are overweight or obese despite the fact that they don’t overeat—they might lack the orexin necessary to activate brown fat and increase energy expenditure,” explains Dr. Devanjan Sikder, senior author of the study and assistant professor in Sanford-Burnham’s Diabetes and Obesity Research Center, located in Orlando’s Medical City at Lake Nona.

Read More

Glucose uptake relies on newly identified protein

by Heather Buschman, Ph.D. on September 7, 2011 at 10:50 am | 0 Comments
Full Article
Dr. Zhen Jiang

Dr. Zhen Jiang

All cells need glucose (sugar) to produce the energy they need to survive. High glucose levels in the bloodstream (such as occur after a meal), trigger the pancreas to produce insulin. In turn, muscle and fat cells respond to insulin by moving GLUT4, a glucose transporter, from intracellular storage out to the cell surface. There, GLUT4 can take up the glucose the cell needs from the bloodstream.

A team led by Dr. Zhen Jiang recently identified the protein—called CDP138—responsible for ensuring that GLUT4 is properly inserted in the cellular membrane. This finding provides a new understanding of glucose metabolism—an important finding considering that impaired insulin action and glucose metabolism contribute to the development of type 2 diabetes.

“This is a newly identified protein that’s involved in an important step in glucose uptake,” said Dr. Jiang, assistant professor in Sanford-Burnham’s Diabetes and Obesity Research Center, located in Orlando’s Medical City at Lake Nona.

Read More

«Older Posts

Search

Find more information

  • About Beaker
  • Contact us
  • Donate

Please take a quick survey

Which of these items describes you?

Select all that apply. (Question 1 of 5)

Categories

  • Basic Research
  • Cancer
    • Apoptosis & Cell Death Research
    • Signal Transduction
    • Tumor Development
    • Tumor Microenvironment
  • Children's Health
    • Genetic Diseases
    • Muscle Development & Regeneration
    • RNA Biology
  • Diabetes & Obesity
    • Cardiovascular Pathobiology
    • Metabolic Signaling & Disease
  • Drug Discovery
  • Events
  • Graduate School of Biomedical Sciences
  • Grants
  • Infectious & Inflammatory Diseases
    • Bioinformatics & Systems Biology
    • Infectious Diseases
    • Inflammatory Diseases
  • Nanomedicine
  • Neuroscience, Aging, & Stem Cells
    • Degenerative Diseases
    • Development & Aging
    • Stem Cells
  • Other
  • People
  • Sanford-Burnham Supporters
  • Translational Medicine

Search by Keyword

Alzheimer's disease CCRA CIRM collaboration commitment communication community Conrad Prebys Center for Chemical Genomics Daniel Kelly Erkki Ruoslahti Evan Snyder Florida Hospital Fred Levine Genetic Disease Program Guy Salvesen Hudson Freeze John Reed Kristiina Vuori La Jolla Lake Nona Metabolic Signaling metabolism NIH Orlando personalized medicine Prebys Center press proteins Rare Diseases Rare disease symposium research publications Robert Wechsler-Reya Santa Barbara Sara Courtneidge Stem Cells Steven Smith Stuart Lipton T. Denny Sanford technology Translational Research Institute tumor microenvironment Tumor Microenvironment Program Video Yu Yamaguchi Ze'ev Ronai

© Sanford-Burnham Medical Research Institute. All rights reserved.

Get Cloud PHP Hosting on CatN