TAG: "Diabetes"

Funding from biotech company to advance diabetes research


Agreement with UC Merced professor an important show of faith.

Rudy Ortiz, UC Merced

Rudy Ortiz, UC Merced

UC Merced biology professor Rudy Ortiz is furthering his innovative research into diabetes with support from a major pharmaceutical company.

Ortiz’ work, developing new applications for medicines used to treat the effects of insulin resistance, has been funded by Amylin Pharmaceuticals LLC, a wholly owned subsidiary of Bristol-Myers Squibb Co., to the tune of $192,000 over two years.

Such funding agreements are common on other UC campuses and in comparable research institutions, and this agreement at UC Merced constitutes an important show of faith from the pharmaceutical industry in the young campus’s research capabilities.

“We will evaluate a drug that is traditionally used to address gluco-regulatory imbalance —the hallmark of diabetes — on a different aspect of diabetes,” Ortiz said. “This drug has also been proposed as a potential alternative to alleviate the hypertension associated with diabetes by improving the kidneys’ ability to regulate sodium.”

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Pediatric diabetes clinic marks 2nd anniversary in new Mission Bay home


UCSF clinic is steps away from the future UCSF Benioff Children’s Hospital.

Kendall Layous, and her mother Shonda, make drawings that are used as table-top covers, part of an art therapy program at the UCSF Madison Clinic for Pediatric Diabetes.

In the two years since the Madison Clinic for Pediatric Diabetes was established through an anonymous, $10 million gift, it has evolved into a state-of-the-art facility with innovative programs and a new home on the Mission Bay campus.

The Madison Clinic at Mission Bay, now located steps away from the future UCSF Benioff Children’s Hospital, offers comprehensive care for children and young adults with diabetes, with an emphasis on patient education, empowerment and the use of advanced technologies. It also has a commitment to advancing research in the management of diabetes in children.

A multidisciplinary team – including endocrinologists, clinical psychologists, nurses, diabetes educators, social workers, dietitians, and administrative staff – ensures patients’ varying needs are met.

“I don’t really manage diabetes. The parents do it all day, every day,” said Saleh Adi, M.D., medical director of the Madison Clinic and a pediatric endocrinologist. “Our job is to teach them how and provide them with the tools they need, and to be there for support and feedback whenever they need it.”

Shonda and Brad Layous know firsthand how much is required of parents with diabetic children. Their daughter Kendall was diagnosed with type 1 diabetes in April 2012, two days after her second birthday.

“Having a child with a serious health condition takes its toll on the entire family, so a bright spot in this emotional year for us was finding the Madison Clinic,” said Shonda Layous. “Our family knows that we are in the best care possible at the UCSF Madison Clinic, and its amazing staff and wonderful space give us comfort and confidence that we will partner with them for life to best manage her disease.”

There currently are 25.8 million children and adults in the United States, or 8.3 percent of the population, living with diabetes, according to the American Diabetes Association. One in every 400 children and adolescents younger than age 20 has the chronic disease, which is characterized by the body’s inability to regulate blood glucose, or blood sugar, levels.

With the incidence of both type 1 and type 2 diabetes in children on the rise, it is increasingly important to have skilled teams of diabetes health care providers who specialize in treating young people.

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International consortium builds ‘Google map’ of human metabolism


Recon 2 is most comprehensive virtual reconstruction of human metabolic network to date.

Researchers liken Recon 2 to Google mapping for its ability to merge complex details into a single, interactive map.

Building on earlier pioneering work by researchers at the University of California, San Diego, an international consortium of university researchers has produced the most comprehensive virtual reconstruction of human metabolism to date. Scientists could use the model, known as Recon 2, to identify causes of and new treatments for diseases like cancer, diabetes and even psychiatric and neurodegenerative disorders. Each person’s metabolism, which represents the conversion of food sources into energy and the assembly of molecules, is determined by genetics, environment and nutrition.

The researchers presented Recon 2 in a paper published online March 3 in the journal Nature Biotechnology.

Doctors have long recognized the importance of metabolic imbalances as an underlying cause of disease, but scientists have been ramping up their research on the connection as a result of compelling evidence enabled by the Human Genome Project and advances in systems biology, which leverages the power of high-powered computing to build vast interactive databases of biological information.

“Recon 2 allows biomedical researchers to study the human metabolic network with more precision than was ever previously possible. This is essential to understanding where and how specific metabolic pathways go off track to create disease,” said Bernhard Palsson, Galletti Professor of Bioengineering at UC San Diego Jacobs School of Engineering.

“It’s like having the coordinates of all the cars in town, but no street map. Without this tool, we don’t know why people are moving the way they are,” said Palsson.

He likened Recon 2 to Google mapping for its ability to merge complex details into a single, interactive map. For example, researchers looking at how metabolism sets the stage for cancerous tumor growth could zoom in on the “map” for finely detailed images of individual metabolic reactions or zoom out to look at patterns and relationships among pathways or different sectors of metabolism. This is not unlike how you can get a street view of a single house or zoom out to see how the house fits into the whole neighborhood, city, state, country and globe.  And just as Google maps brings together a broad set of data – such as images, addresses, streets and traffic flow – into an easily navigated tool, Recon 2 pulls together a vast compendium of data from published literature and existing models of metabolic processes.

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Study links sugar to diabetes


Results provide evidence that not all calories are equal from a diabetes-risk standpoint.

Sanjay Basu, UC San Francisco

Does eating too much sugar cause diabetes?

For years, scientists have said “not exactly.” Eating too much of any food, including sugar, can cause you to gain weight; it’s the resulting obesity that predisposes people to diabetes, according to the prevailing theory.

But now the results of a large epidemiological study conducted at UC San Francisco suggest that sugar may also have a direct, independent link to diabetes.

Researchers examined data on global sugar availability and diabetes rates from 175 countries over the past decade. After accounting for obesity and a large array of other factors, the researchers found that increased sugar in a population’s food supply was linked to higher diabetes rates, independent of obesity rates. Their study was published Feb. 27 in PLOS ONE.

The study provides the first large-scale, population-based evidence for the idea that not all calories are equal from a diabetes-risk standpoint.

Robert Lustig, UC San Francisco

“It was quite a surprise,” said Sanjay Basu, M.D., Ph.D., an assistant professor of medicine at the Stanford Prevention Research Center and the study’s lead author. The research was conducted while Basu was a medical resident at UCSF and working with Robert Lustig, M.D., a pediatric endocrinologist at UCSF Benioff Children’s Hospital and the paper’s senior author.

“We’re not diminishing the importance of obesity at all, but these data suggest that at a population level there are additional factors that contribute to diabetes risk besides obesity and total calorie intake, and that sugar appears to play a prominent role.”

Specifically, more sugar was correlated with more diabetes: For every additional 150 calories of sugar available per person per day, the prevalence of diabetes in the population rose 1 percent, even after controlling for obesity, physical activity, other types of calories and a number of economic and social variables. A 12-ounce can of soda contains about 150 calories of sugar. In contrast, an additional 150 calories of any type caused only a 0.1 percent increase in the population’s diabetes rate.

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Pharmacologist to test new therapy for protecting diabetics from heart failure


UC Davis researcher will focus on blocking the pancreatic hormone amylin.

Florin Despa, UC Davis

A UC Davis pharmacologist has been awarded a two-year, $95,000 Innovation Award from the American Diabetes Association to find out if blocking the pancreatic hormone amylin can reduce diabetic heart failure.

The researcher — Florin Despa — previously found that amylin accumulates in strings of proteins called oligomers in the heart tissue of patients with heart disease and type 2 diabetes or obesity.

“We now want to determine if limiting accumulation of oligomerized amylin in cardiac tissue can delay or even prevent the development of diabetic heart failure,” said Despa, an assistant professor of pharmacology in the UC Davis School of Medicine. “This is a priority for my lab, because heart failure is the number-one killer for people with diabetes.”

In healthy people, amylin circulates in the blood together with insulin — the hormone that controls carbohydrate and fat metabolism — and principally regulates gastric fluxes and the sensation of satiety.

In previous experiments, Despa found widespread amylin deposition in tissue from failing hearts of patients with type 2 diabetes or obesity. Those who were overweight but not obese had some, but not extensive, amylin accumulation, and there was little or none in the heart tissue of lean or non-diabetic people. These studies suggested that cardiac accumulation of the hormone has a role in advancing heart failure for those who are diabetic or obese.

Despa will use the new funding to find out if signaling molecules that have anti-aggregation properties — such as plasmin and eicosanoids — can limit amylin accumulation and its destructive heart-health effects in rats.

“If successful, this project may lead to new therapeutic targets for cardioprotection for those with diabetes,” said Despa.

The American Diabetes Association funds research that accelerates progress toward improved treatments and a cure for diabetes. The program emphasizes innovative and novel projects, along with funding opportunities for early-career researchers. For more information, visit www.diabetes.org.

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UC San Diego awarded NIH grant to expand diabetes, obesity research hub


San Diego Supercomputer Center to host infrastructure.

Computer lab at UC San DiegoResearchers at UC San Diego have been awarded a new National Institutes of Health (NIH) grant to expand and enhance a cyberinfrastructure designed to provide scientists with easily accessible, Web-based resources to help fight diabetes and metabolic diseases.

The grant, awarded through the university’s Center for Research in Biological Systems (CRBS), will focus on establishing, coordinating, and making available large pools of datasets to researchers as part of a project to further develop the National Institute of Diabetes and Digestive and Kidney Diseases’ (NIDDK) Interconnectivity Network community and infrastructure.

About 25.8 million children and adults in the United States, or 8.3 percent of the population, have diabetes, according to the American Diabetes Association. Obesity has been cited as a contributing factor to approximately 100,000 to 400,000 deaths in the U.S. each year.

Established in 2010, a prototype of the current system called dkCOIN was initially created to explore requirements for information sharing between four NIDDK-supported consortia, including the Nuclear Receptor Signaling Atlas (NURSA), the Beta Cell Biology Consortium (BCBC), the Mouse Metabolic Phenotyping Centers (MMPC), and the Diabetic Complications Consortium (DCC).

The new NIH grant will allow UC San Diego researchers to expand the data federation and develop and enhance a user-friendly Web portal that will seamlessly integrate information, resources, and data held by NIDDK-related research groups, with the goal of providing a valuable resource for NIDDK investigators.

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Altman Clinical & Translational Research Institute breaks ground


Institute will speed efforts to deliver new drugs, technologies, procedures to patients.

UC San Diego leaders, philanthropists and community members gathered Thursday to celebrate the official start of construction on the Altman Clinical and Translational Research Institute (CTRI) building, and to show gratitude to the family whose generosity has helped to make the state-of-the-art building possible.

Set to open in 2016, the Altman CTRI will accelerate efforts to deliver new drugs, technologies and procedures to patients who need them most, speakers said. Its location, footsteps from many clinical facilities on the UC San Diego Health System campus in La Jolla, makes it one of only a handful of such centers in the nation.

“This is a building that is going to be a bridge to our future; where we are going to define new cures, where we are going to define how medicine should be practiced,” said Chancellor Pradeep K. Khosla.

The building is named for San Diego philanthropists and longtime residents Lisa and Steve Altman, who have pledged $10 million toward its construction. Steve Altman is vice chairman of Qualcomm Inc.; he and his wife, Lisa, have been generous patrons of many local and national charities.

The Altmans’ gift was inspired by the prevalence of type 1 diabetes in their family. Two of the Altmans’ three children have the disease, and multiple other family members have lived with diabetes since childhood. The Altman CTRI building will be the new home of the UC San Diego Pediatric Diabetes Research Center, and it will welcome patients taking part in clinical trials.

“Other than marrying my wife, Lisa, this was the biggest no-brainer thing for us to do in our lives,” Steve Altman said. “To get these kinds of capabilities here in San Diego, at such a fine institution with so much talent, and putting it all together, it’s something that’s clearly of great need.”

The Altmans were toasted by friend Rich Sulpizio, whose family made a leadership gift to name the Sulpizio Cardiovascular Center, which opened in 2011. Steve Altman and Rich Sulpizio have been longtime colleagues at Qualcomm. Steve Altman shared that he was delighted that the Altman CTRI would be connected to the Sulpizio Cardiovascular Center by a bridge – a lasting symbol of the connection between the two families.

Based on the idea that solving today’s complex medical challenges requires an innovative approach, the facility unites laboratory and clinical researchers with shared resources to support their work in space designed to encourage collaboration. The discoveries that will emerge will benefit patients everywhere.

“That’s what makes this the opportunity of a lifetime,” said UC San Diego Health System CEO Paul Viviano.

UC San Diego is uniquely positioned to host such a center because of its collaborative spirit, talented faculty and staff and its location in the midst of a high concentration of world-class public and private research institutions.

“A facility like this could not exist anywhere else in our region,” said Dr. David A. Brenner, vice chancellor for health sciences and dean of the UC San Diego School of Medicine. “In fact, there are only a handful of places across the nation where it could be successful. I feel lucky to live and work in such a place.”

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Are pear-shaped bodies more healthy than apples?


UC Davis study deflates that notion.

People who are “apple-shaped” — with fat more concentrated around the abdomen — have long been considered more at risk for conditions such as heart disease and diabetes than those who are “pear-shaped” and carry weight more in the buttocks, hips and thighs.

But new research conducted at UC Davis Health System published in The Journal of Clinical Endocrinology and Metabolism provides further evidence that the protective benefits of having a pear-body shape may be more myth than reality. The journal article posted online today (Jan. 10) and will appear in the March print edition.

The UC Davis study found that fat stored in the buttock area — also known as gluteal adipose tissue — secretes abnormal levels of chemerin and omentin-1, proteins that can lead to inflammation and a prediabetic condition know as insulin resistance in individuals with early metabolic syndrome.

Metabolic syndrome refers to a group of risk factors that occur together, doubling the risk for heart disease and increasing the risk for diabetes at least five-fold. Risk factors include having a large waistline, low levels of high-density lipoproteins (HDL), or “good” cholesterol, high blood pressure as well as high fasting blood sugar ( insulin resistance) and high triglyceride levels. According to the Centers for Disease Control and Prevention, metabolic syndrome affects 35 percent of American adults over age 20.

“Fat in the abdomen has long been considered the most detrimental to health, and gluteal fat was thought to protect against diabetes, heart disease and metabolic syndrome,” said Ishwarlal Jialal, lead author of the study and a professor of pathology and laboratory medicine and of internal medicine at UC Davis. ”But our research helps to dispel the myth that gluteal fat is ‘innocent.’ It also suggests that abnormal protein levels may be an early indicator to identify those at risk for developing metabolic syndrome.”

The UC Davis team found that in individuals with early metabolic syndrome, gluteal fat secreted elevated levels of chemerin and low levels of omentin-1 — proteins that correlate with other factors known to increase the risk for heart disease and diabetes.  High chemerin levels, for example, correlated with high blood pressure, elevated levels of C-reactive protein (a sign of inflammation) and triglycerides, insulin resistance, and low levels of HDL cholesterol. Low omentin-1 levels correlated with high levels of triglycerides and blood glucose levels and low levels of HDL cholesterol.

“High chemerin levels correlated with four of the five characteristics of metabolic syndrome and may be a promising biomarker for metabolic syndrome,” said Jialal. “As it’s also an indicator of inflammation and insulin resistance, it could also emerge as part of a biomarker panel to define high-risk obesity states. The good news is that with weight loss, you can reduce chemerin levels along with the risk for metabolic syndrome.”

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Next steps in potential stem cell therapy for diabetes


UC San Diego-based study looks at differentiation of hESCs in endocrine cell progression.

Maike Sander, UC San Diego

Type 1 and type 2 diabetes results when beta cells in the pancreas fail to produce enough insulin, the hormone that regulates blood sugar. One approach to treating diabetes is to stimulate regeneration of new beta cells.

There are currently two ways of generating endocrine cells (cell types, such as beta cells, that secrete hormones) from human embryonic stem cells, or hESCs: either generating the cells in vitro in culture or transplanting immature endocrine cell precursors into mice.

Researchers from the UC San Diego School of Medicine, collaborating with scientists from San Diego-based biotech company ViaCyte Inc., looked at the differences and similarities between these two types of hESC-derived endocrine cell populations and primary human endocrine cells, with the longer-term goal of developing new stem cell therapies for diabetes.

The results of their study will be published online today (Jan. 10), in advance of the Feb. 7 print edition of the journal Cell Stem Cell.

The scientists compared gene expression and chromatin architecture – the structure of combined DNA and proteins that make up the nucleus of the cell, in which dynamic remodeling occurs at various stages of differentiation – in both primary human endocrine cells and hESC-derived cells.

“We found that the endocrine cells retrieved from transplanted mice are remarkably similar to primary human endocrine cells,” said principal investigator Maike Sander, M.D., professor of pediatrics and cellular and molecular medicine, and director of UC San Diego’s Pediatric Diabetes Research Center. “This shows that hESCs can differentiate into endocrine cells that are almost indistinguishable from their primary human counterparts.”

However, the researchers observed that endocrine cells produced in vitro lack features of primary endocrine cells and fail to express the majority of genes that are critical for endocrine cell function. Consistent with this finding, these cells are not able to reverse diabetes in diabetic animal models.

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Pioneering research on type 2 diabetes


Computer modeling eyes cell metabolism as trigger for the increasingly prevalent disease.

Jamey Marth, UC Santa Barbara

While legions of medical researchers have been looking to understand the genetic basis of disease and how mutations may affect human health, a group of biomedical researchers at UC Santa Barbara is studying the metabolism of cells and their surrounding tissue, to ferret out ways in which certain diseases begin. This approach, which includes computer modeling, can be applied to type 2 diabetes, autoimmune diseases and neurodegenerative diseases, among others.

Scientists at UC Santa Barbara have published groundbreaking results of a study of type 2 diabetes that point to changes in cellular metabolism as the triggering factor for the disease, rather than genetic predisposition. Type 2 diabetes is a chronic condition in which blood sugar or glucose levels are high. It affects a large and growing segment of the human population, especially among the obese. The team of scientists expects the discovery to become a basis for efforts to prevent and cure this disease.

The current work is based on a previous major finding by UC Santa Barbara’s Jamey Marth, who determined the identity of the molecular building blocks needed in constructing the four types of macromolecules of all cells when he was based at the Howard Hughes Medical Institute in La Jolla in 2008. These include the innate, genetic macromolecules, such as nucleic acids (DNA and RNA) and their encoded proteins, and the acquired metabolic macromolecules known as glycans and lipids. Marth is a professor in the Department of Molecular, Cellular, and Developmental Biology and the Biomolecular Science and Engineering Program; and holds the John Carbon Chair in Biochemistry and Molecular Biology and the Duncan and Suzanne Mellichamp Chair in Systems Biology. He is also a professor with the Sanford-Burnham Medical Research Institute in La Jolla.

“By studying the four types of components that make up the cell, we can, for the first time, begin to understand what causes many of the common grievous diseases that exist in the absence of definable genetic variation, but, instead, are due to environmental and metabolic alterations of our cells,” said Marth. UC Santa Barbara is the only institution studying these four types of molecules in the cells while also using computational modeling to determine their functions in health and disease, according to Marth.

The new study, published in the Dec. 27 issue of PLOS ONE, relies on computational systems biology modeling to understand the pathogenesis of type 2 diabetes.

“Even in the post-genomic era, after the human genome has been sequenced, we’re beginning to realize that diseases aren’t always in our genes — that the environment is playing a major role in many of the common diseases,” said Marth.

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Communication is key to medication adherence


Patients who give their doctors high marks in communication more likely to fill prescriptions.

Neda Ratonawongsa, UC San Francisco

Even the best medicines in the world can be rendered ineffective if they are not taken as prescribed.  The problem known as medication “non-adherence” is a major health issue in the United States, contributing to worse outcomes for people who have diabetes and other chronic diseases.

Now a study led by researchers at the University of California, San Francisco (UCSF), San Francisco General Hospital and Trauma Center (SFGH) and the Kaiser Permanente Division of Research has identified a significant factor that contributes to poor drug adherence – ineffective communication.

Described in the journal JAMA Internal Medicine, formerly known as the Archives of Internal Medicine, the study looked at 9,377 patients taking medications to lower their blood sugar, blood pressure or cholesterol.

These patients were asked through questionnaires to rate how well their doctors communicated with them. Patient medication adherence was determined by measuring delays in refilling prescriptions. The patients who gave their doctors poor marks in communicating were less likely to adhere to their medications.

The work suggests preparing doctors to be better communicators may help improve medication adherence and ultimately health outcomes, said lead author Neda Ratanawongsa, M.D., M.P.H., an assistant professor in the UCSF Department of Medicine and the UCSF Center for Vulnerable Populations at SFGH.

“Communication matters,” Ratanawongsa said. “Thirty percent of people [in the study] were not necessarily taking their medications the way their doctors thought they were. Rates for non-adherence were 4 to 6 percent lower for patients who felt their doctors listened to them, involved them in decisions and gained their trust. By supporting doctors in developing meaningful relationships with their patients, we could help patients take better care of themselves.”

The work is part of the Diabetes Study of Northern California (DISTANCE), which is designed to evaluate quality of care and to identify reasons for disparities where they exist.

“What is unique about our study is that we found that medication adherence is better if the physician has established a trusting relationship with the patient and prioritizes the quality of communication, even if that communication is not specifically focused on medication adherence,” added Andrew Karter, Ph.D., a senior research scientist with the Kaiser Permanente Division of Research and the principal investigator of DISTANCE.

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Vitamin D deficiency linked to type 1 diabetes


Study suggests preventive role for vitamin D3 in this disease.

Cedric Garland, UC San Diego

A study led by researchers from the UC San Diego School of Medicine has found a correlation between vitamin D3 serum levels and subsequent incidence of type 1 diabetes. The six-year study of blood levels of nearly 2,000 individuals suggests a preventive role for vitamin D3 in this disease. The research appears the December issue of Diabetologia, a publication of the European Association for the Study of Diabetes (EASD).

“Previous studies proposed the existence of an association between vitamin D deficiency and risk of and type 1 diabetes, but this is the first time that the theory has been tested in a way that provides the dose-response relationship,” said Cedric Garland, Dr.P.H., FACE, professor in UCSD’s Department of Family and Preventive Medicine.

This study used samples from millions of blood serum specimens frozen by the Department of Defense Serum Registry for disease surveillance. The researchers thawed and analyzed 1000 samples of serum from healthy people who later developed type 1 diabetes and 1,000 healthy controls whose blood was drawn on or near the same date but who did not develop type 1 diabetes. By comparing the serum concentrations of the predominant circulating form of vitamin D – 25-hydroxyvitamin D (25(OH)D) – investigators were able to determine the optimal serum level needed to lower an individual’s risk of developing type 1 diabetes.

Based mainly on results of this study, Garland estimates that the level of 25(OH)D needed to prevent half the cases of type 1 diabetes is 50 ng/ml. A consensus of all available data indicates no known risk associated with this dosage.

“While there are a few conditions that influence vitamin D metabolism, for most people, 4,000 IU per day of vitamin D3 will be needed to achieve the effective levels,” Garland suggested. He urges interested patients to ask their health care provider to measure their serum 25(OH)D before increasing vitamin D3 intake.

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