UCSF researchers say societal control of sugar needed, similar to alcohol, tobacco.

Sugar should be controlled like alcohol and tobacco to protect public health, according to a team of UCSF researchers, who maintain in a new report that sugar is fueling a global obesity pandemic, contributing to 35 million deaths annually worldwide from non-communicable diseases like diabetes, heart disease and cancer.

Non-communicable diseases now pose a greater health burden worldwide than infectious diseases, according to the United Nations. In the United States, 75 percent of health care dollars are spent treating these diseases and their associated disabilities.

In the Feb. 2 issue of Nature, Robert Lustig, M.D., Laura Schmidt, Ph.D., M.S.W., M.P.H., and Claire Brindis, D.P.H., colleagues at the University of California, San Francisco, argue that sugar’s potential for abuse, coupled with its toxicity and pervasiveness in the Western diet, make it a primary culprit of this worldwide health crisis.

This partnership of scientists trained in endocrinology, sociology and public health took a new look at the accumulating scientific evidence on sugar. Such interdisciplinary liaisons underscore the power of academic health sciences institutions like UCSF.

Sugar, they argue, is far from just “empty calories” that make people fat. At the levels consumed by most Americans, sugar changes metabolism, raises blood pressure, critically alters the signaling of hormones and causes significant damage to the liver — the least understood of sugar’s damages. These health hazards largely mirror the effects of drinking too much alcohol, which they point out in their commentary is the distillation of sugar.

Worldwide consumption of sugar has tripled during the past 50 years and is viewed as a key cause of the obesity epidemic. But obesity, Lustig, Schmidt and Brindis argue, may just be a marker for the damage caused by the toxic effects of too much sugar. This would help explain why 40 percent of people with metabolic syndrome — the key metabolic changes that lead to diabetes, heart disease and cancer — are not clinically obese.

“As long as the public thinks that sugar is just ‘empty calories,’ we have no chance in solving this,” said Lustig, a professor of pediatrics in the division of endocrinology at the UCSF Benioff Children’s Hospital and director of the Weight Assessment for Teen and Child Health (WATCH) Program at UCSF.

“There are good calories and bad calories, just as there are good fats and bad fats, good amino acids and bad amino acids, good carbohydrates and bad carbohydrates,” Lustig said. “But sugar is toxic beyond its calories.”

Limiting the consumption of sugar has challenges beyond educating people about its potential toxicity. “We recognize that there are cultural and celebratory aspects of sugar,” said Brindis, director of UCSF’s Philip R. Lee Institute for Health Policy Studies (IHPS). “Changing these patterns is very complicated.”

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UC Irvine center explores, extols health benefits of exercise in childhood.

Dan Cooper, UC Irvine

Dr. Dan Cooper believes that exercise can be the best medicine — so much so that he’s studying how specifically designed exercise programs for at-risk kids can help curb excessive weight gain, fight diseases and foster long-term fitness.

With childhood obesity and asthma emerging as national health crises, Cooper in 2006 founded UC Irvine’s Pediatric Exercise Research Center, and over the past six years, it has shed light on the full benefits of physical activity.

At any one time, PERC hosts 15 to 20 studies of how — and how much — exercise works to avert type 2 diabetes, limit asthma attacks, thwart arthritis, prevent cancer, encourage mineralization in growing bones, and improve the quality of life for kids with chronic diseases and congenital disorders.

“Our purpose is to recognize the importance of exercise for health and growth in children,” says Cooper, professor and chair of pediatrics at UCI and director of the Institute for Clinical & Translational Science, which supports PERC efforts. “We’re one of the few centers in the country to focus on this crucial issue.”

He and PERC’s associate director, gymnast Shlomit Aizik, maintain that exercise is necessary not only for good childhood health but also to prevent later-in-life maladies such as heart disease and stroke.

Cooper was one of the principal investigators for the nationwide Healthy study, which involved healthier cafeteria choices, longer and more intense periods of physical activity, and robust in-school education programs to lower rates of obesity and other risk factors for type 2 diabetes.

Besides its role in overall fitness, exercise also triggers biochemical mechanisms that activate anti-inflammatory cells and important growth factors, Aizik says.

PERC-supported research on these biochemical mechanisms opened the door to understanding the positive influence of physical activity on immune diseases — most commonly asthma and, to a lesser extent, arthritis, which is increasingly seen in obese children — while addressing a pressing question.

“How much exercise is too much?” Cooper says. “Too much can actually worsen these conditions. The challenge is determining the right ‘dose’ of exercise to achieve anti-inflammatory benefits without causing future harm. PE teachers are not trained for this, so we’re establishing programs to help schools properly integrate the correct amount of exercise.”

PERC researchers are also probing the impact of physical activity during key stages of child development. For example, studies show that diet and exercise are linked to proper mineralization in growing bones, which can stave off osteoporosis in middle and old age.

A PERC group is currently looking at the effects of exercise on infants born two to three months early, missing out on a phase of fetal life marked by lots of body-conditioning physical movement. “This is lost when babies are born prematurely, interfering with a critical growth period,” Cooper says.

His team has created an activity program to offset this deficit. It starts, he says, with passive manipulation of a newborn’s arms and legs and progresses over 12 months to include such motions as head lifting and crawling. After a year, researchers will assess the influence of the exercise on body composition, bone mineralization and additional developmental markers.

Another PERC effort — led by Aizik — seeks to increase physical activity among kids with congenital conditions. College students are being trained to engage spina bifida patients at Miller Children’s Hospital Long Beach in exercise.

“Youngsters with disabilities rarely get enough physical activity,” Aizik says. “And studies show that it improves and extends the quality of life for these children. We want to measure the psychological and physiological results of this mentor-based program to see how we can incorporate an appropriate amount of exercise into their lives.”

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Alliance is UCSF’s third collaboration with Sanofi.

Matthias Hebrok, UC San Francisco

The University of California, San Francisco, has signed an alliance with international pharmaceutical company Sanofi (EURONEXT: SAN and NYSE: SNY) to share expertise in diabetes research and identify drug targets that could lead to new therapies for both type 1 and type 2 diabetes.

The $3.1 million collaboration will bring together scientists in three UCSF labs with deep understanding of the biology of beta cells – insulin-producing cells that are destroyed in type 1 diabetes and often produce too little insulin in type 2 – with Sanofi researchers who are experienced in developing potential drug candidates into actual therapies.

“This is a true partnership between scientists with very different strengths,” said Matthias Hebrok, Ph.D., director of the UCSF Diabetes Center. “UCSF is known for its deep understanding of the underlying biology of diabetes, while Sanofi has great expertise in screening compounds, identifying which molecules have potential, and moving them along to develop a new drug. Such an endeavor is almost impossible to accomplish in a single academic laboratory. Thus, both partners profit from the expertise of the other group.”

The alliance is the university’s third collaboration with Sanofi, alongside brain trauma and oncology research launched last year, since the two signed a master agreement in January 2011 to work together in translating academic science into potential new therapies. Master agreements lay out the fundamental terms of research collaborations, align with the University’s academic mission including broad publication rights, and form part of a core strategy for the UCSF Office of Innovation, Technology and Alliances to expedite that “bench-to-bedside” research.

This also is the first collaboration of its kind for the UCSF Diabetes Center, extending beyond simpler, funded-research agreements to create a two-way partnership in which scientists on both sides contribute technology and expertise to identify drug targets and test their potential.

“Sanofi is pleased to collaborate with the Diabetes Center at UCSF to combine expertise in employing new technologies for the development of innovative diabetes therapies,” said Pierre Chancel, senior vice president in the Diabetes Division at Sanofi. “The potential resulting drug discovery projects will supplement our integrated solutions model for diabetes management and help Sanofi continue to deliver best-in-class solutions to people living with diabetes.”

Together, the team will assess and validate potential drug targets from a UCSF library of roughly 100,000 small interference RNAs (siRNA) – molecules that play a crucial role in turning on and off genes, including the gene that produces insulin. They also will identify Sanofi compounds that might be effective in regulating those molecules, study the impact those compounds have on UCSF laboratory models of diabetes and assess their therapeutic potential.

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By curbing consumption, funding treatment, tens of thousands of lives could be saved.

Kirsten Bibbins-Domingo, UC San Francisco

Every year, Americans drink 13.8 billion gallons of soda, fruit punch, sweet tea, sports drinks, and other sweetened beverages — a mass consumption of sugar that is fueling soaring obesity and diabetes rates in the United States.

Now a group of scientists at the University of California, San Francisco, San Francisco General Hospital and Trauma Center (SFGH) and Columbia University have analyzed the effect of a nationwide tax on these sugary drinks.

They estimate slapping a penny-per-ounce tax on sweetened beverages would prevent nearly 100,000 cases of heart disease, 8,000 strokes, and 26,000 deaths over the next decade.

“You would also prevent 240,000 cases of diabetes per year,” said Kirsten Bibbins-Domingo, M.D., Ph.D., an associate professor of medicine and of epidemiology and biostatistics at UCSF and acting director of the Center for Vulnerable Populations at the UCSF-affiliated SFGH.

In addition to $13 billion per year in direct tax revenue, Bibbins-Domingo and her colleagues estimated that such a tax would save the public $17 billion over the next decade in health care-related expenses due to the decline of obesity-related diseases.

“Our hope is that these types of numbers are useful for policy makers to weigh decisions,” she said.

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19-year-old patient receives rare combination surgery.

Jennifer Golden received the first double lung-liver transplant performed at UCLA.

Jennifer Golden, a 19-year-old college student from Las Vegas, got her Christmas gift early this year — a pair of life-saving lungs and a liver at Ronald Reagan UCLA Medical Center on Dec. 4.

The rare combination surgery, thanks to the gift of one donor, also marked a milestone for the hospital’s organ transplant program: It was the first operation of its kind ever performed at UCLA.

The young woman has a genetic condition called cystic fibrosis, which causes thick, sticky mucus in her lungs that traps infection-causing bacteria. As a result, Jennifer experienced shortness of breath, excess mucus, coughing, an inability to gain weight and diabetes.

Her disease was managed by a routine of “tune-ups” to clear the mucus in her lungs with antibiotics, intravenous medications, physical therapy and other procedures. However, over the years, her lungs developed infections that became increasingly difficult to treat. To make matters more complicated, Jennifer’s liver function was also affected by the disease. By her senior year, she was so sick she could no longer attend high school.

At age 17, with her lungs and liver simultaneously deteriorating, she was told her only chance at life was organ donation.

“I felt every emotion — scared, nervous, but also happy that this could save my life,” Jennifer recalled.

A double lung-liver transplant surgery is rare. According to the most current data available from the United Network for Organ Sharing which manages the country’s organ donation system, only 44 lung-liver transplants have been performed in the United States. It is also unusual for a cystic fibrosis patient to need both lungs and a liver. More commonly, because of the way the disease progresses, the patient needs only one organ or the other.

“Because of her small size and the necessity for both the lungs and liver to be usable, she knew — as did we — that her wait might be long,” said Dr. Sue McDiarmid, professor of pediatrics and surgery, director of the pediatric liver transplant program and Jennifer’s doctor for 10 years.

Meantime, Jennifer’s entire lung and liver transplant team — including surgeons, physicians and anesthesiologists — spent a lot of time planning for her complex surgery. For example, the surgeons decided that the best approach would be for the lung transplant to be performed first.

“We also consulted with reconstructive surgeons to map out where we would make our incisions so that Jennifer’s abdominal muscles, bone and skin would not be impacted,” added Dr. Doug Farmer, professor of surgery and surgical director of the pediatric liver transplant program. “Our goal was to perform the surgery efficiently and with minimal blood loss.”

Two years later, on Saturday, Dec. 3, Jennifer got the call that a donor had been found. She and her mom quickly flew to UCLA while her dad followed behind in the family car.

Jennifer was wheeled into surgery around 4:45 a.m. on Dec. 4. The team’s intense planning paid off, and the 13-hour operation went smoothly.

When Jennifer came out of her surgery, her ability to breath was immediately improved. With the diseased lungs removed, her illness is now gone although her cystic fibrosis is not technically cured since it is part of her genes.

“We are quite optimistic that Jennifer will do well,” said Dr. Abbas Ardehali, professor of cardiothoracic surgery and surgical director of the heart and lung transplant program at UCLA. “This is our mission here at UCLA to expand the horizon of transplant patients we can serve.”

The former high school tennis team captain can now look to the future, and her plans include being with her fiancé, continuing her college studies and hitting the tennis courts again.

She also has a vital message to deliver.

“I hope that if a family out there is ever suffering with the death of loved one, they will consider the priceless gift of organ donation,” Jennifer said. “Someone did that for me, and it saved my life. My family and I cannot thank them enough.”

“Without organ donors and their families,　stories like Jennifer’s would have only tragic endings. Jennifer now breathes with ease — she is pink — her new liver is working very well, and all this because of this one donor whose life lives on in another,” said McDiarmid.

Accomplished UC Irvine scientist and award-winning mentor.

Sheryl Tsai, UC Irvine

Most professors will say that they look at the “Rate My Professor” website with trepidation. It’s easy to get discouraged if a student complains that your grading isn’t fair, or you have dandruff or, even worse, that you’re boring.

Sheryl Tsai has no such fears. Her reviews are unanimous raves, and she has the teaching awards to prove it. “She’s hilarious,” writes one student. “She actually enjoys talking about biology with her students!” writes another.

An associate professor at UC Irvine, Tsai works in the hot new field of chemical biology, harnessing a compendium of scientific disciplines to the task of discovering new drugs.  In 2006, she was named a Pew Scholar for her research on the genetic modification of polyketides, natural products of plants, fungi and bacteria that can form the basis for new treatments for HIV, diabetes and cancer.

Her research has gained international recognition, but she’s just as proud of the teaching awards she’s earned at UC Irvine, including the prestigious Golden Apple Award for Teaching in the Biological Sciences. She mentors five or six students each year through UC Irvine’s Undergraduate Research Opportunities Program.

The UC Berkeley-educated Tsai grew up in Taiwan. (Her first name, Shiou-Chuan, informally became Sheryl after she arrived in the U.S.) By the time she was in high school, cultural and political ferment was loosening the grip of the island’s leaders and, as a result, Tsai says that when she arrived in Berkeley, the famously liberal city felt like home — almost.

Q: Your undergraduate and master’s degrees are from the University of Taiwan. Is university education different there?

A: Most of the professors have Ph.D.s from the United States, so it was very Americanized. Taiwan is a very open country with a big influence from the United States.  I grew up watching “The A-Team” every night.

Q: Berkeley isn’t exactly like the rest of America. Was it a shock?

A: Not really. I think the reason I felt comfortable at Berkeley was the emphasis on social justice. That year, the city of Berkeley increased parking fees, and to show their opposition, people knocked the heads of the parking meters off and planted flowers in them. Everywhere in the city, you saw flowers planted in the beheaded parking meters.

Finding by UC Irvine team could help prevent cardiovascular complications.

N.D. Vaziri, UC Irvine

UC Irvine researchers have uncovered an important source of inflammation seen in people with chronic kidney disease, which is increasingly common due to the epidemic of obesity-related diabetes and hypertension.

Dr. N.D. Vaziri, professor emeritus of medicine and physiology & biophysics, found that CKD causes massive depletion of the key adhesive proteins, called the tight junction, that normally seal the space between the cells lining the intestines. This breakdown in the colon allows the leakage of microbial products and other noxious material into the body’s internal environment, accounting for the persistent systemic inflammation that frequently occurs in CKD patients.

“In fact, low levels of bacterial endotoxins are often noted in the blood of individuals with advanced chronic kidney disease,” Vaziri said. “However, the source and place of entry of these toxins were previously unknown.”

Understanding the connection between CKD and tight junction disintegration, he added, could lead to novel treatments to curb this inflammation and its many adverse consequences. Study results appear online in the journal Nephrology Dialysis Transplantation.

It’s estimated that nearly 25 million people in the U.S. have CKD, and more than 400,000 have end-stage kidney disease requiring dialysis. Many CKD patients develop accelerated cardiovascular disease — the primary cause of premature death in this population — linked to persistent inflammation.

“The relentless inflammation seen in chronic kidney disease has devastating effects on the cardiovascular system and other parts of the body,” Vaziri said.

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UCSF, Kaiser Permanente researchers take aim at genetic links to disease.

An ambitious project, teaming Kaiser Permanente and UC San Francisco researchers, takes aim at genetic links to disease.

At last count, nearly 200,000 members of Kaiser Permanente, one of the nation’s largest health maintenance organizations, had “spit for health” or given blood samples — providing a small supply of their DNA for researchers seeking genetic clues to the causes and prevention of many diseases.

The volunteers are part of the nation’s largest, most thorough effort to identify the genetic variations that underlie the aging process, vulnerability to disease and drug effectiveness.

The project goes well beyond the search for genetic links. It surveys patients’ personal habits, such as smoking, diet and availability of healthy food; it also examines environmental exposures, from pollution and pesticides to housing density and crime.

The research lays the groundwork for understanding how inherited traits and the environment affect health, and how genetic differences influence people’s responses to environmental insults and drug treatments.

Referred to as the Kaiser Permanente Research Program on Genes, Environment, and Health (RPGEH), it draws on Kaiser Permanente’s voluminous electronic patient medical records, which go back at least 15 years.  It is the world’s largest civilian electronic health record, and it is continuously updated to document the health status of all Kaiser members.

The RPGEH is led by Catherine Schaefer of Kaiser Permanente’s Division of Research and Neil Risch, director of UCSF’s Institute for Human Genetics.

The current phase of the RPGEH is funded by a $25 million grant from the National Institutes of Health. This support so far has enabled the researchers to develop genomic profiles of more than 100,000 RPGEH participants.

“Our goal is to provide a powerful resource for research into the genetic and environmental factors that may affect many common health conditions — such as cancer, cardiovascular disease, asthma, diabetes and mental health disorders,” said Schaefer, RPGEH’s executive director.

“We expect this comprehensive approach will accelerate development of new ways to treat and possibly prevent these conditions,” she said.

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Results of mouse tests show promise for drug development, treatment of diabetes.

Human adipose tissue (fat)

By knocking out a key regulatory protein, scientists at the University of California, San Diego School of Medicine and the Ecole Polytechnique Federale de Lausanne (EPFL) in Switzerland dramatically boosted insulin sensitivity in lab mice, an achievement that opens a new door for drug development and the treatment of diabetes.

The research, published in Friday’s (Nov. 11) issue of the journal Cell, reveals a new and previously unsuspected role for nuclear receptor corepressor (NCoR), a transcriptional coregulatory protein found in a wide variety of cells.

“Different transcription factors stimulate genes, turning them on and off, by bringing in co-activators or co-repressors,” said Dr. Jerrold M. Olefsky, associate dean for Scientific Affairs and Distinguished Professor of Medicine at UC San Diego and senior author of the paper. “All transcriptional biology is a balance of these co-activators and co-repressors.”

Olefsky and colleagues focused their attention on NCoR, which was known to be a major co-repressor of Peroxisome Proliferator-Activated Receptor gamma or PPAR-gamma, a ubiquitous protein that regulates fatty acid storage and glucose metabolism, but which also appeared to act on other receptors as well.

“It seemed to be a general purpose co-repressor,” said Olefsky. “It’s unusual for one protein to do so many things. It’s not very efficient and you don’t see it too much in biology.”

The scientists created a knock-out mouse model whose adipocytes or fat cells lacked NCoR. Though bred to be obese and prone to diabetes, Olefsky said the glucose tolerance improved in the NCoR knock-out mice. Moreover, they displayed enhanced insulin sensitivity in liver, muscle and fat, and decreased systemic inflammation. Resistance to insulin, a hormone central to regulating carbohydrate and fat metabolism, is a hallmark of diabetes, as is chronic inflammation.

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Discovery provides insights into interaction between regulated genes and human disease.

Michael Rosenfeld, UC San Diego

Cells develop and thrive by turning genes on and off as needed in a precise pattern, a process known as regulated gene transcription. In a paper published in Wednesday’s (Nov. 9) issue of the Journal of Neuroscience, researchers at the University of California, San Diego, School of Medicine say this process is even more complex than previously thought, with regulated genes actually relocated to other, more conducive places in the cell nucleus.

“When regulated gene transcription goes awry, many human diseases result, such as diabetes, atherosclerosis, cancer and growth defects in children,” said Michael G. Rosenfeld, M.D., a professor in the UC San Diego Department of Medicine, Howard Hughes Medical Institute investigator and senior author of the study. “We’ve shown that rather than being activated at certain, random locations within the cell nucleus, regulated genes can dynamically relocate. The discovery provides a more comprehensive picture of the interaction between regulated genes and human disease.”

Specifically, Rosenfeld and colleagues found that genes regulating cell proliferation responded to growth signals by moving targeted genes from a “silencing environment” in the nucleus called Polycomb bodies to another nuclear compartment called interchromatin granules, which is enriched with activating transcription factors. The movement was precisely guided by two non-coding RNA (ncRNA) molecules called TUG1 and NEAT2.

NcRNA are molecules that are not translated into proteins. In recent years, researchers have ascribed a growing list of duties to them. In this case, Rosenfeld said, TUG1 and NEAT2 move genes to a location in the cell nucleus where they can be more effectively activated and accomplish their function. Cells contain many ncRNAs and it’s likely that others play roles similar to TUG1 and NEAT2 in association with various human diseases.

“A big finding here is the uncovering of a general ncRNA-dependent sensor strategy that relocates a large subset of regulated transcription unit cohorts,” said Liquing Yang, a postdoctoral member of the Rosenfeld lab and co-first author of the study. “Our data suggests that ncRNAs act as regulators and perhaps as modifiers of ‘readers’ and ‘writers’ of the histone code, which implies they have a critical ‘switching’ role in gene transcription regulation.”

“The ability to have signal-dependent relocation of genes in the subnuclear architecture has intriguing implications both in normal regulation and in cancer,” added the other co-first author, Chunru Lin.

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UCSF bioengineer working to create tiny devices that can treat diabetes or kidney failure.

Tejal Desai, UC San Francisco

The same technology used to create integrated circuits may one day be applied to the body to deliver medicine or serve as implants that act as an artificial organ. Tejal Desai, a bioengineer at the University of California, San Francisco, is working with microelectromechanical systems, or MEMS, to create tiny devices that can treat diabetes or kidney failure. But Desai says they’re also looking at different devices which one could potentially inject via catheter.

“Eventually, the goal is to create an implant that actually would just be a simple injection and that injection would be able to have a device,” Desai said. “It’s made out of a really thin film of polymer material and has small channels that can deliver drugs for many months. “

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Adult stem cells can reshape organs in response to changes in the body and environment.

A new study from University of California, Berkeley, researchers demonstrates that adult stem cells can reshape our organs in response to changes in the body and the environment, a finding that could have implications for diabetes and obesity.

Current thinking has been that, once embryonic stem cells mature into adult stem cells, they sit quietly in our tissues, replacing cells that die or are injured but doing little else.

But in working with fruit flies, the researchers found that intestinal stem cells responded to increased food intake by producing more intestinal cells, expanding the size of the intestines as long as the food keeps flowing.

“When flies start to eat, the intestinal stem cells go into overdrive, and the gut expands,” said UC Berkeley postdoctoral fellow Lucy O’Brien. “Four days later, the gut is four times bigger than before, but when food is taken away, the gut slims down.”

Just as in humans and other mammals, O’Brien added, the fly intestine secretes its own insulin. In flies, intestinal insulin seems to be the signal that makes stem cells “supersize the gut.”

“Because of the many similarities between the fruit fly and the human, the discovery may hold a key to understanding how human organs adapt to environmental change,” said David Bilder, UC Berkeley associate professor of molecular and cell biology.

The research will be published in tomorrow’s (Oct. 28) issue of the journal Cell.

Many tissues grow or shrink with usage, including muscle, liver and intestine. Human intestines, for example, regrow after portions have been surgically removed because of cancer or injury, and hibernating animals see their intestines shrink to one-third their normal size during winter.

“One strategy animals use to deal with environmental variability is to tune the workings of their organ systems to match the conditions at hand,” O’Brien said. “How exactly this ‘organ adaptation’ happens, particularly in adult animals that are no longer growing, has long been a mystery.”

Following the surprising discovery of stem cells in the intestines of fruit flies five years ago, O’Brien and Bilder decided to investigate the role of adult stem cells in normal intestinal growth in hopes of finding clues to their role in vertebrates like us.

“I looked at stained stem cells in the fruit fly intestine, and they are studded throughout like jewels. The tissues were so beautiful, I knew I had to study them,” O’Brien said.

O’Brien, Bilder and their colleagues discovered that when fruit flies feed, their intestines secrete insulin locally, which stimulates intestinal stem cells to divide and produce more intestinal cells.

“The real surprise was that the fruit fly intestine is capable of secreting its own insulin,” BIlder said. “This intestinal insulin spikes immediately after feeding and talks directly to stem cells, so the intestine controls its own adaptation.”

Stem cells can divide either asymmetrically, producing one stem cell and one intestinal cell, or symmetrically, producing two stem cells. The team found that, in response to food, intestinal stem cells underwent symmetric division more frequently than asymmetric division, which had the effect of maintaining the proportion of stem cells to intestinal cells, and is a more efficient way of ramping up the total number of cells, O’Brien said.

“Adaptive resizing of the intestine makes sense from the standpoint of physiological fitness,” she said. “Upkeep of the intestinal lining is metabolically expensive, consuming up to 30 percent of the body’s energy resources. By minimizing intestinal size when food is scarce, and maximizing digestive capacity when food is abundant, adaptive intestinal resizing by stem cells helps animals survive in constantly changing environments.”

Bilder and O’Brien’s coauthors on the Cell paper are UC Berkeley staff researchers Sarah S. Soliman and Xinghua Li.

The work was supported by the National Institutes of Health and, for O’Brien, by a Genentech Foundation Fellowship of the Life Sciences Research Foundation.