TAG: "Diabetes"

Community-based weight loss program aids diabetes management


Majority of participants in trial lost weight and reduced medication use.

Cheryl Rock, UC San Diego

Weight loss and control of blood sugar can reduce the risk of complications in patients with diabetes, but this is difficult for many to achieve. A UC San Diego School of Medicine randomized controlled trial of obese adults with type 2 diabetes suggests that participants enrolled in a community-based structured weight loss program are able to shed more pounds, improve blood sugar control and reduce or eliminate insulin use and other medications compared to a control group.

“Support and a tailored lifestyle intervention have been shown to reduce cardiovascular disease risk factors and adverse outcomes in people with diabetes,” said Cheryl L. Rock, Ph.D., R.D., professor of family and preventive medicine and principal investigator of the study. “However, most overweight individuals with type 2 diabetes do not receive this degree of support for changes in diet and physical activity to promote weight loss in their clinical care, due in part to constraints of time and training for most health care providers and clinicians.”

The results of the study, published in today’s (April 23) online issue of Diabetes Care, found that 72 percent of participants on the weight loss program that included portion-controlled foods and personalized counseling were able to change their insulin use compared with 8 percent of the control group. Similarly, other diabetes, cholesterol and blood pressure drugs were decreased or discontinued more often among the weight loss program enrollees.

According to the Centers for Disease Control and Prevention, 35 percent of adults in the United States are obese and 8 percent of adults are affected by diabetes.

“Weight loss is a primary strategy for successful management of type 2 diabetes due to its impact on glycemic control and improvements in cardiovascular disease risk factors,” said Rock. “These study results suggest that patients not only lose weight on structured commercial weight loss programs that include behavioral modification and individual support, but that this weight loss translates to significant improvements in diabetes control and cardio-metabolic parameters.”

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Saving diabetics from blindness in Libya


UC Berkeley grad student, professor, alum join forces in international public service project.

UC Berkeley optometry student Fatima Elkabti and professor Jorge Cuadros discuss a magnified digital image of a healthy retina.

A UC Berkeley graduate student in optometry, one of her professors and a Berkeley alumnus have joined forces to build a long-distance diagnostic project that has the potential to keep a large number of people in crisis-torn Libya from going blind.

The public service project involves training Libyan doctors to take detailed digital photographs inside patients’ eyes, of their retinas, as part of routine health care and put the images online for remote diagnosis of damage caused by diabetes before it’s too late. Too often, diabetes-related retinopathy isn’t caught until it causes symptoms, when treatment can no longer save vision.

The first 11 Libyan doctors underwent training for three days in February in Istanbul, in a seminar organized by the Avicenna Group and taught by Berkeley optometry professor Jorge Cuadros. Turkey was chosen as the training site for security reasons and because it is easily accessible from Libya.

If all goes according to plan, many more doctors will be trained over the next year, both in Libya and out — all because of a project that developed rapidly from a seed planted in a Diabetic Health Clinic class in Berkeley’s School of Optometry.

In the class, Cuadros taught students how to analyze photos of diabetic retinopathy as part of EyePACS, the California-based online initiative he co-founded to train people working in diabetes care to screen patients’ vision for remote diagnosis by certified eye doctors.

In his class was third-year optometry student Fatima Elkabti, who knows firsthand the toll that diabetes is taking in Libya, where the disease is rampant but greatly underdiagnosed. Elkabti’s father, a Libyan, has diabetes, as do about half of her many aunts and uncles.

“I walked out of the class and asked Dr. Cuadros, ‘Can we do this in Libya?’ “ Elkabti relates. Do some research, the professor told her.

Elkabti got to work and within an hour found Ethan Chorin, who earned his Ph.D. at Berkeley in 2000, served in the U.S. diplomatic corps in Libya from 2004 to 2006 and has published a book about the recent Libyan revolution. He founded the not-for-profit Avicenna Group in 2011 with a Libyan-American colleague to catalyze health-related partnerships between Libyan organizations and U.S. universities. Traveling back and forth between Benghazi and Berkeley, he looked for ways to involve Berkeley in Libya’s reconstruction efforts.

“I shot Ethan an email, and within hours we were talking about how to make this happen,” Elkabti says. The Berkeley-Libya retinopathy project was off and running.

Diabetes-related retinopathy is one of the leading causes of blindness in Libya — as well as in the United States and in much of the world. EyePACS has brought retinal screenings to poor and medically underserved areas from California’s Central Valley to Peru, and the Libyan retinopathy project extends the concept to politically unstable and dangerous regions.

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New organ transplant strategy aims to better prevent rejection


UCSF approach might end lifelong drug treatment.

Qizhi Tang, UC San Francisco

Organ-transplant recipients often reject donated organs, but a new, two-pronged strategy developed by UC San Francisco researchers to specifically weaken immune responses that target transplanted tissue has shown promise in controlled experiments on mice.

The hope is that using this novel treatment strategy at the time of transplantation surgery could spare patients from lifelong immunosuppressive treatments and their side effects. The approach might also be used to treat autoimmune diseases such as type 1 diabetes, the researchers said. The study is published and commented upon in a recent issue of American Journal of Transplantation.

The study was conducted in mouse studies of islet-cell transplantation — a procedure used to restore insulin secretion and control over glucose levels in the blood in patients with life-threatening diabetes. The treatment allowed more than 70 percent of mice to accept transplants without requiring any long-term treatment with immunosuppressive drugs.

The approach, led by Diabetes Center member Qizhi Tang, Ph.D., involved using cells from donors to activate immune cells called donor-reactive effector T cells. The researchers then gave the mice a drug called cyclophosphamide, known to specifically kill activated cells.

Up to 80 percent of the donor-reactive effector T cells, which play a major role in transplant rejection, were eliminated by this treatment. However, that procedure alone did not prolong survival of transplanted tissue.

That required a second step: Some of the mice also received cell therapy — an expanded population of cells called TREGs that quell immune activity. Seventy percent to 80 percent of these mice accepted the transplants, without requiring any long-term immunosuppressive drugs.

Significantly, when the cell therapy was used only in those cells that specifically target donor tissue, only one-fifth as many cells were needed to prevent transplant rejection, the UCSF researchers found. The bigger bang per cell may bode well for clinical protocols, Tang suggested.

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Study represents important step toward a cure for type 1 diabetes


Scientists reprogram skin cells into insulin-producing pancreas cells.

Sheng Ding

A cure for type 1 diabetes has long eluded even the top experts. Not because they do not know what must be done—but because the tools did not exist to do it. But now scientists in the laboratory of Gladstone Institutes’ investigator Sheng Ding, M.D., Ph.D., harnessing the power of regenerative medicine, have developed a technique in animal models that could replenish the very cells destroyed by the disease. The team’s findings, published online today (Feb. 6) in the journal Cell Stem Cell, are an important step towards freeing patients from the life-long injections that characterize this devastating disease.

Type 1 diabetes, which usually manifests during childhood, is caused by the destruction of beta-cells (ß-cells). ß-cells are a type of cell that normally resides in the pancreas and produces a hormone called insulin. Without insulin, the body’s organs have difficulty absorbing sugars, such as glucose, from the blood. Once a death sentence, the disease can now be managed with regular glucose monitoring and insulin injections. A more permanent solution, however, would be to replace the missing ß-cells. But these cells are hard to come by, so researchers have looked towards stem cell technology as a way to make them.

“The power of regenerative medicine is that it can potentially provide an unlimited source of functional, insulin-producing ß-cells that can then be transplanted into the patient,” said Ding, who is also a professor at UC San Francisco, with which Gladstone is affiliated. “But previous attempts to produce large quantities of healthy ß-cells — and to develop a workable delivery system — have not been entirely successful. So we took a somewhat different approach.”

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Resetting the metabolic clock


Insight into mammalian circadian rhythms could lead to therapies for obesity, diabetes.

Circadian rhythms are affected by things like travel over time zones, diet and light exposure. (Illustration by Peter Allen)

Circadian rhythms are affected by things like travel over time zones, diet and light exposure.

We’ve all heard about circadian rhythm, the roughly 24-hour oscillations of biological processes that occur in many living organisms. Yet for all its influence in many aspects of our lives — from sleep to immunity and, particularly, metabolism — relatively little is understood about the mammalian circadian rhythm and the interlocking processes that comprise this complex biological clock.

Through intensive analysis and computer modeling, researchers at UC Santa Barbara have gained insight into factors that affect these oscillations, with results that could lend themselves to circadian regulation and pharmacological control. Their work appears in the early edition of the Proceedings of the National Academy of Sciences.

“Our group has been fascinated with circadian rhythms for over 10 years now, as they represent a marvelous example of robust control at the molecular scale in nature,” said Frank Doyle, chair of UCSB’s Department of Chemical Engineering and the principal investigator for the UCSB team. “We are constantly amazed by the mechanisms that nature uses to control these clocks, and we seek to unravel their principles for engineering applications as well as shed light on the underlying cellular mechanisms for medical purposes.”

“Focus is often given to metabolism, cell division and other generic cell processes, but circadian oscillations are just as central to how life is organized,” said Peter St. John, a researcher in the Department of Chemical Engineering and lead author of the study.

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Researchers explain why some wound infections become chronic


Decreasing levels of “reactive oxygen species” can break cycle of unhealing wounds.

Manuela Martins-Green, UC Riverside

Manuela Martins-Green, UC Riverside

Chronic wounds affect an estimated 6.5 million Americans at an annual cost of about $25 billion. Further, foot blisters and other diabetic ulcers or sores account for the vast majority of foot and leg amputations in the United States today.

Why does treating chronic wounds cost so much?  What complicates chronic wound infections, making healing difficult?

Manuela Martins-Green, a professor of cell biology at the University of California, Riverside, reports that two biological activities are out of control in chronic wound infections. These are reactive oxygen species (ROS), which are chemically reactive molecules formed by the partial reduction of oxygen, and biofilms that are formed by selective invading bacteria.

ROS is the natural byproduct of the normal oxygen metabolism and plays a role in cell signaling and homeostasis. However, excessive ROS can induce chronic inflammation, a key characteristic of wounds that do not heal. The biofilms are bacterial defense mechanisms. Together they create a toxic environment that can resist efforts to heal and close a chronic wound.

“By decreasing ROS levels within a chronic wound in a diabetic mouse model, my lab was able to normalize conditions and heal the wound,” Martins-Green said. “Indeed, we saw significant improvement in healing the wound.”

She announced her findings today (Dec. 17) in New Orleans at the 53rd annual meeting of the American Society for Cell Biology.

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Minorities’ health would benefit most from beverage sugar tax


UCSF research team concludes that tax would result in lower rates of diabetes, heart disease.

Kirsten Bibbins-Domingo, UC San Francisco

Kirsten Bibbins-Domingo, UC San Francisco

Taxing sugar-sweetened beverages is likely to decrease consumption, resulting in lower rates of diabetes and heart disease, and these health benefits are expected to be greatest for the low-income, Hispanic and African-American Californians who are at highest risk of diabetes, according to a new analysis led by researchers at UC San Francisco.

Over the course of the next decade, lowered incidence of these diseases would save over half a billion dollars in medical costs, concluded the research team, which includes members from Oregon State University and the Mailman School of Public Health at Columbia University.

The researchers previously modeled the national health effects of a penny-per-ounce tax over the course of 10 years and found that it would reduce consumption among adults by 15 percent, modestly lower the prevalence of diabetes and obesity and prevent tens of thousands of coronary heart events, strokes and premature deaths. The new study considered a range of reductions in sugary beverage consumption among Californians.

In the new study, assuming a decline of 10 to 20 percent in the consumption of soda and other sugary beverages from the tax, researchers concluded that new cases of diabetes and coronary heart disease would drop statewide, and those health benefits would be greatest in poor and minority communities. The analysis, published Dec. 11 in the online journal PLOS ONE, predicted that overall, one in 20,000 Californians would avoid diabetes. This estimate would double for Hispanics and poor Californians and triple for African Americans.

”Poor and minority communities in California and nationally have very high rates of diabetes, a chronic condition with potentially devastating health complications,” said Kirsten Bibbins-Domingo, M.D., Ph.D., UCSF professor of medicine and director of the UCSF Center for Vulnerable Populations at San Francisco General Hospital and Trauma Center. “Although many steps are needed to reverse the rising diabetes trends in the state, our study suggests that efforts to curb sugary beverage consumption can have a significant positive impact, particularly in those most likely to be affected.”

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Islet transplantation gains momentum in type 1 diabetes


UCSF experts improve treatments to prevent rejection.

A close-up of islet cells from a human pancreas. (Image courtesy of Gregory Szot, UC San Francisco)

A close-up of islet cells from a human pancreas.

For the worst cases of type 1 diabetes, islet transplantation already has freed hundreds of people from complete dependence on insulin and from life-threatening consequences of the disease.

However, the procedure still is regarded as experimental by the U.S. Food and Drug Administration (FDA).

Islets are clusters of insulin-making cells in the pancreas that are destroyed in people with type 1 diabetes. After transplanting islet cells from a donor pancreas, the new islet cells can begin to produce insulin.

“Overall the results of islet transplantation are much better than they used to be,” said UC San Francisco transplant surgeon Andrew M. Posselt, M.D., Ph.D.,  “We’re approaching results as good as we see with whole pancreas transplants.”

Posselt, who co-directs the Clinical Islet Transplant Program at UCSF, is part of an international push to bring islet transplantation into the mainstream. As part of that movement, experts gathered in Monterey in September for 14th World Congress of the International Pancreas and Islet Transplant Association (IPITA). World Congress chair, Peter Stock, M.D., Ph.D., is the other co-lead of the UCSF program.

The meeting – sponsored by IPITA, the Transplantation Society and the Department of Surgery at UCSF – included discussions on new ways to foster long-term survival of transplanted islets and to prevent their rejection by the immune system, which is the key to controlling blood sugar without reliance on precisely administered insulin injections.

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Enzyme restores function with diabetic kidney disease


Mouse findings reverse prevailing theory, point to potential treatment options.

Transmission electron micrograph of a cell mitochondrion. (Image courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego)

Transmission electron micrograph of a cell mitochondrion.

Researchers at the UC San Diego School of Medicine say that while a prevailing theory suggests elevated cellular levels of glucose ultimately result in diabetic kidney disease, the truth may, in fact, be quite the opposite. The findings could fundamentally change understanding of how diabetes-related diseases develop – and how they might be better treated.

Writing in today’s (Oct. 25) issue of Journal of Clinical Investigation, Kumar Sharma, M.D., professor of medicine and director of the Center for Renal Translational Medicine (CRTM) at UC San Diego; Laura Dugan, M.D., professor of medicine and Larry L. Hillblom Chair in geriatric medicine; Young You, Ph.D., CRTM; Robert Naviaux, M.D., Ph.D., professor of medicine; and colleagues describe first-ever studies of real-time superoxide production in the kidneys of live mice with type 1 diabetes.

Current theory posits that impaired diabetic kidney function in humans as well as in mice is the result of chronically high glucose (sugar) levels which prompt energy-generating mitochondria in cells to produce an overabundance of superoxide anion – a highly reactive, toxic molecule that ultimately leads to downstream cellular damage, organ dysfunction and disease.

But Sharma, who also works for the Veterans Administration San Diego Healthcare System, and colleagues upend this theory. Rather than detecting higher-than-normal levels of superoxide in the damaged kidneys of the diabetic mice, the researchers discovered reduced superoxide production and suppressed mitochondrial activity. When they stimulated the mitochondria by activating a key energy-sensing enzyme called AMPK, superoxide production increased but evidence of diabetic kidney disease markedly declined.

“Mitochondrial superoxide does not seem to be a causative factor of diabetic kidney disease,” said Sharma. “Indeed, when mitochondrial superoxide is increased with AMPK activation, there is reduced kidney disease, suggesting that improving mitochondrial function and superoxide production is actually beneficial for diabetic complications. This idea is a sea change in the field of diabetic complications.”

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Urine biomarkers reveal mitochondrial dysfunction in diabetic kidney disease


Study suggests suppression of mitochondria is a key characteristic of diabetic kidney disease.

X-ray of human kidneys

X-ray of human kidneys

Researchers at the UC San Diego School of Medicine have identified 13 metabolites – small molecules produced by cellular metabolism – that are significantly different in patients with diabetes and chronic kidney disease compared to healthy controls.

Twelve of the 13 metabolites are linked to mitochondrial function, suggesting that suppression of mitochondria – the powerhouses of cells – is a fundamental characteristic of diabetic kidney disease. The findings are published in the November edition of the Journal of the American Society of Nephology.

“This work provides strong evidence that reduced mitochondrial function is a dominant feature of human diabetic kidney disease,” said first author Kumar Sharma, M.D., professor of medicine and director of the Center for Renal Translational Medicine at UC San Diego. “We found that a specific cellular pathway, AMPK-PGC1a, likely plays a key role to reduce mitochondrial function and content, which means that new therapeutic approaches that restore and increase mitochondrial function and content could ameliorate or perhaps even arrest chronic kidney disease.”

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UCLA, Takeda collaborate on diabetes research


They will explore impact of circadian rhythm disruption on type 2 diabetes development.

Aleksey Matveyenko, UCLA

Aleksey Matveyenko, UCLA

Millions of individuals worldwide are exposed to shift work and numerous environmental conditions that disturb circadian clock function and disrupt normal circadian rhythms. Environmental conditions associated with disrupted circadian rhythms greatly increase the risk for development of type 2 diabetes and metabolic syndrome and also hinder the treatment and management of hyperglycemia in existing patients with diabetes.

A new collaboration effort between the New Frontier Science Group at Takeda Pharmaceutical Co. Ltd. and Dr. Aleksey Matveyenko at UCLA will undertake studies to better understand how disruption of circadian rhythms globally and at the level of pancreatic beta-cells promotes development of type 2 diabetes and, specifically, loss of pancreatic beta-cell function and mass.  This research will provide an enhanced molecular understanding of the relationship between circadian clock disruption, beta-cell dysfunction and loss, and type 2 diabetes that may lead to the development of innovative circadian medicines.

Opened in November 2004, the Larry L. Hillblom Islet Research Center at UCLA is the first center dedicated to the study of the islets of Langerhans, which include the insulin-producing cells in the pancreas. An understanding of the causes of islet cell destruction is key to finding a cure for diabetes. The center’s faculty members, recruited from around the world, provide leadership in the worldwide fight against the disease. The center is made possible through a grant from the Larry Hillblom Foundation, established to support medical research in the state of California.

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Researchers discover biological link between diabetes and heart disease


Discovery helps explain why diabetes is significant independent risk factor for heart disease.

(From left) Lianguo Wang, Crystal Ripplinger and Donald Bers, UC Davis

(From left) Lianguo Wang, Crystal Ripplinger and Donald Bers, UC Davis

UC Davis Health System researchers have identified for the first time a biological pathway that is activated when blood sugar levels are abnormally high and causes irregular heartbeats, a condition known as cardiac arrhythmia that is linked with heart failure and sudden cardiac death.

Reported online today (Sept. 29) in the journal Nature, the discovery helps explain why diabetes is a significant independent risk factor for heart disease.

“The novel molecular understanding we have uncovered paves the way for new therapeutic strategies that protect the heart health of patients with diabetes,” said Donald Bers, chair of the UC Davis Department of Pharmacology and senior author of the study.

While heart disease is common in the general population, the risk is up to four times greater for diabetics, according to the National Institutes of Health. The American Heart Association estimates that at least 65 percent of people with diabetes die from heart disease or stroke and has emphasized the need for research focused on understanding this relationship.

Through a series of experiments, Bers, his UC Davis team and their collaborators at the Johns Hopkins University School of Medicine showed that the moderate to high blood glucose levels characteristic of diabetes caused a sugar molecule (O-linked N-acetylglucosamine, or O-GlcNAc) in heart muscle cells to fuse to a specific site on a protein known as calcium/calmodulin-dependent protein kinase II, or CaMKII.

CaMKII has important roles in regulating normal calcium levels, electrical activity and pumping action of the heart, according to Bers. Its fusion with O-GlcNAc, however, led to chronic overactivation of CaMKII and pathological changes in the finely tuned calcium signaling system it controls, triggering full-blown arrhythmias in just a few minutes. The arrhythmias were prevented when CaMKII or its union with O-GlcNAc was inhibited.

“While scientists have known for a while that CaMKII plays a critical role in normal cardiac function, ours is the first study to identify O-GlcNAc as a direct activator of CaMKII with hyperglycemia,” said Bers.

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