Posts Tagged ‘Diabetes’

Sleep Apnea and Type 2 Diabetes

May 21st, 2009 BMI

Study finds sleep apnea widely undiagnosed among obese type 2 diabetics

Sleep apnea has long been known to be associated with obesity. But a new study published in the June issue of Diabetes Care finds that the disorder is widely undiagnosed among obese individuals with type 2 diabetes – nearly 87 percent of participants reported symptoms, but were never diagnosed.

For those with untreated sleep apnea, it doesn’t just mean their sleep is disrupted; existing research shows that it can also mean an increased risk of heart disease and stroke.

“The high prevalence of undiagnosed, and therefore, untreated sleep apnea among obese patients with diabetes constitutes a serious public health problem,” said Gary Foster, PhD, lead author and director of the Center for Obesity Research and Education at Temple University.

The new study, called Sleep AHEAD, looked at 306 obese patients with type 2 diabetes already enrolled in the Look AHEAD trial, a 16-site study investigating the long-term health impact of an intensive lifestyle intervention in 5, 145 overweight or obese adults with type 2 diabetes.

Each participant had a sleep study (polysomnogram) that measures various breathing and brain activity during sleep. Participants also filled out a series of questions about symptoms related to sleep (snoring, sleepiness during the day), and had their weight, height, waist and neck circumferences measured.

Researchers found that 86.6 percent of participants had sleep apnea, yet reported never being diagnosed. More than 30 percent of these had between 16 and 20 episodes per hour where they would stop breathing, and 22 percent had more than 30 episodes per hour, considered severe sleep apnea. Most of these also had a larger waist circumference, which researchers found, along with higher BMI, to be significantly associated with sleep apnea.

Obesity has long been known to be associated with sleep apnea, but researchers say that these findings are alarming.

“Doctors who have obese patients with type 2 diabetes need to be aware of the possibility of sleep apnea, even if no symptoms are present, especially in cases where the patient has a high BMI or waist circumference,” said Foster.

Currently, more than half of obese or overweight individuals have diabetes, the seventh leading cause of death in the United States.

Source: Temple University

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How gastric bypass rapidly reverses diabetes symptoms

May 15th, 2009 BMI

A report in the September Cell Metabolism, a publication of Cell Press, offers new evidence to explain why those who undergo gastric bypass surgery often show greater control of their diabetes symptoms within days. It also helps to explain why lap-band surgery doesn’t offer the same instant gratification. By studying mice that have undergone both procedures, the researchers show that changes in the intestine are the key.

In addition to removing about two-thirds of the stomach, gastric bypass in effect produces a “double intestine,” said Gilles Mithieux of Institut National de la Sante et de la Recherche Medicale in France. The portion closest to the stomach is taken out of the loop so that it receives no nutrients. The segment normally farther down is then attached directly to the stomach, where it receives all the nutrients coming in.

In both cases, those positional changes ramp up production of blood sugar by the small intestine, Mithieux said. He noted that fasting normally induces blood sugar production by the upper small intestine. By placing the lower small intestine, which doesn’t normally produce much glucose, in close proximity to the stomach, it starts to act more like the upper portion.

That blood sugar synthesized in the intestine pours into the portal vein (a large vein that carries blood from the digestive tract to the liver) where it sends a signal to the brain, he and his colleagues earlier found. “The walls of the portal vein system detect the glucose and inform the brain,” he said. “It’s an important signal for decreasing hunger.”

They now find an important new element of glucose production by the intestine. It also increases insulin sensitivity and lowers blood sugar, improving the symptoms of diabetes. Mithieux said that’s in part because glucose production by the intestine lowers glucose production by the liver, which accounts for a much greater overall proportion of blood sugar synthesis. These metabolic changes take place within days of surgery, well before any weight loss takes place.

While gastric banding, in which a prosthetic band is placed around the upper stomach, works for weight loss, it doesn’t affect the intestine at all and lacks the immediate metabolic benefits of bypass, they report.

Further evidence for the mechanism involved came from studies of mice lacking GLUT-2, a glucose transporter required for glucose sensing in the portal vein. Gastric bypass lost its insulin-sensitizing benefits in those GLUT-2-deficient mice. Similarly, mice whose portal veins had lost their nerve supply also stopped responding to the surgical procedure.

The bottomline, according to Mithieux: the intestine deserves more respect. “Up to now, the intestine had been considered like a machine to assimilate nutrients. We’ve now begun to realize that it is a complex endocrine organ” with particular importance when it comes to glucose metabolism.

As for what patients weighing gastric bypass versus lap-band surgery should do, Mithieux recommends they talk to their doctors about the possible benefits and risks of both procedures. The new findings do support the notion that gastric bypass may be an effective treatment for diabetes in obese patients. It might even have potential for people who are diabetic, whether they are obese or not, he said.

Source: Cell Press

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Early trigger for type 1 diabetes found in mice, Stanford scientists report

May 15th, 2009 BMI

STANFORD, Calif. – Scientists at the Stanford University School of Medicine are shedding light on how type-1 diabetes begins.

Doctors have known the disease is caused by an autoimmune attack on the pancreas, but the exact trigger of the attack has been unclear. Now, a new study in mice implicates the immune signal interferon-alpha as an early culprit in a chain of events that upend sugar metabolism and make patients dependent on lifelong insulin injections.

“We never considered that interferon-alpha could be a major player in early type-1 diabetes,” said Qing Li, MD, PhD, a postdoctoral scholar in microbiology and immunology who was the primary author of a paper describing the new result. The study is published in today’s issue of Proceedings of the National Academy of Sciences. “This was a pretty surprising finding.”

Interferon-alpha normally helps the body fight viruses. Synthetic interferon-alpha is injected as a drug for treating hepatitis C and some forms of cancer, Li noted.

“Everybody’s been wondering what process initiates type-1 diabetes,” said Hugh McDevitt, MD, professor of microbiology and immunology and the study’s senior author.

Type-1 diabetes is caused by complete deficiency of insulin, a hormone that helps the body store and burn sugar. About 1 million Americans have the disease, also known as juvenile diabetes because it tends to be diagnosed in children and young adults, for which there is no effective prevention or cure. Diabetes is a leading cause of heart disease, blindness, limb amputations and kidney failure.

The early pathology of type-1 diabetes is hard to study in humans, McDevitt said, because it’s almost impossible to predict who will get the disease and when it will develop. Scientists have relied on animal models, such as diabetic mice, because they predictably develop high blood sugar and other features of the human disease.

To pinpoint interferon-alpha, Li and McDevitt worked backwards from what they knew about how type-1 diabetes starts. Prior studies in diabetic mice showed a pathogenic role for immune cells called CD4+ T cells. These cells are an early player in the immune attack on the body’s insulin factories, pancreatic beta cells. The scientists used silicon gene-chip technology to measure which genes are revved up in the CD4+ T cells just before they assault the pancreas. The measurements fell into a pattern: many of the upregulated genes were known to be controlled by interferon-alpha.

To confirm the signal’s nefarious role, the researchers gave mice an antibody that blocks interferon-alpha activity several weeks before the animals were expected to develop diabetes. Thwarting interferon-alpha delayed the start of the disease by an average of four weeks, and, in 60 percent of treated mice, it prevented diabetes entirely.

The finding confirmed the importance of interferon-alpha and helped the scientists connect the dots between normal mouse physiology and early diabetes. Mice are born with more pancreatic beta cells than they need, Li noted. The extras soon undergo programmed cell death, leaving plenty of working beta cells to pump out insulin. However, in mice that develop diabetes, debris left behind by the dying cells triggers an inappropriate immune response, with lots of interferon-alpha. The interferon-alpha cues immune destruction of more and more beta cells, causing insulin deficiency and diabetes.

The mechanism may be more complex in humans, the scientists cautioned, explaining that while their new finding goes a long way toward explaining the beginnings of diabetes in the mice, additional genetic and environmental factors influence the human disease. But the basic principle of disease is likely the same in diabetic mice and humans, they said.

“A normal process – programmed cell death – causes a normal response,” McDevitt said. “But it does this in such a way that, in a small subset of the population, it starts them on the road to type-1 diabetes.”

Source: Stanford University Medical Center

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Low cholesterol associated with cancer in diabetics

May 15th, 2009 BMI

Low levels of LDL cholesterol as well as high levels are associated with cancer in patients with type 2 diabetes, found a prospective cohort study http://www.cmaj.ca/press/pg427.pdf published in CMAJ.

Researchers from the Hong Kong Institute of Diabetes and Obesity, the Li Ka Shing Institute of Health Sciences and The Chinese University of Hong Kong conducted a study of 6107 Chinese patients with type 2 diabetes and found a V-shaped risk relation between LDL cholesterol and cancer in patients not receiving statin therapy.

“LDL cholesterol levels below 2.80 mmol/L and levels of at least 3.90 mmol/L were both associated with markedly elevated risk of cancer among patients who did not use statins,” state Dr. Juliana Chan and coauthors.

The study excluded people on statins as statins obscured the association between LDL cholesterol and all-site cancer.

Increasing data suggests an association between type 2 diabetes and an elevated risk of cancer, including breast, colorectal, pancreatic and liver cancers. An elevated risk of cancer in patients with low LDL was linked to cancers of digestive organs and peritoneum, genital and urinary organs, lymphatic and blood tissues as well as other areas. Patients with an LDL cholesterol level above 3.80 mmol/L had heightened risks of oral, digestive, bone, skin, connective tissue, breast and other cancers.

Regarding clinical implications, the authors suggest “the use of these levels as risk markers may help clinicians to assess their patients more fully and thus to prevent premature deaths in patients who have high risk.”

They call for re-analysis of data from clinical trials to confirm or refute these findings.

In a related commentary, Drs. Frank Hu and Eric Ding of Harvard School of Public Health (Todd Datz, Public Relations, Harvard School of Public Health, 617-432-3952 for Dr. Frank Hu) say confounding factors such as indication for the use of statins, lifestyle and socioeconomic status must be considered when looking at the association of high levels of LDL cholesterol and the risk of cancer.

“Low serum cholesterol is commonly observed in individuals with ill health (e.g. cancer patients) and those with unhealthy lifestyle characteristics such as smoking and heavy drinking,” states Hu.

Source: Canadian Medical Association Journal

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Stroke incidence declines among Swedish diabetics

May 15th, 2009 BMI

The incidence of strokes among diabetics in Northern Sweden declined between 1985 and 2003, according to a population-based study published in Stroke: Journal of the American Heart Association.

Researchers also found that survival rates improved leading to a rapid decline in the number of fatal events among diabetic people.

“Prior research has suggested that the trend in strokes was increasing, but our study shows declining incidence in stroke for non-diabetic men, both for first and recurrent stroke, and in recurrent strokes in non-diabetic women,” said Mats Eliasson, M.D., Ph.D., co-author of the study and a senior lecturer in the Department of Public Health and Clinical Medicine at Umeå University and the Department of Medicine at Sunderby Hospital in Luleå, Sweden.

The reasons for the overall decline of strokes among diabetics are uncertain. The decline may be the result of more intensive treatment of hypertension in diabetics and smoking cessation and cholesterol-lowering efforts, Eliasson said.

“The impressive decline in smoking and large decreases in cholesterol levels, and to a lesser degree blood pressure levels, in the population of northern Sweden may have contributed to the declining incidence in both diabetic and non-diabetic subjects over the study period,” he said. “On the other hand, we found more recurrent events among diabetic subjects than non-diabetic subjects, indicating a need for even more intensive secondary prevention among diabetic patients.”

Researchers examined data on 15,382 stroke patients, 35- to 74-years-old, who were part of the Northern Sweden MONICA (Multinational Monitoring of Trends and Determinants in Cardiovascular Disease) Project Stroke Registry, an international collaboration sponsored by the World Health Organization.

Over the 19 years, 11,605 subjects suffered a first stroke and 3,777 had a recurrent stroke. Twenty-two percent of the men and women had previously been diagnosed with diabetes. Although the total number of strokes per 100,000 in diabetics was significantly greater than in non-diabetics, researchers found no significant difference in the rate of decline over time and death rates between the two groups.

Among the major findings:

  • Diabetic women had a yearly decrease in incidence of first-ever stroke of 1.5 percent, while incidence remained unchanged over the observation period for non-diabetic women.
  • Non-diabetic men had a significant declining trend in incidence rates of first-ever stroke of .8 percent per year, while there was an insignificant decline in diabetic men.
  • All groups, except diabetic women with first-ever stroke, had a significant decline in deaths over time.
  • Incidence rates per 100,000 of all strokes among male diabetics fell from 1,961 to 1,815.
  • The incidence rates per 100,000 of all stroke in women fell from 1,921 to 1,176.
  • In non-diabetics, the incidence rates per 100,000 fell from 358 for men and 204 for women to 284 and 183, respectively.
  • For recurrent strokes, the decline was significant for all but diabetic men, with the greatest decline (5.4 percent a year) in diabetic women. Non-diabetic women showed a 2.7 percent yearly drop. Researchers found no apparent explanation for the gender differences. An earlier study in the United States didn’t find gender differences in care or treatment adherence between male and female diabetics.

“The fact that patients with diabetes, to a great extent, had favorable time trends similar to those of non-diabetics is particularly interesting considering that diabetic patients with heart attack, from the same population, did not show any positive trends over the 19-year study,” Eliasson said.

Control of hypertension may have a greater impact in stroke than in coronary heart disease, he said.

Source: American Heart Association

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New research suggests diabetes transmitted from parents to children

May 12th, 2009 BMI

A new study in the September issue of the Journal of Lipid Research suggests an unusual form of inheritance may have a role in the rising rate of diabetes, especially in children and young adults, in the United States.

DNA is the primary mechanism of inheritance; kids get half their genes from mom and half from dad. However, scientists are just starting to understand additional kinds of inheritance like metabolic programming, which occurs when an insult during a critical period of development, either in the womb or soon after birth, triggers permanent changes in metabolism.

In this study, the researchers looked at the effects of a diet high in saturated fat on mice and their offspring. As expected, they found that a high-fat diet induced type 2 diabetes in the adult mice and that this effect was reversed by stopping the diet.

However, if female mice continued a high-fat diet during pregnancy and/or suckling, their offspring also had a greater frequency of diabetes development, even though the offspring were given a moderate-fat diet. These mice were then mated with healthy mice, and the next generation offspring (grandchildren of the original high-fat fed generation) could develop diabetes as well.

In effect, exposing a fetal mouse to high levels of saturated fats can cause it and its offspring to acquire diabetes, even if the mouse goes off the high-fat diet and its young are never directly exposed.

The study used mice so it’s not time to warn women to eat differently during pregnancy and breastfeeding but earlier research has shown that this kind of inheritance is at work in humans. For example, there is an increased risk of hypertension and cardiovascular disease in children born of malnourished mothers.

American Society for Biochemistry and Molecular Biology

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Overweight Hispanic children at significant risk for pre-diabetes, according to new USC study

May 12th, 2009 BMI

A study by researchers at the University of Southern California (USC) found that overweight Hispanic children are at significant risk for pre-diabetes, a condition marked by higher than normal blood glucose levels that are not yet high enough for a diagnosis of diabetes. The persistence of pre-diabetes during growth is associated with progression in risk towards future diabetes, according to the study, which will be published in an upcoming issue of the journal Diabetes, and is now available online.

With a population of more than 35 million, Hispanics are the largest and fastest growing minority group in the United States. Despite the fact that Hispanics are at high risk for developing type 2 diabetes, few previous studies have looked at physiological causes of the disease within this population.

Researchers led by Michael I. Goran, Ph.D., professor of preventive medicine, physiology and biophysics and pediatrics, and director of the USC Childhood Obesity Research Center at the Keck School of Medicine of USC, followed a cohort of 128 overweight Hispanic children in East Los Angeles. The children were tested over four consecutive years for glucose tolerance, body mass index, total body fat and lean mass and other risk factors for type 2 diabetes. The study found that an alarming 13% of the children had what the investigators termed “persistent pre-diabetes.”

Most prior studies examining pre-diabetes in overweight and obese children looked at a one-time assessment of metabolic risk factors for type 2 diabetes, but fluctuations over time led to poor reliability for these tests. In the new study, Goran and colleagues examined longitudinal data to look at a progression of risk factors over four years. Children were identified as having persistent pre-diabetes if they had three to four positive tests over four annual visits. The children who had persistent pre-diabetes had signs of compromised beta-cell function, meaning that their bodies were unable to fully compensate to maintain blood glucose at an appropriate level, and they had increasing accumulation of visceral fat or deposition of fat around the organs. Both of these outcomes point towards progression in risk towards type 2 diabetes.

“What this study shows is that doctors should be doing regular monitoring of these children over time, because a one-time checkup might not be enough to tell if they are at risk for developing diabetes,” Goran says.

Visceral fat, which pads the spaces between abdominal organs, has been linked to metabolic disturbances and increased risk for cardiovascular disease and type 2 diabetes.

Increased obesity has been identified as a major determinant of insulin resistance. Lower beta-cell function is a key component in the development of type 2 diabetes, as the cells are unable to produce enough insulin to adequately compensate for the insulin resistance.

“To better treat at-risk children we need better ways to monitor beta-cell function and visceral fat buildup,” Goran says. “Those are tough to measure but are probably the main factors determining who will get type 2 diabetes.”

Future studies will examine different interventions, including improving beta-cell function and reducing visceral fat.

“The study provides great insight into the risk factors that lead to the progression towards type 2 diabetes in this population,” says Francine Kaufman, professor of pediatrics at the Keck School of Medicine at USC and head of the division of endocrinology and metabolism at Childrens Hospital Los Angeles, who was not directly involved in the study. “Only by understanding how this devastating disease develops will be able to begin taking steps to prevent it.”

Source: University of Southern California

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