all endocrinology stories

New insight into skin-tanning process suggests novel way of preventing skin cancer

70652986 — Mon, 26 Mar 2007 06:28:08 -0400

Findings from a study led by researchers at Dana-Farber Cancer Institute and Children's Hospital Boston have rewritten science's understanding of the process of skin tanning - an insight that has enabled them to develop a promising way of protecting fair- skinned people from skin cancer caused by exposure to sunlight.

Moms who breastfeed may be protected from type 2 diabetes

70652986 — Mon, 26 Mar 2007 05:42:34 -0400

Researchers have demonstrated that breastfeeding a child for one year may reduce a woman's risk of developing type 2 diabetes by 15 percent. This study appeared in the Nov. 23, 2005 issue of the Journal of the American Medical Association.

"We've known for a long time that breastfeeding is good for babies," said lead author and Brigham and Women's Hospital researcher Alison Stuebe, MD. "In this study, we found that it's good for moms, too."

The production of milk requires a breastfeeding mother to use an average of 500 calories each day - the equivalent of running four to five miles. According to Stuebe, the additional energy required for lactation is associated with short-term changes in insulin, and glucose. Her study was among the first to look at the long-term association between breastfeeding and incidence of type 2 diabetes. "Our study supports the theory that breastfeeding may be associated with important metabolic changes that influence diabetes risk," she said. "However, more research is needed to determine what hormonal and biological factors are involved."

Study identifies fat-secreted protein linked to insulin resistance

70652986 — Mon, 26 Mar 2007 07:10:39 -0400

According to senior author Barbara B. Kahn, M.D., chief of the Division of Endocrinology, Diabetes, and Metabolism at BIDMC, these findings in mice and humans show that elevated levels of retinol-binding protein 4 (RBP4) contribute to insulin resistance, a primary risk factor for diabetes.

Produced by the pancreas, insulin helps cells take in glucose and convert the sugar to energy. In insulin-resistant individuals, the body's cells cannot properly respond to the hormone, resulting in a build-up of glucose and insulin in the blood, which can lead to diabetes and cardiovascular disease.

Earlier work in Kahn's lab had focused on the role of the glucose transporter protein GLUT4 in insulin resistance. Knowing that down-regulation of GLUT4 expression in fat tissue is an almost universal feature of insulin-resistant states, Kahn's lab developed two transgenic mouse models: one with fat cell overexpression of GLUT4 and one with fat cell reduction of GLUT4. They found that the mice with overexpression of GLUT4 demonstrated enhanced glucose tolerance and insulin sensitivity, while the mice with reduced GLUT4 expression became insulin-resistant and had an increased risk of diabetes.

Kahn's team then conducted a global microarray analysis to identify the protein RBP4 and found elevation of RBP4 can cause insulin resistance and that decrease of the protein in insulin- resistant states would ameliorate the condition.

How the brain keeps extra calories from becoming extra pounds

70652986 — Mon, 26 Mar 2007 05:23:17 -0400

What determines whether excess calories are turned into fat or are burned off? The key lies in a process known as diet-induced thermogenesis, an intricate system of communications masterminded by the brain which literally means “heat production,” according to the senior author of a new study, Bradford B. Lowell, of Beth Israel Deaconess Medical Center's department of endocrinology. “The body requires a certain number of calories in order to function and maintain good health,” explains Lowell, who is also an associate professor of medicine at Harvard Medical School. “When the body takes in more calories than it needs, it either converts the extra into stored fat, which sticks around and can lead to obesity, or it converts them into heat, which is subsequently dissipated.” In a study with mice, Lowell and his collaborators discovered that mice burn off extra calories when a group of molecules called beta adrenergic receptors are "turned on" by neurotransmitters released from sympathetic nerve endings. The findings, which could ultimately aid researchers in identifying mutations that cause obesity as well as in developing anti-obesity drugs.

Diabetes treatment linked to increased blood pressure

70652986 — Mon, 26 Mar 2007 05:21:28 -0400

Type II diabetes accounts for the majority of cases of the disease, and is a huge public health problem: As many as 16 million individuals in the United States have Type II diabetes, which puts them at risk for a number of serious complications, including stroke and heart disease. Although diabetes can often be controlled through diet, exercise and existing medications, the magnitude of the problem has given rise to the development of a number of new drugs to better manage the disease, including GLP-1 agonists. These agents, being tested in clinical trials, work by targeting the rate of gastric emptying and by stimulating insulin secretion from islet cells in the pancreas.

Death protein may cause neural tube defects in babies of diabetic mothers

70652986 — Mon, 26 Mar 2007 05:20:44 -0400

A research report provides a possible explanation for a class of birth defects that appears to be on the rise. A protein normally involved in programmed cell death may, as a consequence of high blood sugar, mistakenly tell cells of the nascent neural tube to die. Even with good control of diabetes, the risk for neural tube and other birth defects is two to five times higher than normal if a mother has the disease. That risk could increase as diabetes and obesity, both of which can cause high blood sugar, make inroads into younger populations.

Hormone leptin tied to fat breakdown in muscle

70652986 — Mon, 26 Mar 2007 05:18:55 -0400

Research has shown that leptin is an important hormone with a hand in many metabolic processes. It undoubtedly has widespread effects that may influence diabetes as well as obesity. Recent work from Harvard researchers has tied leptin to a crucial pathway in fat metabolism in muscle. This pathway suggests a role for leptin in clearing fat out of cells and sheds light on the connection between diabetes and obesity. In the Jan. 17, 2002, issue of the journal Nature, a team led by Barbara Kahn, Harvard Medical School professor of medicine and chief of the Division of Endocrinology, Diabetes and Metabolism at Beth Israel Deaconess Medical Center, and Yasuhiko Minokoshi, visiting associate professor of medicine, established the new connection in the body's metabolic machinery.

Single enzyme may be linked to obesity

70652986 — Mon, 26 Mar 2007 05:17:37 -0400

Fat is harmful to health -- we all know that -- and abdominal, or "beer belly" fat, is the worst. “Obesity is a massive problem in our population,” says researcher Jeffrey S. Flier, who has been studying the molecular mechanisms of obesity for the past decade. “It's linked to a huge burden of disease -– hypertension, coronary disease, atherosclerosis, cancers, reproductive disorders, diabetes. In fact, an estimated 80 percent of diabetes cases would not exist in the absence of obesity. If we could attack obesity, not only would people feel better, it would also improve all of these other disease states.” Flier, an endocrinologist at Beth Israel Deaconess Medical Center and the George C.

Immune system discovery may lead to preventive therapy for diabetes

70652986 — Mon, 26 Mar 2007 05:18:27 -0400

The job of cells known as iNKT cells is to regulate the immune system's response to infections and other disorders, ensuring that only diseased tissue, not healthy tissue, is targeted for attack. Type I diabetes, an "autoimmune" disorder, occurs when the immune system mistakenly attacks healthy insulin-producing cells in the pancreas. A new study involved the body's mechanism for activating iNKT cells. The mechanism involves a class of cells known as dendritic cells, whose role is to alert the rest of the immune system to the presence of infection or another health problem. The surface of dendritic cells is studded with proteins called CD1d, which display lipids, or fat, molecules. One such potent activating lipid is known as alpha-galactosylceramide.

Common aspirin reveals mechanism of insulin resistance

70652986 — Mon, 26 Mar 2007 05:13:10 -0400

In 1876, a German professor described a treatment that led to rapid improvement in two men who were suffering from what doctors now recognize as classic type 2 diabetes. In the late 1950s, scattered reports about this treatment for diabetes symptoms again appeared in the medical literature; the results were equally dramatic. What was this mysterious medicine? Aspirin. Doctors have long known that aspirin can lower blood sugar and the amount of insulin in the blood streams of diabetic patients. But the high dosages of aspirin required to treat diabetes symptoms -- and the harmful, even potentially fatal, side-effects of those high dosages -- made it impractical as a therapy. Now Harvard researchers working at Joslin Diabetes Center in Boston have figured out how high dosages of aspirin reverse the effect of a particular protein that can cause insulin resistance. Steven Shoelson, Harvard Medical School associate professor of medicine at Joslin, was senior author of the scientific report appearing in the Aug. 31, 2001, issue of Science. Shoelson envisions the development of a new selective drug that can target the key protein without aspirin's potentially fatal side-effects.

Diet and exercise dramatically delay type 2 diabetes

70652986 — Mon, 26 Mar 2007 05:15:18 -0400

Diabetes afflicts more than 16 million people in the United States; type 2 diabetes accounts for up to 95 percent of all diabetes cases. New findings from the Diabetes Prevention Program (DPP), a major clinical trial conducted by Massachusetts General Hospital (MGH) and 26 other medical centers nationwide, show that modifications in diet and exercise can dramatically delay the onset of type 2 diabetes in people predisposed to the disease. Participants randomly assigned to intensive lifestyle intervention reduced their risk of getting type 2 diabetes by 58 percent. The same study found that treatment with the oral diabetes drug metformin (Glucophage®) also reduces diabetes risk, though less dramatically.

Adult stem cells effect a cure

70652986 — Mon, 26 Mar 2007 05:14:19 -0400

Using stem cells from the unborn to treat adult diseases has created an anguished public debate. Now research news from Harvard Medical School scientists may help to end that debate by showing that adult stem cells can be coaxed into performing new functions. Researchers working with diabetic mice first killed cells responsible for the diabetes. The animals' adult stem cells took over and regenerated missing cells needed to produce insulin and eliminate the disease. "It was a miracle that we didn't expect," says researcher Denise Faustman, the associate professor of medicine who leads the research. Setting up a trial for patients to test the technique has already begun at Massachusetts General Hospital in Boston.

A familiar drug gives surprising hope against diabetic blindness

70652986 — Mon, 26 Mar 2007 05:12:47 -0400

A common complication of diabetes is diabetic retinopathy, which can lead to blindness. Diabetic retinopathy is caused by changes in the blood vessels of the retina. This form of retinopathy has long been suspected of being the result of tiny blood clots in the capillaries of the eye that lead to blockages in blood circulation which, in turn, result in tissue damage and eventually cell death.

Fat cells tied to whole-body insulin resistance

70652986 — Mon, 26 Mar 2007 05:12:14 -0400

Research done by Barbara Kahn, professor of medicine at Beth Israel Deaconess Medical Center, and colleagues now shows that glucose uptake by fatty tissue is important for maintaining the body's ability to respond to insulin. Their results also point to a mechanism by which an abnormality in fat cells may trigger insulin resistance and ultimately diabetes. Skeletal muscle is the primary tissue for insulin-stimulated glucose uptake. Yet in obesity and Type II diabetes, expression of the primary insulin-stimulated glucose transporter, GLUT4, is normal in muscle but reduced in fatty tissue. This paradox led Kahn and colleagues to ask what role fatty tissue-expressed GLUT4 may play in the development of insulin resistance. The results clearly show that "fat is important for whole-body insulin action," said Kahn.

Brain found to play unexpected role in Type II diabetes

70652986 — Mon, 26 Mar 2007 05:03:49 -0400

Until now, the brain was assumed to be a side player in diabetes. "For the most part, diabetes researchers have not been looking at the brain," said C. Ronald Kahn, the Mary K. Iacocca professor of medicine and president of Joslin Diabetes Center. But a report appearing in the Sept. 22, 2000, Science suggests that defects in the brain's ability to respond to insulin could contribute to some of the central symptoms of adult, or Type II, diabetes, including obesity and lowered fertility. The findings, made in mice, contribute to our understanding of the brain's role. More importantly, if confirmed in humans, the discovery could call into question a longstanding dogma about how insulin resistance, the hallmark of diabetes, paves its ruinous course through the body. The new findings by Kahn and his colleagues are already pointing to an alternative view of the disease which, if confirmed, could lead to new diabetes treatments.