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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.

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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.

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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."

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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