NEWS AGOSTO 2009

 

27 Agosto 2009:

Molecular Link Found Between Insulin Resistance And Inflammation

ScienceDaily — An exploration of the molecular links between insulin resistance and inflammation may have revealed a novel target for diabetes treatment, say scientists at the John G. Rangos Sr. Research Center, Children's Hospital of Pittsburgh of UPMC. Their findings were published earlier this month in the online version of Diabetes, one of the journals of the American Diabetes Association.

Signs of low-grade systemic inflammation are not uncommon among people who have the pre-diabetic condition known as metabolic syndrome, as well as in animal models of obesity and type 2, or insulin-resistant, diabetes, said senior author H. Henry Dong, Ph.D., assistant professor, Department of Pediatrics, University of Pittsburgh School of Medicine.

"But it's not yet clear if there is a cause-and-effect relationship between chronic exposure to low-grade inflammation and the onset of insulin resistance," he explained. "Other studies have shown that in patients who have inflammation and diabetes, insulin-sensitizing drugs seem to reduce inflammation while anti-inflammatory therapies improve sensitivity to insulin."

Dr. Dong's team examined the role played by a protein called Forkhead Box 01 (Fox01), which his previous research showed contributes to elevations in triglycerides in an animal model of obesity and diabetes.

In the current paper, the researchers found in cultured cells and mouse experiments that Fox01 stimulates inflammatory white blood cells called macrophages, which migrate to the liver and adipose, or fat, tissue in insulin-resistant states, to increase production of a cytokine called interleukin-1 beta (IL-1B). The cytokine in turn interferes with insulin signaling. Insulin typically inhibits Fox01, setting up a feedback loop in healthy tissues that helps regulate insulin levels.

"The findings suggest that when there is a lack of insulin or when cells such as macrophages are resistant to its presence, there are no brakes on Fox01's stimulation of IL-1B and its further interference with insulin signaling," Dr. Dong said. "That might explain why chronic inflammation often is coupled with obesity and type 2 diabetes. Also, a drug that acts on Fox01 might be able to better control blood sugar."

According to the ADA, an estimated 24 million Americans have type 2 diabetes, formerly known as adult-onset diabetes. As obesity becomes more common, however, the prevalence is rising in children. In type 2 diabetes, the body becomes resistant to the effect of insulin, leading to elevated blood sugar levels.

Co- authors of the paper include lead author Dongming Su, M.D., Gina M. Coudriet, Dae Hyun Kim, Ph.D., German Perdermo, Ph.D., Shen Qu, M.D., Sandra Slusher, Hubert M. Tse, Ph.D., Jon Piganelli, Ph.D., and Nick Giannoukakis, Ph.D., all of the Division of Immunogenetics, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC and Pitt School of Medicine, and Yi Lu, Ph.D., and Jian Zhang, M.D., Division of Hematology and Oncology, Department of Medicine, Pitt School of Medicine.

The study was funded by the American Diabetes Association and the National Institutes of Health.

 

26 Agosto 2009:

Clinical Depression Causes Early Malfunctions In The Brain’s Pleasure Center, Study Shows. ScienceDaily — Clinically depressed individuals are less capable of finding pleasure in activities they previously enjoyed, a recent study has proven. Research featured in the August 26 issue of the NeuroReport shows reduced brain function in the reward center of the brain in depressed individuals, when compared to healthy subjects.

The study was conducted by Dr. Elizabeth Osuch, a researcher at the Lawson Health Research Institute, and is the first scientific publication of data obtained by the newly developed First Episode Mood & Anxiety Program (FEMAP) research arm at the London Health Sciences Centre in Ontario, Canada.

To investigate the effects of depression on brain activity, Dr. Osuch and her team asked 15 healthy subjects and 16 recently depressed subjects to provide a list of their favourite music as well as identify music that they neither liked nor disliked (neutral music). The subjects then listened to their musical selections for three minutes while a functional magnetic resonance imaging (fMRI) scanner measured the neural activity in their brain.

The researchers found that the healthy subjects showed more brain activity in specific regions when they listed to their favourite music compared to the depressed subjects. More specifically, several regions of the brain that are associated with reward processing were shown to be less activated in the depressed individuals, suggesting that even the most basic capacity of enjoyment seems to be malfunctioning in this area of the brain in those who have depression. This was true in spite of no difference in how enjoyable the two groups rated listening to the music in the scanner.

"Our results revealed significant responses within the areas of the brain that are associated with reward processing in healthy individuals. They also showed significant deficits in these neurophysiological responses in recently depressed subjects compared to the healthy subjects,” explains Dr. Osuch. “It is known that depressed individuals experience anhedonia—a loss of enjoyment in previously pleasurable activities. The study results show that for recently depressed individuals this loss of enjoyment is linked to very specific parts of the brain which are involved with experiencing pleasure. If we can target these areas of the brain through treatment, we have the potential to treat depression earlier, right at the source.”

Journal reference:

Osuch, Elizabeth A; Bluhm, Robyn L; et al. Brain activation to favorite music in healthy controls and depressed patients. Neuroreport, 2009; 20 (13): 1204 DOI:10.1097/WNR.0b013e32832f4da3

 

 

25 Agosto 2009:

Autopsia a Michael Jackosn Revela muerte por propofol. ¿Qué es el PROPOFOL?