Posts tagged metabolic syndrome

Posts tagged metabolic syndrome
While the search continues for the Fountain of Youth, researchers may have found the body’s “fountain of aging”: the brain region known as the hypothalamus. For the first time, scientists at Albert Einstein College of Medicine of Yeshiva University report that the hypothalamus of mice controls aging throughout the body. Their discovery of a specific age-related signaling pathway opens up new strategies for combating diseases of old age and extending lifespan. The paper was published today in the online edition of Nature.

“Scientists have long wondered whether aging occurs independently in the body’s various tissues or if it could be actively regulated by an organ in the body,” said senior author Dongsheng Cai, M.D., Ph.D., professor of molecular pharmacology at Einstein. “It’s clear from our study that many aspects of aging are controlled by the hypothalamus. What’s exciting is that it’s possible — at least in mice — to alter signaling within the hypothalamus to slow down the aging process and increase longevity.”
The hypothalamus, an almond-sized structure located deep within the brain, is known to have fundamental roles in growth, development, reproduction, and metabolism. Dr. Cai suspected that the hypothalamus might also play a key role in aging through the influence it exerts throughout the body.
“As people age,” he said, “you can detect inflammatory changes in various tissues. Inflammation is also involved in various age-related diseases, such as metabolic syndrome, cardiovascular disease, neurological disease and many types of cancer.” Over the past several years, Dr. Cai and his research colleagues showed that inflammatory changes in the hypothalamus can give rise to various components of metabolic syndrome (a combination of health problems that can lead to heart disease and diabetes).
To find out how the hypothalamus might affect aging, Dr. Cai decided to study hypothalamic inflammation by focusing on a protein complex called NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells). “Inflammation involves hundreds of molecules, and NF-κB sits right at the center of that regulatory map,” he said.
In the current study, Dr. Cai and his team demonstrated that activating the NF-κB pathway in the hypothalamus of mice significantly accelerated the development of aging, as shown by various physiological, cognitive, and behavioral tests. “The mice showed a decrease in muscle strength and size, in skin thickness, and in their ability to learn — all indicators of aging. Activating this pathway promoted systemic aging that shortened the lifespan,” he said.
Conversely, Dr. Cai and his group found that blocking the NF-κB pathway in the hypothalamus of mouse brains slowed aging and increased median longevity by about 20 percent, compared to controls.
The researchers also found that activating the NF-κB pathway in the hypothalamus caused declines in levels of gonadotropin-releasing hormone (GnRH), which is synthesized in the hypothalamus. Release of GnRH into the blood is usually associated with reproduction. Suspecting that reduced release of GnRH from the brain might contribute to whole-body aging, the researchers injected the hormone into a hypothalamic ventricle (chamber) of aged mice and made the striking observation that the hormone injections protected them from the impaired neurogenesis (the creation of new neurons in the brain) associated with aging. When aged mice received daily GnRH injections for a prolonged period, this therapy exerted benefits that included the slowing of age-related cognitive decline, probably the result of neurogenesis.
According to Dr. Cai, preventing the hypothalamus from causing inflammation and increasing neurogenesis via GnRH therapy are two potential strategies for increasing lifespan and treating age-related diseases. This technology is available for licensing.
(Source: einstein.yu.edu)

Lack of nutrients and metabolic syndrome linked to different subtypes of depression
A low intake of folate and vitamin B12 increases the risk of melancholic depressive symptoms, according to a study among nearly 3,000 middle-aged and elderly Finnish subjects. On the other hand, non-melancholic depressive symptoms are associated with an increased risk for the metabolic syndrome. Based on these new observations, melancholic and non-melancholic depression may be separate depressive subtypes with different etiologies in terms of proinflammation and diet. The study was the first to look at these depressive sub-types separately.
"The findings have practical implications in the care of patients with depressive symptoms. For example, it may be wise to avoid medication causing weight gain among patients with non-melancholic depression, whereas melancholic depressive symptoms may call for a closer look at the quality of the patient’s diet," says Mr Jussi Seppälä, MD, Chief of the Department of Psychiatry of the Hospital District of Southern Savo.
Melancholic depression involves typical depressive symptoms, such as a depressed mood. Non-melancholic depression is characterized by other types of symptoms, such as low self-esteem and feelings of worry and anxiety.
Among subjects with the highest folate intake, the risk for melancholic depressive symptoms was almost 50 per cent lower than among those with the lowest intake. In addition, among those with the highest vitamin B12 levels, the risk for melancholic depressive symptoms was almost three times lower than among those with the lowest levels. Both findings are new. A similar association with non-melancholic depressive symptoms was not observed.
Another novel observation is that the risk for the metabolic syndrome was twofold among those with non-melancholic depressive symptoms, as compared to those with melancholic symptoms or those with no depressive symptoms.
Mr Seppälä’s doctoral thesis “Depressive symptoms, metabolic syndrome and diet" was published at the University of Eastern Finland. The study was conducted as part of the Finnish Type 2 Diabetes Prevention Programme. The findings were originally published in Journal of Affective Disorders.
ScienceDaily (Sep. 3, 2012) — A new study by researchers at NYU School of Medicine reveals for the first time that metabolic syndrome (MetS) is associated with cognitive and brain impairments in adolescents and calls for pediatricians to take this into account when considering the early treatment of childhood obesity.
The study, funded by the National Institutes of Health under award number DK083537, and in part by award number 1ULIRR029892, from the National Center for Research Resources, appears online September 3 in Pediatrics.
As childhood obesity has increased in the U.S., so has the prevalence of metabolic syndrome — a constellation of three or more of five defined health problems, including abdominal obesity, low HDL (good cholesterol), high triglycerides, high blood pressure and pre-diabetic insulin resistance. Lead investigator Antonio Convit, MD, professor of psychiatry and medicine at NYU School of Medicine and a member of the Nathan Kline Research Institute, and colleagues have shown previously that metabolic syndrome has been linked to neurocognitive impairments in adults, but this association was generally thought to be a long-term effect of poor metabolism. Now, the research team has revealed even worse brain impairments in adolescents with metabolic syndrome, a group absent of clinically-manifest vascular disease and likely shorter duration of poor metabolism.
"The prevalence of MetS parallels the rise in childhood obesity," Dr. Convit said. "There are huge numbers of people out there who have problems with their weight. If those problems persist long enough, they will lead to the development of MetS and diabetes. As yet, there has been very little information available about what happens to the brain in the setting of obesity and MetS and before diabetes onset in children."
7/18/2012
Metabolic syndrome, a term used to describe a combination of risk factors that often lead to heart disease and type 2 diabetes, seems to be linked to lower blood flow to the brain, according to research by the University of Wisconsin School of Medicine and Public Health.
Dr. Barbara Bendlin, researcher for the Wisconsin Alzheimer’s Disease Research Center and an assistant professor of medicine (geriatrics) at the UW School of Medicine and Public Health, said study participants with multiple risk factors connected to metabolic syndrome, including abdominal obesity, high blood pressure, high blood sugar and high cholesterol averaged 15 percent less blood flow to the brain than those in a control group, according to results of brain scans to measure cerebral blood flow.
"We thought the cerebral blood flow measurements of the metabolic syndrome group would be lower, but it was striking how much lower it was," said Bendlin.
Although lower blood flow could result in an eventual reduction in memory skills, Bendlin said it is not known if people with metabolic syndrome will get Alzheimer’s disease.
"Having metabolic syndrome at middle age does have an effect on the brain, and there is some suggestion that if you have lower blood flow, certain types of memory functions are reduced," she said. "The key will be to follow these people over time, because we want to know if lower blood flow will lead to a gradual loss of memory and cognitive skills. But it’s too early to say if these people will develop Alzheimer’s."
The study, presented today at the Alzheimer’s Association International Conference in Vancouver, British Columbia, involved 71 middle-aged people recruited from the Wisconsin Registry for Alzheimer’s Prevention (WRAP). Of this group, 29 met the criteria for metabolic syndrome and 42 did not.
Bendlin said the next steps will be to conduct additional brain scans on people with metabolic syndrome to get more specifics on why they have reduced cerebral blood flow.
"By comparing people with metabolic syndrome with those who don’t, we don’t know which of the risk factors are worst," she said. "Is having a high blood-glucose level worse than having high blood pressure or is it different than having abdominal obesity? All of these risk factors have been linked to increased risk for dementia, but they are clustered together. If we knew which ones were the worst, those would be the ones to target with specific treatments."
Source: Bio-Medicine