09 March 2006

Metabolic Syndrome: Mitochondria in Diabetes and Heart Disease


In a previous post, I discussed the relationship of mitochondrial dysfunction to neurological disorders such as Alzheimer's, Huntington's, Parkinson's disease, and ALS. In another post, I discussed mitochondrial biomarkers of aging. Now evidence is mounting that mitochondria are involved in metabolic syndrome, including diabetes, obesity, heart disease, and related disorders including hypertension and hyperlipidemia. This syndrome accounts for millions of deaths around the world yearly, and accounts for the ongoing disability of many millions more yearly.

In this JCI research article, scientists from Howard Hughes Medical Institute, and Yale University School of Medicine discovered that there were 38% fewer mitochondria in the muscles of healthy but insulin resistant offspring of diabetic parents. This reduction in muscle mitochondria apparently led to a 60% increase in intramyocellular fat, inside the muscle cells, which likely contributes to insulin resistance, and eventually type 2 diabetes. That is an intriguing finding. Read the entire article online here.

Furthermore, Douglas Wallace at UCI has received a sizable grant to study how genetic changes in mitochondria can lead to metabolic disorders, such as type 2 diabetes. According to this newsreport:

"Our receipt of this prestigious Doris Duke Charitable Foundation award is the direct consequence of UCI's vision of becoming a world leader for the new biomedical discipline of mitochondrial medicine," said Wallace, director of the Center for Molecular and Mitochondrial Medicine and Genetics (MAMMAG) at UC Irvine and National Academy of Sciences member.

Mitochondrial medicine offers innovative new perspectives and approaches for addressing the common age-related diseases associated with the metabolic syndrome as well as with forms of blindness, deafness, movement disorders and dementias -- clinical problems that remain elusive to traditional biomedical concepts and approaches.

With the Doris Duke Clinical Interfaces Award -- which will provide funding for five years -- Wallace will lead a multidisciplinary team of UCI researchers, which include physicians Dr. Ping Wang, Dr. Lee-Ming Chuang and Dr. Jay Gargus; biomedical engineer Bruce Tromberg, director of the Beckman Laser Institute; and atmospheric chemists Donald Blake and F. Sherwood Rowland, who received the Nobel Prize in Chemistry in 1995.

The team will study genetic variation in the DNA of mitochondria and its association with the various symptoms of the metabolic syndrome. Wang, Chuang and Gargus will collect mitochondrial samples from metabolic syndrome patients of Chinese heritage in Taiwan and in Southern California. Wallace's team at MAMMAG then will conduct extensive molecular and biochemical studies of these samples to see if variations in mitochondrial DNA as well as environmental factors affect individual predisposition to the clinical symptoms of metabolic syndrome.


Read more here.

Because of the intimate connection to both aging and many debilitating and fatal diseases, mitochondrial medicine presents a tremendous opportunity. Reversing the age-related changes in mitochondria is one of the seven prime interventions of the SENS rejuvenation approach.

Hat tip to New Hope Cancer Blog.

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