New drug potential for treating diabetes and Alzheimer's

Cell proteins with the ability to prevent the death of nerve cells can also help improve the effect of insulin and lower blood glucose levels, according to a new study of the Albert Einstein School of Medicine at Yeshiva University. Working with the University of California in Los Angeles.

Research conducted on rats will be published in the PloS One this month. This is the first study to show the role of humanin, a small protein (peptide) in glucose metabolism.Scientists have also demonstrated that humanin is similar to peptide leptin in that it also acts on the brain affecting glucose metabolism.

Humanin is found in mitochondria - a type of structure in the cytoplasm and provides energy for cells. This peptide was first detected in nerve cells in the brain in 2001, and subsequent studies have shown that they protect nerve cells from harm when the body gets Alzheimer's. many other diseases of the brain.

'This new function of humanin in glucose metabolism and its role for Alzheimer's disease is very interesting, because scientists have long shown a link between type 2 diabetes and Alzheimer's, ' Professor Nir Barzilai, senior author of the project, director of the Geriatric Research Institute at Einstein College of Medicine, said. 'Humanin may be a treatment option for these two debilitating diseases in millions of people. In addition, humanin may help treat other diseases related to old age. '

In the study, Dr. Barzilai and his colleagues introduced humanin into the brains of diabetic mice to determine the effect of peptides on glucose metabolism.Humanin then works to improve insulin sensitivity clearly, both in the liver and in skeletal muscle. In addition, a single dose of highly effective form of humanin also significantly reduced blood glucose levels in infected mice.

A single dose of Humanin could almost normalize glucose levels in experimental mice with type 2 diabetes. (Photo: Albert Einstein School of Pharmacy)

'Increasing insulin sensitivity under humanin central control may be one of the main mechanisms for humanin to determine cell survival,' said Dr. Barzilai. 'This could be a positive mechanism by which humanin protects the body from Alzheimer's attack.'

The link between humanin and age-related diseases - particularly Alzheimer's and type 2 diabetes - has prompted researchers to examine whether changes in humanin levels during aging appear. in mice and people or not.They found that the amount of humanin in skeletal muscle and in the two brain structures (the hypothalamus - the region that controls body temperature, hunger, thirst, . - and the cortex) decreases with the aging process. chemistry in mice, and that circulating blood levels of peptide chains decrease during aging in humans.

'From these results, we came to the conclusion that reducing the amount of humanin in old age is the reason why Alzheimer's and type 2 diabetes are more common in older people than others,' said Dr. Barzilai said.

Furthermore, 'the unusual activity of this strange peptide poses a new role for a type of endogenous molecule that has been underdeveloped from mitochondria, which has been underestimated and may suggest treatment for many different diseases. , ' Dr. Pinchas Cohen, co-author of the study, head of endocrinology at Mattel Children's Hospital at the University of California, Los Angeles, revealed.

Scientists are currently studying the level of safety as well as the chemical and physical effects of humanin on the human body.

The results of the study are published in PLoS One issue July 22, 2009.

The lead author of this time is Radhika H. Muzumdar, professor of pediatrics and pharmacy at Einstein College of Pharmacy. Along with a group of senior authors, there were also Dr. Barzilai and Cohen. The work also recognized the participation of scientists including Gil Atzmon, Tamuri Budagov, Linguang Cui, Francine Einstein, Sigal Fishman, and Derek Huffman from Einstein University; Aruna Poduval is from the Montefiore Children's Hospital; Christoph Buettner from Mount Sinai Pharmacy School; and Laura Cobb and David Hwang from the University of California in Los Angeles.

The project is fully funded by the National Institutes of Health. There are no commercial sponsorships or conflicts of interest related to the study.