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April 13, 2012--------News Archive Return to: News Alerts

The new study shows how glucagon’s effect on glucose could be disrupted without disturbing glucagon’s other duties, raising prospects for a safer anti-glucagon diabetes treatment.

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Targeting Glucagon May Offer a New Approach to Treating Diabetes

Maintaining the right level of sugar in the blood is the responsibility not only of insulin, which removes glucose, but also of a hormone called glucagon, which adds glucose

For decades, treatments for type II diabetes have taken aim at insulin, but a new study suggests that a better approach may be to target glucagon’s sweetening effect.

The findings were published today in the online edition of Cell Metabolism.

“What we’ve found is a way to reduce glucagon’s influence on blood sugar without the side effects of global glucagon repression,” said Ira Tabas, MD, PhD, Richard J. Stock Professor and Vice Chair of Research in the Department of Medicine and professor of Anatomy & Cell Biology (in Physiology and Cellular Biophysics), who led the study with Lale Ozcan, PhD, associate research scientist.

Though glucagon was discovered at the same time as insulin, research on it has languished compared with that of its cousin, and treatments have almost exclusively targeted the latter.

In the last decade, the success of incretins, a new class of drugs for type II diabetes, has sparked a renaissance in glucagon research. When they were first introduced, incretins were known to stimulate insulin secretion. But recent studies show that a significant part of their clinical success can be attributed to previously unsuspected inhibiting effects on glucagon secretion.

The experience with incretin has led to a renewed search for other drugs that act against glucagon, including compounds that block glucagon in the liver, where it acts to free glucose. Drugs that block the glucagon receptor in the liver have been tested, but glucagon has multiple roles, and recent early clinical trials show that it can raise cholesterol and lead to fat accumulation in the liver.

The new study shows how glucagon’s effect on glucose could be disrupted without disturbing glucagon’s other duties, raising prospects for a safer anti-glucagon diabetes treatment.

Drs. Tabas and Ozcan found that once glucagon binds to its receptor, glucose is fully released only after an enzyme called CaMKII is activated. When activated, CaMKII sends a protein called FoxO1 into the cell nucleus, where it turns on the genes needed for glucose secretion. A related pathway, working in parallel to this one, sends a FoxO1 helper protein into the cell nucleus, as reported in a paper on which Dr. Tabas is a co-author, published online on April 8 in Nature.

“Even when their disease is well controlled, most patients with type II diabetes have excess glucagon action, so blocking CaMKII could potentially be a new way to lower blood sugar and better treat the disease,” said Dr. Tabas.

When the researchers blocked CaMKII in obese, diabetic mice, the animals’ blood sugar went down, with no negative side effects. Instead, cholesterol declined, insulin sensitivity improved, and the liver became less fatty.

“Until now, it has been difficult to block glucagon’s effect on blood sugar without interfering with glucagon’s other functions,” said Dr. Tabas, “but we think CaMKII is different.”

Dr. Tabas is now working on the possibility of developing a CaMKII inhibitor to treat diabetes.

Drs. Ozcan’s and Tabas’ paper is titled, “Calcium signaling through CaMKII regulates hepatic glucose production in fasting and obesity.” Domenico Accili, MD, Russell Berrie Foundation Professor of Diabetes (in Medicine) and a world-renowned diabetes expert, was a major contributor to this study.

Additional authors are: Catherine C.L. Wong (Scripps Research Institute); Gang Li (CUMC); Tao Xu (Scripps Research Institute); Utpal Pajvani (CUMC); Sung Kyu Robin Park (Scripps Research Institute); Anetta Wronska (CUMC); Bi-Xing Chen (CUMC); Andrew R. Marks (CUMC); Akiyoshi Fukamizu (University of Tsukuba, Japan); Johannes Backs (University of Heidelberg, Germany); Harold A. Singer (Albany Medical College); and John R. Yates, III (Scripps Research Institute).

The researchers declare no financial or other conflict of interest.

This work was supported by an American Heart Association Scientist Development Grant to L. Ozcan; Emmy Noether-DFG grant 2258/2-1 to J. Backs; and NIH grants P41 RR011823 to C.C.L. Wong and J. Yates III NHLBI Proteomic Centers grant HHSN268201000035C to T. Xu, HL49426 to H.A. Singer, HL087123 and DK057539 to D. Accili, and HL087123 and HL075662 to I. Tabas.

Columbia University Medical Center provides international leadership in basic, pre-clinical and clinical research, in medical and health sciences education, and in patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Established in 1767, Columbia’s College of Physicians and Surgeons was the first institution in the country to grant the M.D. degree and is among the most selective medical schools in the country. Columbia University Medical Center is home to the largest medical research enterprise in New York City and state and one of the largest in the United States. For more information, please visit www.cumc.columbia.edu.

Original article: http://www.cumc.columbia.edu/news-room/2012/04/glucagon-pathway-inhibitor-may-offer-a-new-approach-to-treating-diabetes/