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Scientists ID Gene Regulating Blood Glucose Levels

(HealthDay News) -- Researchers who've identified a gene that regulates glucose levels but does not increase the risk of type 2 diabetes say their finding may help improve understanding of the underlying causes of diabetes.

"Elevations of blood glucose are diagnostic of diabetes. This finding demonstrates there are gene variants that are important in day-to-day regulation of glucose, but they do not appear to play a significant role in disease risk," co-senior author Richard M. Watanabe, an associate professor of preventive medicine and physiology & biophysics at the Keck School of Medicine at the University of Southern California, said in a prepared statement.

"The identification of these variants increases our basic knowledge about regulation of glucose and may also be useful in future genetic studies to help discriminate between genetic variants that do or do not contribute to disease susceptibility," Watanabe said.

The researchers analyzed genetic information from thousands of people and concluded a gene on chromosome 2 that encodes for the enzyme glucose-6-phosphatase catalytic 2 (G6PC2) is associated with fasting glucose levels.

"G6PC2 is primarily expressed in the beta cells of the pancreas and is responsible for converting glucose-6-phosphate back to glucose. Genetic variation of G6PC2 may be responsible for reducing insulin secretion and causing the glucose concentration to increase," Watanabe said.

With each additional copy of the higher frequency variant of the gene, glucose concentrations increased. Chronically elevated glucose levels may be a precursor to type 2 diabetes, Watanabe noted.

The study is published in the July issue of The Journal of Clinical Investigation.

"Genetics is identifying a whole new set of genes, proteins and pathways that are related to diabetes and blood sugar control. Our next challenge is to figure out how these genes work," study co-author Dr. Thomas A. Buchanan, professor of endocrinology at Keck, said in a prepared statement.

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Decoding Muscle Stem Cell Development

(HealthDay News) -- Muscle stem cells can't grow into mature muscle cells if there aren't enough nutrients, according to a study that offers new insight into how developing muscle cells sense and respond to nutrient levels.

The research, part of ongoing investigations into the effects of caloric restriction on physiology and aging, may help in the development of new treatments for muscle wasting.

In this study, National Institutes of Health researchers examined how the availability of glucose affects the ability of muscle stem cells (myoblasts) to develop into mature skeletal muscle fibers.

According to a news release about the study, the researchers "found that glucose restriction (GR) impaired differentiation of skeletal myoblasts and activated AMP-activated protein kinase (AMPK). These results define a pathway in which activation of AMPK in response to low glucose levels stimulates expression of the NAD+ biosynthetic enzyme Nampt. NAD+ is a known co-factor of SIRT1, which plays an important role in numerous physiological processes, including differentiation of skeletal muscle cells, and has been implicated in regulation of life span and aging. Importantly, inhibition of AMPK, Nampt or SIRT1 resulted in skeletal muscle cells that were oblivious to a nutrient-poor environment and were able to differentiate under conditions that otherwise would not be suitable."

The researchers said their findings, published in the May issue of Developmental Cell, show that a specific pathway controls muscle cell differentiation in response to low nutrient levels.

"We speculate that, functioning as a cellular checkpoint, the AMPK-Nampt-SIRT1 pathway may be activated by reduced nutrient availability to prevent cells from undertaking energy-demanding processes -- such as cell differentiation -- during calorie-unfavorable conditions. On the other hand, once nutrients become available, the pathway is inactivated to allow resumption of physiological development," researcher Vittorio Sartorelli said in a prepared statement.

This same mechanism also operates in adult tissues, which means it would be part of the response to a diet with reduced calorie intake. The researchers also found that both glucose restriction or treatment of skeletal muscle cells with metformin (a drug used to treat type 2 diabetes) had similar outcomes and activated SIRT1.

"It is therefore possible that the well-known benefits that diabetics derive from lowering the calorie intake in their diet may be attributable to activation of the AMPK-Nampt-SIRT1 axis," Sartorelli said.

He added that AMPK and SIRT1 may prove good targets for treatment of muscle-wasting.

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The U.S. National Institutes of Health has more about stem cells.