The discovery is based on the development of image analysis methods that make possible the detailed study of events immediately inside the plasma membrane of the insulin-secreting cells.

Cyclic AMP (cAMP) is a universal messenger molecule that controls a number of different functions inside the cell. For example, it plays a role in the release of insulin from the beta cells in the pancreas (see Facts). It is well-known that the production of cAMP explains how certain hormones can amplify insulin secretion. On the other hand, it has been unclear to what extent cAMP also contributes to the major release of insulin triggered by an increase in blood sugar (glucose).

Anders Tengholms research team at Uppsala University has developed methods that make it possible for the first time to measure both the secretion of insulin and the cAMP concentration in individual beta cells. The results show that ATP, the energy-rich molecule that is produced when glucose is metabolized, causes an increase in cAMP concentration right at the cell membrane where the release of insulin takes place. This increase varies rhythmically and coincides with similarly regular variations in another stimulant messenger, the calcium ion, resulting in pulsatile secretion of insulin.

Optimal glucose-induced insulin secretion requires that the varying cAMP and calcium signals are coordinated in time. The study sheds new light on the cellular mechanisms that underlie the pulsatile release of insulin in healthy individuals, says Anders Tengholm.

The discovery that the cell metabolism directly stimulates the production of cAMP illustrates a new principle for the regulation of this messenger molecule. The connection between metabolism and cAMP is not only important for the secretion of insulin; it also plays a role in gene regulation, cell growth, and cell survival. The observations thereby pave the way for understanding of the disturbed beta cell function in type 2 diabetes and for the development of new drugs for the disease.

uu.se/

According to researchers from City of Hope National Medical Center in Duarte, California, UVB light is more harmful to our skin because our bodies are less able to repair the DNA damage it causes than the damage caused by UVA light. To reach their conclusions, scientists exposed three sets of cells to UVA light, UVB light and simulated sunlight. Then they compared these cells to an unexposed control group to analyze how well these cells were able to repair the damage. In addition, they analyzed published data on the genetics involved in human skin cancers. The researchers found that cells were more easily able to repair the damage caused by the UVA light, which explains why UVA light has been perceived as "safer" than UVB light. Despite this perception, scientists and public health experts caution that UVA light can and does cause serious damage that can and does lead to skin cancer.

"We know that sunlight causes skin cancer and that breakdown of the ozone layer exposes us to ever more ultraviolet radiation. This work tells us that both forms of UVA and UVB in sunlight cause damage to DNA. It forms a missing link in the chain of events from sun exposure to tumor formation," said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal. "This research article gives us information that could lead to better sunscreens or effective 'after sun' products. It promises new ways to prevent - and perhaps to treat - the epidemic of skin cancer brought on by modern life."

faseb/