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Resveratrol, obesity and diabetes. Eur J Pharmacol. 2010 Jun 10;635(1-3):1-8 Authors: Szkudelska K, Szkudelski T Resveratrol belongs to the large group of biologically active substances found in plants. This compound is classified as phytoestrogen because of its ability to interact with estrogen receptor. Numerous beneficial effects of resveratrol described in the literature involve cardioprotective, anti-cancer, anti-inflammatory and antioxidant action. Recently, this broad spectrum of effects is enlarged by new data demonstrating a great potency of this compound in relation to obesity and diabetes. It is well established that resveratrol exerts beneficial effects in rodents fed a high-calorie diet. In some studies, resveratrol was reported to reduce body weight and adiposity in obese animals. The action of this compound involves favourable changes in gene expressions and in enzyme activities. The accumulating evidence also indicates the benefits of resveratrol in diabetes and diabetic complications. It is known that resveratrol affects insulin secretion and blood insulin concentration. In animals with hyperinsulinemia, resveratrol was found to reduce blood insulin. Moreover, numerous data indicate that in diabetic rats, resveratrol is able to reduce hyperglycemia. The mechanism of resveratrol's action is complex and is demonstrated to involve both insulin-dependent and insulin-independent effects. These data point to the potential possibility of use of resveratrol in preventing and/or treating both obesity and diabetes.

A new study published in the journal Population and Health Metrics predicts that the incidence of diabetes in the United States will almost double by 2050. A summary of the study follows:

Background
People with diabetes can suffer from diverse complications that seriously erode quality of life. Diabetes, costing the United States more than $174 billion per year in 2007, is expected to take an increasingly large financial toll in subsequent years. Accurate projections of diabetes burden are essential to policymakers planning for future health care needs and costs.

Methods
Using data on prediabetes and diabetes prevalence in the United States, forecasted incidence, and current US Census projections of mortality and migration, the authors constructed a series of dynamic models employing systems of difference equations to project the future burden of diabetes among US adults. A three-state model partitions the US population into no diabetes, undiagnosed diabetes, and diagnosed diabetes. A four-state model divides the state of “no diabetes” into high-risk (prediabetes) and low-risk (normal glucose) states. A five-state model incorporates an intervention designed to prevent or delay diabetes in adults at high risk.

Results
The authors project that annual diagnosed diabetes incidence (new cases) will increase from about 8 cases per 1,000 in 2008 to about 15 in 2050. Assuming low incidence and relatively high diabetes mortality, total diabetes prevalence (diagnosed and undiagnosed cases) is projected to increase from 14% in 2010 to 21% of the US adult population by 2050. However, if recent increases in diabetes incidence continue and diabetes mortality is relatively low, prevalence will increase to 33% by 2050. A middle-ground scenario projects a prevalence of 25% to 28% by 2050. Intervention can reduce, but not eliminate, increases in diabetes prevalence.

Conclusions
These projected increases are largely attributable to the aging of the US population, increasing numbers of members of higher-risk minority groups in the population, and people with diabetes living longer. Effective strategies will need to be undertaken to moderate the impact of these factors on national diabetes burden. Our analysis suggests that widespread implementation of reasonably effective preventive interventions focused on high-risk subgroups of the population can considerably reduce, but not eliminate, future increases in diabetes prevalence.

A link between obesity and diabetes has been take for granted for a long time, but the exact relationship has been elusive. New evidence suggest that excess fat may be contributing to the accumulation of pollutants that eventually influence the appearance of tye 2 diabetes.

Certain pollutants present in the environment tend to accumulate in the fatty tissues of animals. An example if these substances in PCB, which occurs in many types of electrical equipment. Another example is the pesticide DDT, which in spite of being banned still persists in the environment. Some pollutants are directly conmumed by people, and in other cases they are ingested by animals, entering the food chain and end up in people as well.

Researchers at the Kyungpook National University in South Korea found out that people that had elevated levels of six different kinds of pollutants in their fatty tissues had more chances to develop diabetes than people with low levels of these pollutants (for more info see New Scientist, 30 September 2006, p 18). This study was backed by further evidence suggesting a link between PCB and some pesticides and development of insulin resistance in non-diabetics. The hypothesis is that fat people will tend to accumulate more pollutants as their fat acts as a storage agent. Although the theory is appealing, other investigators warn that the relationship is much more complex and other factors may be at play.