The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Insulin resistance in obesity as analyzed by the response of glucose kinetics to glucagon infusion.

A new approach has been developed to examine insulin sensitivity and resistance in vivo in man. In it, tracer methods are used, which permit the assessment of nonsteady state glucose kinetics by a method that is noninvasive and does not use pharmacologic agents. Graded doses of glucagon, infused intravenously, are used to drive glucose out of steady state and to stimulate the release of insulin into the portal circulation. By relating the changes in the rates of glucose production, utilization, and fractional disappearance to immunoreactive glucagon and insulin, it is possible to assess the body's sensitivity to physiologic levels of these two hormones. The utility of this approach was examined in obesity, a known human model of insulin resistance. The data demonstrated that glucose production in the obese subjects responded normally to glucagon. They also showed that insulin was much less effective in promoting glucose utilization in the obese persons than it was in the normal ones. In the obese subjects who were studied, the pancreatic B-cells were shown to be normally responsive to the stimulatory effects of either glucose or glucagon. Hence, they did not release sufficient insulin to overcome the insulin resistance, and these obese individuals had impaired glucose tolerance. Thus, it is suggested that, in the presence of insulin resistance, the responsiveness of B-cells will determine whether the glucose tolerance will be nore homeostasis in other conditions associated with glucose intolerance, the metabolic basis of which is undefined.[1]

References

 
WikiGenes - Universities