Dietary Diversity,Diet Cost,and Incidence of Type 2 Diabetes in the United Kingdom: A Prospective Cohort Study

BackgroundDiet is a key modifiable risk factor for multiple chronic conditions, including type 2 diabetes (T2D). Consuming a range of foods from the five major food groups is advocated as critical to healthy eating, but the association of diversity across major food groups with T2D is not clear and the relationship of within-food-group diversity is unknown. In addition, there is a growing price gap between more and less healthy foods, which may limit the uptake of varied diets. The current study had two aims: first, to examine the association of reported diversity of intake of food groups as well as their subtypes with risk of developing T2D, and second, to estimate the monetary cost associated with dietary diversity.ConclusionsA diet characterized by regular consumption of all five food groups and by greater variety of dairy, fruit, and vegetable subtypes, appears important for a reduced risk of diabetes. However, such a diet is more expensive. Public health efforts to prevent diabetes should include food price policies to promote healthier, more varied diets.     

Potential reversal of a phase shift: the rapid decrease in the cover of the invasive green macroalga <Emphasis Type="Italic">Dictyosphaeria cavernosa</Emphasis> Forsskål on coral reefs in Kāne‘ohe Bay,Oahu, Hawai‘i

The native green macroalga Dictyosphaeria cavernosa dominated most of the reef slope habitat in Kāne‘ohe Bay, Hawai‘i for 40 years prior to 2006 and had displaced corals from the habitats they created. This has been one of the most oft-cited examples of a phase shift occurring on a coral reef. After decades of relatively constant, high abundance of the alga, percent cover declined dramatically throughout the bay between February and June 2006. The sudden decrease in cover of this alga appears to be the result of an unusually protracted cloudy, rainy period in March 2006, which may have reduced irradiance and caused the alga to lose weight. Corals and red macroalgae living at the same depths and in some of the same habitats were apparently not affected by this 42-day period of rain and overcast skies. Competition between corals and D. cavernosa for space on reef slopes has been virtually eliminated by the death of this alga, but the unstable rubble formations, which remain in much of the area formerly covered by D. cavernosa may not be conducive to rapid increase in cover by the remaining corals or to establishment by coral recruits. Two years later, there was still no recovery of D. cavernosa. This represents a rare example of decline in macroalgal dominance on a reef and a partial reversal, possibly only temporary, of a phase shift.     

Engineering the melanocortin-4 receptor to control constitutive and ligand-mediated G(S) signaling in vivo

The molecular and functional diversity of G protein-coupled receptors is essential to many physiological processes. However, this diversity presents a significant challenge to understanding the G protein-mediated signaling events that underlie a specific physiological response. To increase our understanding of these processes, we sought to gain control of the timing and specificity of G(s) signaling in vivo. We used naturally occurring human mutations to develop two G(s)-coupled engineered receptors that respond solely to a synthetic ligand (RASSLs). Our G(s)-coupled RASSLs are based on the melanocortin-4 receptor, a centrally expressed receptor that plays an important role in the regulation of body weight. These RASSLs are not activated by the endogenous hormone alpha-melanocyte-stimulating hormone but respond potently to a selective synthetic ligand, tetrahydroisoquinoline. The RASSL variants reported here differ in their intrinsic basal activities, allowing the separation of the effects of basal signaling from ligand-mediated activation of the G(s) pathway in vivo. These RASSLs can be used to activate G(s) signaling in any tissue, but would be particularly useful for analyzing downstream events that mediate body weight regulation in mice. Our study also demonstrates the use of human genetic variation for protein engineering.