Meta-studies in land use science: Current coverage and prospects

Land use science has traditionally used case-study approaches for in-depth investigation of land use change processes and impacts. Meta-studies synthesize findings across case-study evidence to identify general patterns. In this paper, we provide a review of meta-studies in land use science. Various meta-studies have been conducted, which synthesize deforestation and agricultural land use change processes, while other important changes, such as urbanization, wetland conversion, and grassland dynamics have hardly been addressed. Meta-studies of land use change impacts focus mostly on biodiversity and biogeochemical cycles, while meta-studies of socioeconomic consequences are rare. Land use change processes and land use change impacts are generally addressed in isolation, while only few studies considered trajectories of drivers through changes to their impacts and their potential feedbacks. We provide a conceptual framework for linking meta-studies of land use change processes and impacts for the analysis of coupled human–environmental systems. Moreover, we provide suggestions for combining meta-studies of different land use change processes to develop a more integrated theory of land use change, and for combining meta-studies of land use change impacts to identify tradeoffs between different impacts. Land use science can benefit from an improved conceptualization of land use change processes and their impacts, and from new methods that combine meta-study findings to advance our understanding of human–environmental systems.

Brain-borne IL-1 adjusts glucoregulation and provides fuel support to astrocytes and neurons in an autocrine/paracrine manner.

It is still controversial which mediators regulate energy provision to activated neural cells, as insulin does in peripheral tissues. Interleukin-1β (IL-1β) may mediate this effect as it can affect glucoregulation, it is overexpressed in the 'healthy' brain during increased neuronal activity, and it supports high-energy demanding processes such as long-term potentiation, memory and learning. Furthermore, the absence of sustained neuroendocrine and behavioral counterregulation suggests that brain glucose-sensing neurons do not perceive IL-1β-induced hypoglycemia. Here, we show that IL-1β adjusts glucoregulation by inducing its own production in the brain, and that IL-1β-induced hypoglycemia is myeloid differentiation primary response 88 protein (MyD88)-dependent and only partially counteracted by Kir6.2-mediated sensing signaling. Furthermore, we found that, opposite to insulin, IL-1β stimulates brain metabolism. This effect is absent in MyD88-deficient mice, which have neurobehavioral alterations associated to disorders in glucose homeostasis, as during several psychiatric diseases. IL-1β effects on brain metabolism are most likely maintained by IL-1β auto-induction and may reflect a compensatory increase in fuel supply to neural cells. We explore this possibility by directly blocking IL-1 receptors in neural cells. The results showed that, in an activity-dependent and paracrine/autocrine manner, endogenous IL-1 produced by neurons and astrocytes facilitates glucose uptake by these cells. This effect is exacerbated following glutamatergic stimulation and can be passively transferred between cell types. We conclude that the capacity of IL-1β to provide fuel to neural cells underlies its physiological effects on glucoregulation, synaptic plasticity, learning and memory. However, deregulation of IL-1β production could contribute to the alterations in brain glucose metabolism that are detected in several neurologic and psychiatric diseases.Molecular Psychiatry advance online publication, 8 December 2015; doi:10.1038/mp.2015.174.