Chemerin is an adipokine involved in obesity, inflammation, and innate immune system that is highly expressed in the liver. In the present study, we find that chemerin mRNA expression is decreased in the livers of rodents with nonalcoholic fatty liver disease as well as in HepG2 cells after lipid overloading. Moreover, we report that chemerin expression and secretion are induced in HepG2 cells and primary hepatocytes from wild-type mice, but not farnesoid X receptor (FXR)-/- mice, in response to the synthetic FXR ligand GW4064. Hepatic chemerin expression is decreased in FXR-/- mice but up-regulated by GW4064 administration in wild-type mice. Dual-luciferase reporter assay and chromatin immunoprecipitation analyses further identified a functional FXR response element located in the -258-bp /+121-bp region of the chemerin gene. These data demonstrate that chemerin, a novel target gene of FXR, is related to nonalcoholic steatohepatitis.
Adiponectin, a metabolic hormone secreted by adipocytes, can cross the blood-brain barrier to act on neurons in different brain regions, including those involved in stress-related disorders. Here we show that dopamine neurons in the ventral tegmental area (VTA) express adiponectin receptor 1 (AdipoR1). Intra-VTA infusion of adiponectin or the adiponectin mimetic AdipoRon in wild-type mice decreases basal dopamine neuron population activity and firing rate and reverses the restraint stress-induced increase in dopamine neuron activity and anxiety behavior. Adiponectin haploinsufficiency leads to increased dopamine neuron firing and anxiety behavior under basal conditions. Ablation of AdipoR1 specifically from dopamine neurons enhances neuronal and anxiogenic responses to restraint stress. The effects of intra-VTA infusion of adiponectin on neuronal activity and behavior were abolished in mice lacking AdipoR1 in dopamine neurons. These observations indicate that adiponectin can directly modulate VTA dopamine neuron activity and anxiety behavior, and that AdipoR1 is required for adiponectin-induced inhibition of dopamine neurons and anxiolytic effects. These results strengthen the idea of adiponectin as a key biological factor that links metabolic syndrome and emotional disorders.
Mixed integer linear programming (MILP) a b s t r a c tMicrogrids are promising in reducing energy consumption and carbon emissions, compared with the current centralised energy generation systems. Smart homes are becoming popular for their lower energy cost and provision of comfort. Flexible energy-consuming household tasks can be scheduled coordinately among multiple smart homes to reduce economic cost and CO 2 . However, the electricity tariff is not always positively correlated with CO 2 intensity. In this work, a mixed integer linear programming (MILP) model is proposed to schedule the energy consumption within smart homes using a microgrid system. The daily power consumption tasks are scheduled by coupling environmental and economic sustainability in a multi-objective optimisation with e-constraint method. The two conflicting objectives are to minimise the daily energy cost and CO 2 emissions. Distributed energy resources (DER) operation and electricity-consumption household tasks are scheduled based on electricity tariff, CO 2 intensity and electricity task time window. The proposed model is implemented on a smart building of 30 homes under three different price schemes. Electricity tariff and CO 2 intensity profiles of the UK are employed for the case study. The Pareto curves for cost and CO 2 emissions present the trade-off between the two conflicting objectives.
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