Aerobic glycolysis involves increased glycolysis and decreased oxidative catabolism of glucose even in the presence of an ample oxygen supply. Aerobic glycolysis, a common metabolic pattern in cancer cells, was recently discovered in both the healthy and diseased human brain, but its functional significance is not understood. This metabolic pattern in the brain is surprising because it results in decreased efficiency of adenosine triphosphate (ATP) production in a tissue with high energetic demands. We report that highly aggressive honey bees (Apis mellifera) show a brain transcriptomic and metabolic state consistent with aerobic glycolysis, i.e. increased glycolysis in combination with decreased oxidative phosphorylation. Furthermore, exposure to alarm pheromone, which provokes aggression, causes a metabolic shift to aerobic glycolysis in the bee brain. We hypothesize that this metabolic state, which is associated with altered neurotransmitter levels, increased glycolytically derived ATP and a reduced cellular redox state, may lead to increased neuronal excitability and oxidative stress in the brain. Our analysis provides evidence for a robust, distinct and persistent brain metabolic response to aggression-inducing social cues. This finding for the first time associates aerobic glycolysis with naturally occurring behavioral plasticity, which has important implications for understanding both healthy and diseased brain function.
Nonalcoholic fatty liver disease (NAFLD) is an increasingly prevalent liver pathology characterized by hepatic steatosis and commonly accompanied by systematic inflammation and metabolic disorder. Despite an accumulating number of studies, no pharmacological strategy is available to treat this condition in the clinic. In this study, we applied extensive gain‐ and loss‐of‐function approaches to identify the key immune factor leukocyte immunoglobulin‐like receptor B4 (LILRB4) as a negative regulator of NAFLD. The hepatocyte‐specific knockout of LILRB4 (LILRB4‐HKO) exacerbated high‐fat diet–induced insulin resistance, glucose metabolic imbalance, hepatic lipid accumulation, and systematic inflammation in mice, whereas LILRB4 overexpression in hepatocytes showed a completely opposite phenotype relative to that of LILRB4‐HKO mice when compared with their corresponding controls. Further investigations of molecular mechanisms demonstrated that LILRB4 recruits SHP1 to inhibit TRAF6 ubiquitination and subsequent inactivation of nuclear factor kappa B and mitogen‐activated protein kinase cascades. From a therapeutic perspective, the overexpression of LILRB4 in a genetic model of NAFLD, ob/ob mice, largely reversed the inherent hepatic steatosis, inflammation, and metabolic disorder. Conclusion: Targeting hepatic LILRB4 to improve its expression or activation represents a promising strategy for the treatment of NAFLD as well as related liver and metabolic diseases. (Hepatology 2018;67:1303‐1319)
Spirotetramat is a new pesticide against a broad spectrum of sucking insects and exhibits a unique property with a two-way systemicity. In order to formulate a scientific rationale for a reasonable spray dose and the safe interval period of 22.4 % spirotetramat suspension concentrate on controlling vegetable pests, we analyzed degradation dynamics and pathways of spirotetramat in different parts of spinach plant (leaf, stalk, and root) and in the soil. We conducted experimental trials under field conditions and adopted a simple and reliable method (dispersive solid phase extraction) combined with liquid chromatography-triple quadrupole tandem mass spectrometry to evaluate the dissipation rates of spirotetramat residue and its metabolites. The results showed that the spirotetramat was degraded into different metabolite residues in different parts of spinach plant (leaf, stalk, and root) and in the soil. Specifically, spirotetramat was degraded into B-keto, B-glu, and B-enol in the leaf; B-glu and B-enol in the stalk; and only B-enol in the root. In the soil where the plants grew, spirotetramat followed a completely different pathway compared to the plant and degraded into B-keto and B-mono. Regardless of different degradation pathways, the dissipation dynamic equations of spirotetramat in different parts of spinach plant and in the soil were all based on the first-order reaction dynamic equations. This work provides guidelines for the safe use of spirotetramat in spinach fields, which would help prevent potential health threats to consumers.
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