Abstract

Adiponectin, an adipose tissue-derived hormone, plays integral roles in lipid and glucose metabolism in peripheral tissues, such as the skeletal muscle, adipose tissue, and liver. Moreover, it has also been shown to have an impact on metabolic processes in the central nervous system. Astrocytes comprise the most abundant cell type in the central nervous system and actively participate in metabolic processes between blood vessels and neurons. However, the ability of adiponectin to control nutrient metabolism in astrocytes has not yet been fully elucidated. In this study, we investigated the effects of adiponectin on multiple metabolic processes in hypothalamic astrocytes. Adiponectin enhanced glucose uptake, glycolytic processes and fatty acid oxidation in cultured primary hypothalamic astrocytes. In line with these findings, we also found that adiponectin treatment effectively enhanced synthesis and release of monocarboxylates. Overall, these data suggested that adiponectin triggers catabolic processes in astrocytes, thereby enhancing nutrient availability in the hypothalamus.

Highlights

  • The brain constitutes a metabolically active organ that requires the highest energy demands in the human body

  • Based on the evidence that astrocytes respond to metabolic alterations and reactive astrocytes display morphological changes [12], we evaluated the number of astrocytes and their pattern of interaction with blood vessels in the hypothalamus assessed by immunohistochemistry with an antibody against glial fibrillary acidic protein (Gfap), a molecular maker for the astrocyte after central administration of adiponectin

  • We further examined the contact ratio between astrocytes and blood vessels by performing fluorescence immunohistochemistry combined with a visualization of blood vessels by cardiac infusion of lectin to speculate whether adiponectin participates in nutrient shuttling between astrocytes and blood vessels

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Summary

Introduction

The brain constitutes a metabolically active organ that requires the highest energy demands in the human body. As neurons expend high levels of energy resources, such as glucose and lactate, to initiate and propagate their action potentials [4,5], impairment of the energy supply can lead to perturbation of neuronal excitability. Consistent with these concepts, multiple brain disorders are deeply associated with abnormalities of energy metabolism in the CNS. Astrocytes are responsible for the metabolic processing of glucose absorbed by the brain [4,7], they do not require as much energy as they uptake. The primary driving factor underlying astrocyte participation in glucose uptake and utilization is the provision of energy sources from astrocytes to neurons

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