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1 Introduction The dysregulation of glucose and fatty acids is commonly observed in metabolic diseases such as obesity and diabetes. High glucose and fatty acid levels could cause compound pathological insults termed glucolipotoxicity, which was initially referred to for their adverse impacts on pancreatic β-cells [1].
Abstract Metabolic disorders could cause dysregulated glucose and lipid at the systemic level, but how inter-tissue/organ communications contribute to glucolipotoxicity is difficult to dissect in animal models. To solve this problem, myocardium and nerve tissues were modeled by 3D engineered heart tissues (EHTs) and neural organoids (NOs), which were co-cultured in a generalized medium with normal or elevated glucose/fatty acid contents.
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