This study raises important questions: Are hypoxic conditions and elevated HIF-1α levels during obesity involved in A2 upregulation? Does A2 deletion reduce HIF-1α levels and thus mitigate adipocyte dysfunction? What is the interplay between endothelial cells and adipocyte dysfunction? And which one precedes the other? Also, what is the impact of A2 deletion in other tissues involved in metabolism, including muscle, liver and brown adipose tissue? Although the expression of UCP-1 in VAT is low [ 58 ], A2 deletion showed a trend towards increased expression of this browning/beiging protein.
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Role of Arginase 2 in Systemic Metabolic Activity and Adipose Tissue Fatty Acid Metabolism in Diet-Induced Obese Mice.
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