Trivalent Chromium Ameliorates Lipid Accumulation and Enhances Glucose Metabolism in the High-NEFA Environment of Bovine Hepatocytes by Regulating PI3K/AKT Pathways.

During the periparturient transition period, dairy cows are often accompanied by disorders of liver glycolipid metabolism. The PI3K/AKT signaling pathway plays an important role in the homeostasis of glycolipid metabolism. Trivalent chromium [Cr(III)] is an essential trace element in the body. Here, we investigated the protective effect of chromium trivalent on nonesterified fatty acid (NEFA)-induced glycolipid metabolism disorder in bovine hepatocytes and elucidated the potential mechanism. First, the effects of Cr(III) on glycolipid metabolism disorder induced by 1.2 mM NEFA were studied by pretreating bovine hepatocytes with Cr(III). Then, after pretreatment with PI3K pathway inhibitor LY294002 (2 μM), we investigated whether the PI3K/AKT signaling pathway of Cr(III) plays a role in maintaining glycolipid metabolism homeostasis. The results showed that Cr(III) pretreatment effectively inhibited lipid synthesis, promoted lipid oxidation and VLDL assembly, and increased glycogen generation, thereby improving the glycolipid metabolism disorder induced by NEFA in bovine hepatocytes. However, the beneficial effects of Cr(III) on glycolipid homeostasis were eliminated after pretreatment with inhibitors of the PI3K/AKT signaling pathway. Therefore, Cr(III), as an essential trace element, ameliorates NEFA-induced glucose and lipid metabolism disorders while promoting gluconeogenesis in dairy cow hepatocytes by relying on the PI3K/AKT signaling pathway.