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Regulation of glucose metabolism from a liver-centric perspective

2016; Springer Nature; Volume: 48; Issue: 3 Linguagem: Inglês

10.1038/emm.2015.122

2092-6413

Hye-Sook Han, Geon Kang, Jun Seok Kim, Byeong Hoon Choi, Seung‐Hoi Koo,

Metabolism, Diabetes, and Cancer

Glucose homeostasis is tightly regulated to meet the energy requirements of the vital organs and maintain an individual’s health. The liver has a major role in the control of glucose homeostasis by controlling various pathways of glucose metabolism, including glycogenesis, glycogenolysis, glycolysis and gluconeogenesis. Both the acute and chronic regulation of the enzymes involved in the pathways are required for the proper functioning of these complex interwoven systems. Allosteric control by various metabolic intermediates, as well as post-translational modifications of these metabolic enzymes constitute the acute control of these pathways, and the controlled expression of the genes encoding these enzymes is critical in mediating the longer-term regulation of these metabolic pathways. Notably, several key transcription factors are shown to be involved in the control of glucose metabolism including glycolysis and gluconeogenesis in the liver. In this review, we would like to illustrate the current understanding of glucose metabolism, with an emphasis on the transcription factors and their regulators that are involved in the chronic control of glucose homeostasis. Hundreds of liver enzymes are involved in the body's processing of glucose. Together these enzymes help the body to maintain blood glucose levels and convert excessive carbohydrates into fatty acids. Seung-Hoi Koo and colleagues at Korea University. The researchers explain how these different liver enzymes are tightly regulated by several key transcription factors, including sterol regulatory element binding protein 1c (SREBP-1c), carbohydrate response element binding protein (ChREBP), cAMP response element-binding protein (CREB) and forkhead box protein O1 (FoxO1). Specifically, SREBP-1c and ChREBP are responsible for the chronic activation of glycolysis and fatty acid biosynthesis, while CREB and FoxO1 are responsible for the chronic activation of gluconeogenesis—the production of glucose from non-carbohydrate sources.