Abstract
Gluconeogenesis in the liver converts lipids and several other noncarbohydrate precursors into glucose, ensuring that blood sugar levels are maintained at healthy levels, especially during fasting. Effective regulation of gluconeogenesis is therefore critical for maintaining systemic metabolic homeostasis. Zhang and colleagues have discovered that the ubiquitous transcriptional regulator nuclear factor Y (NF-Y) confers cAMP responsiveness to key gluconeogenic genes and up-regulates hepatic glucose production. The study expands our understanding of transcriptional regulation of hepatic gluconeogenesis and also presents critical insights into the function of NF-Y in the liver.
Highlights
Besides its many other functions in the body, the liver is a major storage organ for glucose in its immobile form, glycogen
Previous observations have indicated that cAMP signaling extensively controls gluconeogenesis via cAMP response element– binding protein (CREB), but other, yet unknown effectors besides CREB appear to be required for regulating gluconeogenesis
Nuclear factor Y (NF-Y) is a ubiquitous, evolutionarily conserved transcription factor that is a cAMP target in other cells that respond to sugar, such as those in the pancreas
Summary
Besides its many other functions in the body, the liver is a major storage organ for glucose in its immobile form, glycogen. Epigenetic regulators of glucose homeostasis control gluconeogenic gene transcription (6). Previous observations have indicated that cAMP signaling extensively controls gluconeogenesis via CREB, but other, yet unknown effectors besides CREB appear to be required for regulating gluconeogenesis.
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