Abstract
The ability to detect changes in nutrient levels and generate an adequate response to these changes is essential for the proper functioning of living organisms. Adaptation to the high degree of variability in nutrient intake requires precise control of metabolic pathways. Mammals have developed different mechanisms to detect the abundance of nutrients such as sugars, lipids and amino acids and provide an integrated response. These mechanisms include the control of gene expression (from transcription to translation). This review reports the main molecular mechanisms that connect nutrients’ levels, gene expression and metabolism in health. The manuscript is focused on sugars’ signaling through the carbohydrate-responsive element binding protein (ChREBP), the role of peroxisome proliferator-activated receptors (PPARs) in the response to fat and GCN2/activating transcription factor 4 (ATF4) and mTORC1 pathways that sense amino acid concentrations. Frequently, alterations in these pathways underlie the onset of several metabolic pathologies such as obesity, insulin resistance, type 2 diabetes, cardiovascular diseases or cancer. In this context, the complete understanding of these mechanisms may improve our knowledge of metabolic diseases and may offer new therapeutic approaches based on nutritional interventions and individual genetic makeup.
Highlights
The discovery of the galactose operon in bacteria represented a key finding for the study of the regulation of metabolism
Provided evidence function is essential for the fructose-dependent increase of plasmatic levels of fibroblast growth factor-21 (FGF21), and that under suggests that AKT2 drives de novo lipogenesis in this tissue by inducing ChREBPβ transcription
We have summarized the molecular mechanisms of diet-induced gene expression, which allows the integration of nutrient signaling to metabolic homeostasis
Summary
The discovery of the galactose operon in bacteria represented a key finding for the study of the regulation of metabolism. The risk of having a metabolic syndrome (MetS) caused by a disruption of energy homeostasis is associated with overweight and obesity. This association stresses the link between lipid and glucose metabolism. How knowledge of the mechanisms that control gene expression expression offer therapeutic. The purpose of this review is tobalance; highlight current knowledge of how transcriptional participates in homeostatic energy how carbohydrates, lipids and control amino participates in homeostatic energy balance; how carbohydrates, lipids and amino acids—nutrients that can be used as energy sources—modulate transcriptional activity to achieve acids—nutrients that can be used as energy sources—modulate transcriptional activity to achieve metabolic homeostasis (Figure 1).
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