Energetic cell sensors: a key to metabolic homeostasis

Naïmi, Mustapha; Arous, Caroline; Obberghen, Emmanuel Van

doi:10.1016/j.tem.2009.09.003

Cited by 29 publications

(20 citation statements)

References 72 publications

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“…In general, these systems are robust against random mutations but are vulnerable to attacks against the hub [17]. Acetyl-CoA is a key hub metabolite of the metabolic network and plays a critical role in maintaining cellular homeostasis [20]. Previous studies have implicated branchedchain amino acid degradation [21], fatty acid oxidation [22,23] and citrate cycle [22,23] dysregulation as a characteristic feature of type 2 diabetes and related traits.…”

Section: Discussionmentioning

confidence: 99%

“…Acetyl-CoA lies at the crossroads of glycolysis, citrate cycle, ketogenesis, lipid synthesis, amino acid and fatty acid metabolism, suggesting that the metabolite may play a key role as an energy sensor in the cell [20]. Carbon skeletons of sugars, amino acids and fatty acids are degraded to the acetyl group to form acetyl-CoA, which enters the citric acid cycle for energy generation.…”

Section: Discussionmentioning

confidence: 99%

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Downregulation of the acetyl-CoA metabolic network in adipose tissue of obese diabetic individuals and recovery after weight loss

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Downregulation of the acetyl-CoA metabolic network in adipose tissue of obese diabetic individuals and recovery after weight loss

et al. 2014

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“…In turn, the core clock genes receive inputs from the periphery to ensure proper between-function synchronization. For example, NAD+, a major contributor of cell metabolism, shows 24-hour oscillations [9] and has been shown to modulate the circadian activity of different key metabolites such as SIRT1 [10], AMPK [11] or PGC1-α [12]. Overall, there is growing evidence that circadian rhythms and metabolic processes maintain intricate interactions in order to ensure energy homeostasis [13–16].…”

Section: The Circadian Clock Exerts Central and Peripheral Effects Thmentioning

confidence: 99%

Nocturnin: at the crossroads of clocks and metabolism

Stubblefield¹,

Terrien²,

Green³

2012

Trends in Endocrinology & Metabolism

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Many aspects of metabolism exhibit daily rhythmicity under the control of endogenous circadian clocks, and disruptions in circadian timing result in dysfunctions associated with the metabolic syndrome. Nocturnin (Noc) is a robustly rhythmic gene that encodes a deadenylase thought to be involved in the removal of polyA tails from mRNAs. Mice lacking the Noc gene display resistance to diet-induced obesity and hepatic steatosis, due in part to reduced lipid trafficking in the small intestine. In addition, Noc appears to play important roles in other tissues and has been implicated in lipid metabolism, adipogenesis, glucose homeostasis, inflammation and osteogenesis. Therefore, Noc is a potential key post-transcriptional mediator in the circadian control of many metabolic processes.

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“…During fasting and feeding, cellular energy and metabolic states are reflected in fluctuations in levels of NAD + and acetyl-CoA [112]. Upon feeding, the levels of acetyl-CoA, coenzyme of KATs, increase (Figure 1).…”

Section: Dietary Sirtuin Activation and Metabolic Impact On K-acetmentioning

confidence: 99%

“…Upon feeding, the levels of acetyl-CoA, coenzyme of KATs, increase (Figure 1). Increased KAT activity then causes changes in chromatin dynamics and leads to the development of a certain epigenetic profile [112]. On the other hand, fasting elevates cellular NAD + levels and leads to activation of sirtuins.…”

Section: Dietary Sirtuin Activation and Metabolic Impact On K-acetmentioning

confidence: 99%

Dietary, Metabolic, and Potentially Environmental Modulation of the Lysine Acetylation Machinery

Kim

Gocevski

et al. 2010

International Journal of Cell Biology

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Healthy lifestyles and environment produce a good state of health. A number of scientific studies support the notion that external stimuli regulate an individual's epigenomic profile. Epigenetic changes play a key role in defining gene expression patterns under both normal and pathological conditions. As a major posttranslational modification, lysine (K) acetylation has received much attention, owing largely to its significant effects on chromatin dynamics and other cellular processes across species. Lysine acetyltransferases and deacetylases, two opposing families of enzymes governing K-acetylation, have been intimately linked to cancer and other diseases. These enzymes have been pursued by vigorous efforts for therapeutic development in the past 15 years or so. Interestingly, certain dietary components have been found to modulate acetylation levels in vivo. Here we review dietary, metabolic, and environmental modulators of the K-acetylation machinery and discuss how they may be of potential value in the context of disease prevention.

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Energetic cell sensors: a key to metabolic homeostasis

Cited by 29 publications

References 72 publications

Downregulation of the acetyl-CoA metabolic network in adipose tissue of obese diabetic individuals and recovery after weight loss

Downregulation of the acetyl-CoA metabolic network in adipose tissue of obese diabetic individuals and recovery after weight loss

Nocturnin: at the crossroads of clocks and metabolism

Dietary, Metabolic, and Potentially Environmental Modulation of the Lysine Acetylation Machinery

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