What it is
Lipid metabolism in fat cells (adipocytes) is coordinated by circadian rhythms, diet and environmental temperature, but how these diverse signals are integrated at the molecular level was unknown. The authors show that the three cues converge on SLC25A34, an orphan mitochondrial transporter (one whose cargo had not been identified), to orchestrate lipid cycling. During the sleep phase, the fat cell's own clock suppresses expression of the Slc25a34 gene through REV-ERB transcriptional repressors. Entering the active phase, eating lipid-rich diets or exposure to cold lifts that repression, and lipolytic signals (signals that trigger fat breakdown) stimulate the gene's transcription through peroxisome proliferator-activated receptors.
Why it matters
The authors conclude that SLC25A34 confers circadian, dietary and temperature control on the lipid metabolism of fat cells: one carrier where all three signals meet. It is proposed to import oxaloacetate into mitochondria, supporting both the tricarboxylic acid cycle (a central metabolic pathway in mitochondria) and the production of acetyl-coenzyme A (acetyl-CoA) in the cytosol, outside the mitochondria. The extra cytosolic acetyl-CoA then fuels the synthesis of lipids and promotes the transcription of genes that enhance mitochondrial oxidation.
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Filed underCircadian rhythm and melatonin, Adipose Tissue and Metabolism, Dietary Effects on Health
