Highlights d COQ9 specifically accesses and binds membraneembedded aromatic isoprenes d An exposed tryptophan and an amphipathic helix control lipid and membrane binding d Interactions with the peripheral membrane enzyme COQ7 suggest lipid presentation d In vivo CoQ production relies on COQ9's membrane, lipid, and protein interactions
Thermogenesis is an energy demanding process by which endotherms produce heat to maintain their body temperature in response to cold exposure. Mitochondria in the brown and beige adipocytes play a key role in thermogenesis, as the site for uncoupling protein 1 (UCP1), which allows for the diffusion of protons through the mitochondrial inner membrane to produce heat. To support this energy demanding process, the mitochondria in brown and beige adipocytes increase oxidation of glucose, amino acids, and lipids. This review article explores the various mitochondria-produced and processed lipids that regulate thermogenesis including cardiolipins, free fatty acids, and acylcarnitines. These lipids play a number of roles in thermogenic adipose tissue including structural support of UCP1, transcriptional regulation, fuel source, and activation of cell signaling cascades.
Background
Chronic pain in adolescence is associated with diminished outcomes, lower socioeconomic status in later life, and decreased family well-being. Approximately one third of adolescents with chronic pain have obesity compared to the general population. In obesity, lipid signals regulate insulin sensitivity, satiety, and pain sensation. We determined whether there is a distinct lipid signature associated with chronic pain and its co-occurrence with obesity in adolescents.
Methods
We performed global lipidomics in serum samples from female adolescents (N = 67, 13–17 years old) with no pain/healthy weight (Controls), chronic pain/healthy weight (Pain Non-obese), no pain/obesity (Obese), or chronic pain/obesity (Pain Obese).
Results
The Pain Non-obese group had lipid profiles similar to the Obese and Pain Obese groups. The major difference in these lipids included decreased lysophosphatidylinositol (LPI), lysophosphatidylcholine (LPC), and lysophosphatidylethanolamine (LPE) in the three clinical groups compared to the Control group. Furthermore, ceramides and sphingomyelin were higher in the groups with obesity when compared to the groups with healthy weight, while plasmalogens were elevated in the Pain Obese group only.
Conclusions
Serum lipid markers are associated with chronic pain and suggest that specific lipid metabolites may be a signaling mechanism for inflammation associated with co-occurring chronic pain and obesity.
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