This Research Topic is part of the
'Regulation of Lipid Metabolism in Adipose Tissue and Skeletal Muscle' series:
Regulation of Lipid Metabolism in Adipose Tissue and Skeletal MuscleObesity due to excessive deposition of lipids in adipose tissue (AT) has become a global epidemic. Together with the associated risks of chronic diseases including Type 2 Diabetes (T2D), chronic inflammation, hypertension and cancer, obesity pose formidable challenges to human health. Adipocytes are highly plastic and can uptake, esterificate and store excess lipids in the form of triacylglycerols (TAG) within lipid droplets (LDs), as well as undergo lipolysis to provide energy when nutrition is limited. Non-AT such as skeletal muscle, which has a comparatively high capacity for fatty acid oxidation to generate energy, becomes dysfunctional with 'lipid overload'. The dysregulation of lipid metabolism in skeletal muscle highly contributes to obese-related insulin resistance. Thus, understanding how lipid storage and utilization are regulated in AT and skeletal muscle are critical for the development of therapeutics to overcome obesity. Indeed, interventions that increase AT/muscle fatty acid oxidation and/or limit lipid storage have been postulated as therapies for treating obesity-related conditions.
There are two types of AT: brown adipose tissue (BAT) and white adipose tissue (WAT). BAT dissipates glucose and fatty acid (FA) to generate heat, and thus it has an important role in cold- and diet-induced thermogenesis. WAT is the main organ responsible for fat storage.
TAG serves as the predominant form of lipid storage and is synthesized within the bilayer of endoplasmic reticulum (ER) membrane. The first step for TAG synthesis is converting glycerol 3-phosphate (G-3-P) and fatty acyl CoA (FA-CoA) to lysophosphatidate (LPA). TAG and other neutral lipids are then packaged into nascent LD which is budded from ER into the cytosol. After initial budding, newly formed LDs retain a functional connectivity with the ER, and keep expanding through fusion or local lipid synthesis. Under fasting, thermogenic or exercise conditions, TAG in LDs could be hydrolyzed by an enzymatic process called lipolysis to release FAs. FAs are taken up by BAT/muscle through membrane transporters and subsequently be utilized via ß-oxidation within the mitochondria. The aim of this article collection is to promote our understanding of the whole processes of lipid metabolism within in the AT and skeletal muscle.
This Research Topic is intended to provide readers the basic research on the regulatory mechanisms of lipid metabolism in AT and skeletal muscle. We welcome Original research, Review, Mini-Review, Short communications and Perspectives articles that are related, but not limited to the following subtopics:
- White adipocyte, brown adipocyte and muscle cell differentiation.
- TAG synthesis in WAT.
- LD biogenesis and maintenance in WAT.
- Lipolysis in WAT and BAT.
- FA uptake by BAT and skeletal muscle.
- FA ß-oxidation and mitochondria function in BAT and skeletal muscle.
- Dysregulated lipid metabolism in AT and skeletal muscle from any diseases.
- Potential therapeutic strategies to target lipid metabolism in AT and skeletal muscle.
- Circadian control of lipid metabolism in AT and skeletal muscle
