Tissue-specific fat metabolism and insulin actions regulate ectopic fat accumulation, with outcomes of de novo lipogenesis and adipogenesis differing across subcutaneous adipose tissue, liver, and muscle.
BACKGROUND: The accumulation of ectopic fats is related to metabolic syndromes with insulin resistance, which is considered as the first hit in obesity-related diseases. However, systematic understanding of the occurrence of ectopic fats is limited, since organisms are capable of orchestrating complicated intracellular signaling pathways to ensure that the correct nutritional components reach the tissues where they are needed. Interestingly, tissue-specific mechanisms lead to different consequences of fat metabolism with different insulin sensitivities. AIM OF REVIEW: To summarize the mechanisms of fat deposition in different tissues including adipose tissue, subcutis, liver, muscle and intestines, in an attempt to elucidate interactive mechanisms involving insulin actions and establish a potential reference for the rational uptake of fat. KEY SCIENTIFIC CONCEPTS OF REVIEW: Tissue-specific fat metabolism serves as a trigger for developing abnormal fat metabolism or as a compensatory agent for regulating normal fat metabolism. Outcomes of de novo lipogenesis and adipogenesis differ in the subcutaneous adipose tissue (SAT), liver and muscle, with the participation of insulin actions. Overload of lipid metabolic capability results in SAT fat expansion, and ectopic fat accumulation implicates impaired lipo-/adipogenesis in SAT. Regulating insulin actions may be a key measure on fat deposition and metabolism in individuals.
Wu et al. (Sat,) conducted a review in Metabolic syndromes with insulin resistance and ectopic fat accumulation. Tissue-specific fat metabolism and insulin actions was evaluated. Tissue-specific fat metabolism and insulin actions regulate ectopic fat accumulation, with outcomes of de novo lipogenesis and adipogenesis differing across subcutaneous adipose tissue, liver, and muscle.