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Background: There is a myriad of metabolic roles of omega-3 fatty acids. More recently, studies have looked at omega-3 fatty acids effects on skeletal muscle. Objectives: The objective was to determine their effects in situations such as physical activity, obesity, sarcopenia and cachexia. Methods: Bibliographic searches focused on the PubMed database, looking in priority at systematic reviews, until November 2023. Twenty-seven papers were finally included. Results: Omega-3 fatty acids could increase protein anabolism, reduce protein catabolism in the context of exercise-related muscle damages, and could induce beneficial mitochondrial modifications. In obesity, omega-3 fatty acids participate in weight loss and its maintenance, and can help decrease insulin resistance. In sarcopenia atrophic conditions, omega 3 fatty acids allow muscle mass and function maintenance. In cancer cachexia, omega 3 fatty acids are more efficient at the pre-cachectic stage, as they can reduce protein catabolism and increase protein anabolism, but cannot reverse energy imbalance. Conclusions: Omega 3 fatty acids have multiple beneficial effects on skeletal muscle in physical activity, obesity, sarcopenia and cachexia. Yet, these effects are mediated by EPA and DHA, whose sources are solely of marine origins. As marine resources are overexploited, finding diverse sources of omega-3 fatty acids is crucial.

In addition to the major fatty acids widely studied, our diet contains many bioactive fatty acids less frequently investigated such as n-3 docosapentaenoic acid (n-3 DPA), natural trans fatty acids, conjugated fatty acids (CLAs), furan fatty acids (FuFAs), branched chain fatty acids (BCFAs) and fatty acid esters of hydroxyl fatty acids (FAHFAs). Many of them may have beneficial health effects, particularly in the prevention of cardiovascular diseases, inflammation and metabolic disorders such as diabetes. This review aims to give a brief overview of the current knowledge on these lipids. Thus, information about biosynthesis, food and tissue content, daily intake, biological and potential health effects of these fatty acids is provided.

Thyroid hormone exerts a diversity of physiological influences over developmental and metabolic processes. Searching for receptors able to mediate this extended regulation led to the identification of triiodothyronine (T3) nuclear receptors encoded by two different genes, c-erbA alpha (TR alpha) and c-erbA beta (TR beta). More recently, two N-terminally truncated forms of the triiodothyronine nuclear receptor TR alpha 1, with molecular weights of 43 and 28 kDa, have been discovered in mitochondria. Synthesized through the use of internal initiation sites of translation occurring in the TR alpha 1 transcript, they are addressed into mitochondria according to an atypical process. Two mitochondrial import sequences have been characterized in the C-terminal part of these proteins; in addition, their N-terminal part, devoid of negative charges, plays a permissive role in this import. Whereas the function of p28 remains unknown, p43 is a T3-dependent transcription factor of the mitochondrial genome, acting through dimeric complexes involving at least two other truncated forms of nuclear receptors, mtRXR and mtPPAR. P43 activation by T3 stimulates mitochondrial protein synthesis, respiratory chain activity and mitochondriogenesis. Through the mitochondrial/nuclear crosstalk, this direct T3 mitochondrial pathway influences the expression of nuclear genes involved in the regulation of cell proliferation and differentiation. In particular, in myoblasts, p43 overexpression stimulates terminal differentiation and induces a preferential expression of slow myosin, by down-regulating c-Myc expression and up-regulating calcineurin and myogenin expression. Comparison of the respective influences of the nuclear and mitochondrial T3 pathways demonstrates either both additivity (myoblast differentiation), complementarity (mitochondriogenesis, myoblast differentiation) or opposite influences (myosin expression), thus indicating that these two pathways introduce a fine-tuning of the hormone influence.