Skeletal muscle is composed of multinuclear cells called myofibres, which are formed by the fusion of myoblasts during development. The size of the muscle fiber and mass of skeletal muscle are altered in response to several pathological and physiological conditions. Skeletal muscle regeneration is primarily mediated by muscle stem cells called satellite cells (SCs). In response to injury, these SCs replenish myogenic progenitor cells to form new myofibers to repair damaged muscle. During myogenesis, activated SCs proliferate and differentiate to myoblast and then fuse with one another to form muscle fibers. A reduced number of SCs and an inability to undergo myogenesis may contribute to skeletal muscle disorders such as atrophy, cachexia, and sarcopenia. Myogenic regulatory factors (MRF) are transcription factors that regulate myogenesis and determines whether SCs will be in the quiescent, activated, committed, or differentiated state. Mitochondria oxidative phosphorylation and oxidative stress play a role in the determination of the fate of SCs. The potential activation and function of SCs are also affected by inflammation during skeletal muscle regeneration. Omega-3 polyunsaturated fatty acids (PUFAs) show promise to reduce inflammation, maintain muscle mass during aging, and increase the functional capacity of the muscle. The aim of this critical review is to highlight the role of omega-3 PUFAs on the myogenic differentiation of SCs and pathways affected during the differentiation process, including mitochondrial function and inflammation from the current body of literature.

Maternal body mass index is associated with breast milk (BM) fatty acid composition. This study investigated the effects of BM omega (n)-6:n-3 polyunsaturated fatty acids (PUFAs) from non-obese women and women with obesity on the process of adipogenesis in 3T3-L1 preadipocytes. BM samples were collected from non-obese women (BMNO) and women with obesity (BMO) at one month postpartum. The fatty acid composition was measured, and BMNO and BMO groups with the lowest (Q1) and highest (Q4) quartiles of n-6:n-3 PUFA ratios were identified. 3T3-L1 preadipocytes were differentiated in the presence or absence of BM. Lipid accumulation and the expression of genes involved in lipogenesis and lipolysis were measured. Treatment with BMNO containing high (vs. low) n-6:n-3 PUFA ratios significantly increased the mRNA expression of lipogenic genes (acetyl-CoA carboxylase, fatty acid synthase, and stearoyl-CoA desaturase); however, there was no effect when cells were treated with BMO (with either low or high n-6:n-3 PUFA ratios). Treatment with BMO (high n-6:n-3 PUFA ratio) caused larger lipid droplets. Our findings demonstrated that BMNO with a high n-6:n-3 PUFA ratio was associated with a higher expression of lipogenic genes, while BMO with a high n-6:n-3 PUFA ratio showed larger lipid droplets, suggesting adipocyte dysfunction. These findings may have implications in the BM-mediated programming of childhood obesity.

Cancer treatment evokes impediments to liver metabolism that culminate in fatty liver. This study determined hepatic fatty acid composition and expression of genes and mediators involved in lipid metabolism following chemotherapy treatment. Female rats bearing the Ward colon tumor were administered Irinotecan (CPT-11) +5-fluorouracil (5-FU) and maintained on a control diet or a diet containing eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) (2.3 g/100 g fish oil). Healthy animals provided with a control diet served as a reference group. Livers were collected one week after chemotherapy. Triacylglycerol (TG), phospholipid (PL), ten lipid metabolism genes, leptin, and IL-4 were measured. Chemotherapy increased TG content and reduced EPA content in the liver. Expression of SCD1 was upregulated by chemotherapy, while dietary fish oil downregulated its expression. Dietary fish oil down-regulated expression of the fatty acid synthesis gene FASN, while restoring the long chain fatty acid converting genes FADS2 and ELOVL2, and genes involved in mitochondrial β-oxidation (CPT1α) and lipid transport (MTTP1), to values similar to reference animals. Neither leptin nor IL-4 were affected by chemotherapy or diet. Depletion of EPA is associated with pathways evoking enhanced TG accumulation in the liver. Restoring EPA through diet may pose a dietary strategy to attenuate chemotherapy-associated impediments in liver fatty acid metabolism.

No abstract

Objectives Fatty acid esters of hydroxy fatty acids (FAHFAs) are a novel class of endogenous lipids with suspected anti-inflammatory and anti-diabetic properties in adults. They have been reported to be present in breast milk (BM), but there is no data about their role in infant growth and nutrition. Our objective was to determine the role of maternal body mass index (BMI) on BM FAHFA composition and to delineate the association of these BM fatty acids on infant growth and adiposity. Methods This is a secondary analysis of a randomized controlled trial of maternal vitamin D supplementation during lactation (NCT00412074). We included 40 control mother-infant dyads who had BM samples at one (V1) and four (V4) months and outcome data available. At V1 and V4, maternal and infant anthropometrics were measured, dual energy absorptiometry (DXA) scans conducted, and BM samples collected. BM lipids were measured using established methods of UHPLC-C30RP/HRAM mass spectrometry. Our primary infant growth outcomes were percentage of fat and lean mass, fat mass index, and fat-free mass index. Redundancy analysis (RDA) was used to analyze the relation between individual lipids, maternal BMI, and infant growth. Focusing on V1 measurements, we computed the unadjusted associations between maternal BMI with BM lipids; BM lipids with infant growth using Pearson's correlations; and the adjusted associations of BM lipids at V1 with infant growth using linear regression with adjustment for relevant covariates. Results The mean maternal BMI was 29 kg/m2. There was no correlation between maternal BMI and reported dietary intake of fat. Higher maternal BMI was associated with a higher concentration of saturated and monounsaturated FAHFAs, and a lower concentration of polyunsaturated FAHFAs in BM at V1. In an unadjusted model, saturated and monounsaturated FAHFAs were associated with higher infant fat mass and lower lean mass. The converse was seen with polyunsaturated FAHFAs which were associated with lower infant fat mass and higher lean mass. In a fully adjusted model, these associations were attenuated but the overall pattern persisted (Table 1). Conclusions Maternal BMI influences the FAHFA composition of BM. In turn, BM FAHFA composition may play a role in programming infant growth patterns. Funding Sources The Nutritional Obesity Research Consortium Grant. Supporting Tables, Images and/or Graphs