Abstract
An association between sulfur amino acids (methionine, cysteine, homocysteine and taurine) and lipid metabolism has been described in several experimental and population-based studies. Changes in the metabolism of these amino acids influence serum lipoprotein concentrations, although the underlying mechanisms are still poorly understood. However, recent evidence has suggested that the enzyme stearoyl-CoA desaturase-1 (SCD-1) may be the link between these two metabolic pathways. SCD-1 is a key enzyme for the synthesis of monounsaturated fatty acids. Its main substrates C16:0 and C18:0 and products palmitoleic acid (C16:1) and oleic acid (C18:1) are the most abundant fatty acids in triglycerides, cholesterol esters and membrane phospholipids. A significant suppression of SCD-1 has been observed in several animal models with disrupted sulfur amino acid metabolism, and the activity of SCD-1 is also associated with the levels of these amino acids in humans. This enzyme also appears to be involved in the etiology of metabolic syndromes because its suppression results in decreased fat deposits (regardless of food intake), improved insulin sensitivity and higher basal energy expenditure. Interestingly, this anti-obesogenic phenotype has also been described in humans and animals with sulfur amino acid disorders, which is consistent with the hypothesis that SCD-1 activity is influenced by these amino acids, in particularly cysteine, which is a strong and independent predictor of SCD-1 activity and fat storage. In this narrative review, we discuss the evidence linking sulfur amino acids, SCD-1 and lipid metabolism.
Highlights
Methionine, homocysteine, cysteine and taurine metabolism are highly linked
cystathionine β-synthase (CβS) deficiency is the most common type of severe hyperhomocysteinemia, with an estimated worldwide prevalence of 1 in 344,000 individuals [13]. This deficiency results in classical homocystinuria, a disease characterized by increased plasma levels of homocysteine, methionine and AdoMet and decreased levels of cystathionine and cysteine
Among the main factors is SREBP-1c, a transcription factor that regulates the biosynthesis of fatty acids, LXRα and LXRβ receptors, PPARs, nuclear receptors involved in adipocyte differentiation and lipid storage and estrogen receptors, which regulate lipogenesis [28,32]
Summary
Methionine, homocysteine, cysteine and taurine metabolism are highly linked. These main sulfur amino acids are involved in several metabolic pathways such as glutathione synthesis, protein synthesis and the methylation of several substances, such as DNA, RNA, proteins and lipids [1,2,3]. The concentration of AdoMet increases, favoring sulfur amino acid metabolism through the transsulfuration pathway, via activating cystathionine β-synthase (CβS) and inhibiting 5,10-methylene-tetrahydrofolate reductase (MTHFR). CβS deficiency is the most common type of severe hyperhomocysteinemia, with an estimated worldwide prevalence of 1 in 344,000 individuals [13] In humans, this deficiency results in classical homocystinuria, a disease characterized by increased plasma levels of homocysteine, methionine and AdoMet and decreased levels of cystathionine and cysteine. A frequent polymorphism in the MTHFR gene (c.677C > T) makes the enzyme thermolabile and decreases enzymatic activity in homozygotes to 70% If their folate status is low to normal, homocysteine can increase dramatically [63]. The most frequent symptoms are developmental delays, psychiatric disorders, microangiopathy, and ocular and hematologic abnormalities [13,14]
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