Sirtuin 1 (SIRT1) is a deacetylase enzyme that plays crucial roles in controlling many cellular processes and its downregulation has been implicated in different metabolic disorders.
The inhibition of miR-122 protects hepatocytes from lipid metabolic disorders such as NAFLD and suppresses lipogenesis via elevating Sirt1 and activating the AMPK pathway.
Sirtuin 1 (SIRT1), an NAD<sup>+</sup>-dependent deacylase, has been identified to be associated with renal tubular inflammatory conditions and metabolic disorders, which are risk factors of nephrolithiasis.
In this study we investigate whether SIRT1 activation in early childhood can mitigate metabolic disorders due to maternal and postnatal high-fat feeding in mice.
SIRT1 plays a key role in the pathophysiology of metabolic diseases and neurodegenerative disorders, and is considered to protect against age-related diseases including cancer.
SIRT1 is a key member of Sirtuins, playing important roles in aging and energy metabolism, which has been reported to be involved in various metabolic diseases and tumors.
Our study points out that targeting the activation of the AMPK/Sirt1/PGC1α pathway by GA or its derivatives might be a potential therapeutic intervention for insulin resistance in metabolic diseases.
HCV core protein induces alterations in cellular redox state (decrease in the NAD(+)/NADH ratio), which could influence the activity of SIRT1 and secondarily AMPK, then change the expression profile of glucose and lipid metabolism-related genes, thereby causing metabolism disorders of hepatocytes.
This review will discuss the latest advances in this field, focusing on beneficial roles of SIRT1 in hepatic lipid metabolism including its potential as a therapeutic target for treatment of steatosis and other obesity-related metabolic diseases.
Although the extrapolation of data obtained from yeast Sir2p to mammalian SIRT1cannot be automatic, animal studies provide convincing evidence that SIRT1 is a potent protector against aging-associated pathologies, in particular metabolic disorders and cardiovascular diseases.
These attractive features have validated SIRT1 as a therapeutic target in the management of metabolic disease and prompted an intensive search to identify pharmacological SIRT1 activators.
Thus, both GCN5 and SIRT1 may be pharmacological targets to regulate the activity of PGC-1α, providing a potential treatment for metabolic disorders in which hepatic glucose output is altered.
A deeper understanding of the mechanistic underpinnings of Sirt1's metabolic functions is necessary to effectively design Sirt1-based therapeutic interventions for metabolic disorders.
Sirt1 targets numerous proteins, including peroxisome proliferator-activated receptor (PPAR)-gamma, PPAR-gamma coactivator (PGC)-1alpha, uncoupling protein 2 (UCP2), and nuclear factor-kappa B, which play key roles in various metabolic disorders.