Our data suggest that genetic variation in SIRT1 increases the risk for obesity, and that SIRT1 genotype correlates with visceral obesity parameters in obese men.
In 6,251 elderly subjects from the prospective, population-based Rotterdam Study, three single nucleotide polymorphisms (SNPs) in the SIRT1 gene were studied in relation to BMI and risk of obesity (BMI > or =30 kg/m(2)) and prospectively with BMI change after 6.4 years of follow-up.
To evaluate the role of mammalian Sirt1 and Sirt1 activators in the protection from metabolic disorders such as diet-induced obesity, diabetes type 2, or nonalcoholic fatty liver disease.
Replication of our findings and further in-depth studies of dietary patterns that modify SIRT1 may lead to clinical studies of dietary modification of SIRT1 to influence obesity.
The purpose of this study was to determine whether variation in SIRT1 affects susceptibility to obesity or type 2 diabetes in Pima Indians, a population with very high prevalence and incidence rates of these diseases.
Here, we demonstrate that adenovirus-mediated overexpression of SIRT1 in the liver of diet-induced insulin-resistant low-density lipoprotein receptor-deficient mice and of genetically obese ob/ob mice attenuates hepatic steatosis and ameliorates systemic insulin resistance.
Transcript expression was significantly correlated to BMI in the lean siblings (r(2) = 0.13, P value = 3.36 × 10(-7)) and lower SIRT1 expression was associated with obesity (P value = 1.56 × 10(-35)).
SIRT1 gene has been connected to many cellular processes and implicated in human diseases, such as obesity, type 2 diabetes, cancer and neurodegenerative diseases.
SIRT1 has been involved in many cellular processes and implicated in human diseases, such as obesity, type 2 diabetes, cancer and neurodegenerative diseases.
To develop a SIRT1 and circadian locomotor output cycles kaput (CLOCK) combined genotype and to assess its associations with the chronotype of subjects and their potential resistance to weight loss in a behavioral treatment for obesity based on a Mediterranean diet.
Aside from adiposity itself, the high caloric intake that leads to obesity also may heighten chronic kidney disease risk via the circuitous loop between Sirt1 and adiponectin and podocyte effacement.
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.
Under lean conditions, CREB acetylation was low due to an association with the energy-sensing NAD(+)-dependent deacetylase SirT1; amounts of acetylated CREB were increased in obesity, when SirT1 undergoes proteolytic degradation.
Central Sirt1 regulates body weight and energy expenditure along with the POMC-derived peptide α-MSH and the processing enzyme CPE production in diet-induced obese male rats.
In addition, an α-MG supplement up-regulated hepatic AMPK, SirT1, and PPARγ levels compared with the high-fat diet states, suggesting that α-MG regulates hepatic steatosis and obesity through the SirT1-AMPK and PPARγ pathways in high-fat diet-induced obese mice.
SIRT1 polymorphisms exhibited no main effects, but modified the association between obesity measures and FEV1/FVC and FEF25-75 decline (p = 0.009-0.046).
The effects of green cardamom on blood glucose indices, lipids, inflammatory factors, paraxonase-1, sirtuin-1, and irisin in patients with nonalcoholic fatty liver disease and obesity: study protocol for a randomized controlled trial.
These findings indicate that zerumbone ameliorated diet-induced obesity and inhibited adipogenesis, and that the underlying mechanisms involved AMPK and the microRNA-146b/SIRT1 pathway.