Association between handgrip strength and metabolic syndrome in relation to gender and adiposity among middle aged and older Saudi populations.

AIM: This cross-sectional study investigated the association between metabolic syndrome (MetS) and handgrip strength (HGS) with respect to sex and adiposity in Saudi men (n = 287) and women (n = 268). MATERIAL AND METHODS: Anthropometry, body composition, HGS, and blood biochemistry were measured. The average age of the study population was 57.65 ± 9.3 years (men = 55.1 ± 9.3 years, women = 60.4 ± 9.3 years). We report that HGS/body mass index (BMI), HGS/weight, and HGS/fat (%) were significantly higher in controls than in patients with MetS in men but not in women. According to the ROC analysis, relative HGS (RHGS) was higher than HGS alone in the association with MetS, which was significant for men (p < 0.01). At lower quartiles of HGS, the probability of MetS was higher in women, and the same was found in men in the lower quartiles of HGS/%Fat. Multinomial regression revealed significant associations between age and adiposity and MetS in men and HGS in women. Additionally, the linear regression of age, HGS, and weight exhibited significant associations between HGS with WC in both sexes. CONCLUSION: A higher risk of MetS in the lower quartiles of HGS was found in women, and adiposity moderated the relationship between HGS and MetS in men.

Isoliquiritigenin prevents Doxorubicin-induced hepatic damage in rats by upregulating and activating SIRT1.

This study evaluated if the hepatic protective effect of Isoliquiritigenin (ISL) against doxorubicin (DOX)-treated rats involves upregulating sirtuin-1 (SIRT1) signaling. Adult male was divides into 5 groups (n = 6 rats/each) as control (vehicle), ISL (25 mg/kg), DOX (15 mg/kg), DOX + ISL, and DOX + ISL + EX-527 (a SIRT1 inhibitor, 5 mg/kg). ISL and EX-527 were administered 10 days before and after the single treatment of DOX. Also, cultured AML-12 hepatocytes (5 ×104) were treated with 10 µM of ISL for 24 h with or without DOX-treatments (10 µM) and in the presence or absence of EX-527 (5 µM). ISL prevented hepatocyte damage and decreased serum levels of hepatic transaminases, hepatic levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and hepatic mRNA levels of Bax and caspases-3,8, and 9. In the liver of the control and DOX-treated rats, ISL reduced levels of malondialdehyde (MDA) but increased hepatic levels of glutathione (GSH), superoxide dismutase (SOD), and catalase, as well as mRNA levels of Bcl2. In vitro, ISL stimulated cell survival and lowered levels of ROS but increased GSH levels. In vivo and in vitro, in the livers of control and DOX-treated animals, ISL significantly increased the nuclear activity and mRNA levels of SIRT1, enhanced the nuclear levels of Nrf2, and reduced nuclear levels of NF-κB p65. In conclusion, ISL alleviates DOX-induced hepatocyte toxicity by stimulating the Nrf2/antioxidants axis and concomitant suppression of NF-κB, mainly by upregulating/activating SIRT1.