The study was performed to confirm the high prevalence of metabolic syndrome in gouty patients and to define the relationship between insulin resistance and gouty arthritis. We recruited 83 patients with gouty arthritis and checked clinical factors according to the diagnostic criteria of metabolic syndrome from the ATP III guidelines and WHO Asia-Pacific obesity criteria recommendations. We also assessed the clinical characteristics of subjects and homeostasis model assessment of insulin resistance (HOMA-IR) and compared with previous study groups as controls. The prevalence of metabolic syndrome in patients with gout was 30.1% according to ATP III criteria and 50.6% with WHO Asia-Pacific adjustment and is significantly higher than the previous control study groups (ATP III: 5.2, 10.6%, WHO Asia-Pacific adjustment: 9.8, 13.9%). The mean value of HOMA-IR in patients with gout was 2.63 ± 1.36 and is significantly higher than control study (1.91 ± 1.01, P < 0.05). There were significant correlations between 24-h urinary uric acid excretion and waist circumference (r(2) = 0.225, P = 0.049), fasting insulin (r(2) = 0.241, P = 0.035), and insulin resistance (HOMA-IR) (r(2) = 0.271, P = 0.017). There were significant correlations between insulin resistance and waist circumference (r(2) = 0.341, P < 0.01), BMI (r(2) = 0.390, P < 0.01). The value of HOMA-IR (insulin resistance) and the prevalence of metabolic syndrome in patients with gout are significantly higher than normal healthy control groups. The hyperuricemia in gout might be caused by the increased adiposity associated with insulin resistance.
Eucommia ulmoides Oliver is a natural product widely used as a dietary supplement and medicinal plant. Here, we examined the potential regulatory effects of Eucommia ulmoides Oliver extracts (EUE) on hepatic dyslipidemia and its related mechanisms by in vitro and in vivo studies. EUE and its two active constituents, aucubin and geniposide, inhibited palmitate-induced endoplasmic reticulum (ER) stress, reducing hepatic lipid accumulation through secretion of apolipoprotein B and associated triglycerides and cholesterol in human HepG2 hepatocytes. To determine how EUE diminishes the ER stress response, lysosomal and proteasomal protein degradation activities were analyzed. Although proteasomal activity was not affected, lysosomal enzyme activities including V-ATPase were significantly increased by EUE as well as aucubin and geniposide in HepG2 cells. Treatment with the V-ATPase inhibitor, bafilomycin, reversed the inhibition of ER stress, secretion of apolipoprotein B, and hepatic lipid accumulation induced by EUE or its component, aucubin or geniposide. In addition, EUE was determined to regulate hepatic dyslipidemia by enhancing lysosomal activity and to regulate ER stress in rats fed a high-fat diet. Together, these results suggest that EUE and its active components enhance lysosomal activity, resulting in decreased ER stress and hepatic dyslipidemia.
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