Expression of proinflammatory genes PPARγ, PDK4, Rantes, interferon-inducible protein 10, and inducible nitric oxide synthase were all increased in hepatoma cells following transfection of WT IKKε, but not a kinase-inactive mutant IKKε. This indicates IKKε functions to regulate hepatic inflammation and provides further evidence supporting a direct role for IKKε in the phenotype of the IKKε knockout Barasertib ic50 mice independent of decreased obesity. This study by Chiang and coworkers has important clinical implications but raises many additional questions. For instance, what are the cellular signals regulating IKKε, potentiating its role in inflammation, insulin resistance, and regulation

of energy balance? Do the results of this study translate to humans and does increased activation of IKKε cause obesity in humans? Although it is intriguing to speculate that IKKε may emerge as an attractive therapeutic target for obesity and obesity-related diseases, the critical role of IKKε in viral immunity cannot be Trichostatin A order overlooked; IKKε knockout mice are prone to lethal viral infections.17 If the role of IKKε in inflammation and energy balance can be dissected from its function in innate immunity either by specific pharmacologic inhibitors or

conditional/tissue-specific genetic modification, it is possible that IKKε may indeed represent an attractive therapeutic target for obesity. “
“The nutritional state of living donor liver transplantation (LDLT) recipients is one of the most important factors affecting postoperative outcome. Although the assessment of health-related quality of life (HRQOL) is of increasing importance, few studies have examined this in conjunction with LDLT recipient nutritional state. Ten LDLT recipients 上海皓元 with end-stage liver disease were recruited for this study. Measurements of energy expenditure, anthropometrics and laboratory data were performed before and 1, 6 and 12–24 months after

LDLT. HRQOL was measured by using the 36-item Short-Form (SF-36) before and 1, 3, 6 and 12–24 months after LDLT. The preoperative value of non-protein respiratory quotient (npRQ) was 0.796 ± 0.026 and it increased significantly after the operation. Serum non-esterified fatty acid (NEFA) levels were high in the preoperative state, but had significantly decreased 1 month after the operation. A negative correlation between npRQ and NEFA was observed throughout the study period. Cholinesterase and albumin levels improved to normal levels within 6 and 12–24 months, respectively. The recovery of the physical component summary of the SF-36 was observed after the improvement of all domains of laboratory data and energy metabolism based on the nutritional state. This study demonstrated that the recovery of metabolic function, laboratory data and HRQOL in LDLT recipients are variable, and it took more than 6 months to normalize the liver protein synthetic capacity and physical HRQOL score periods.