Nonalcoholic hepatic steatosis in Zucker diabetic rats: spontaneous evolution and effects of metformin and fenofibrate. These abnormalities may generate cardiac hypertrophy and dysfunction, eventually leading to congestive heart failure [1, 21]. In accordance with the guiding principles established by George Ellery Hale in 1914, PNAS publishes brief first announcements of Academy Members’ and Foreign Associates’ more important contributions to research and of work that appears to a Member to be of particular importance. One of the first studies with rats consuming spirulina showed a reduction in total cholesterol levels when examining the lipid profile . Male C57BL/KsJ-db/db mice were fed a normal diet with CPE (2 g/100 g diet) or rosiglitazone (0.001 g/100 g diet) for 6 weeks. Over time, expression of DGAT1 in the heart resulted in the development of a significant cardiomyopathy. Of 6 patients with 2+ hepatic xenon, 4 had a drinking history, 1 had no drinking history recorded, and 1 was diabetic; 2 had abnormal liver-function studies.
Expression of genes associated with lipoapoptosis was decreased, whereas antioxidant protein metallothioneins were increased in diabetic Tg hearts. Indexes of diastolic function, including the ratio of maximal left ventricular early peak filling rate and the maximal left ventricular atrial peak filling rate (E/A) and E peak deceleration, were significantly impaired in T2DM compared with those in healthy subjects (1.08 ± 0.04 ml/s2 × 10−3 vs. Conversely, C/EBPβ overexpression in wild-type mice increased PPARγ2 and stearoyl-CoA desaturase-1 mRNA and hepatic triglyceride content. These results suggest the possible utility of hepatic radioxenon accumulation as a diagnostic test for fatty infiltration of the liver. Interestingly, PF-04991532 decreased intracellular AMP concentrations and increased hepatic futile cycling. Hepatic xenon-133 accumulation was studied in paired rat litter mates, one with alcohol-induced fatty liver, the control fed isocaloric glucose. Xenon accumulation was increased in fatty livers and paralleled the amount of liver fat.
During routine ventilation studies in 42 patients, hepatic xenon accumulation and retention were correlated with alcoholic drinking history and hepatic function studies. Of 15 patients without xenon accumulation, 1 had a drinking history. Of 13 patients with 1+ hepatic xenon, 5 had a drinking history, 3 were diabetic, 2 were obese, and 2 had elevated lipid levels. Of 6 patients with 2+ hepatic xenon, 4 had a drinking history, 1 had no drinking history recorded, and 1 was diabetic; 2 had abnormal liver-function studies. All 5 patients with 3+ hepatic xenon had a drinking history and abnormal liver function. Of three patients with 4+ hepatic xenon, 2 had a drinking history and abnormal liver function; the other was an obese diabetic. There was a parallel between the degree of hepatic xenon accumulation and the degree of suspected alcoholic fatty infiltration or diabetes determined from the clinical data.
These results suggest the possible utility of hepatic radioxenon accumulation as a diagnostic test for fatty infiltration of the liver.