NASH was established and compared between hepatocyte-specific p38α knockout (p38α<sup>ΔHep</sup>), macrophage-specific p38α knockout (p38α<sup>ΔMΦ</sup>) and wild-type (p38α<sup>fl/fl</sup>) mice fed with high-fat diet (HFD), high-fat/high-cholesterol diet (HFHC), or methionine-and choline-deficient diet (MCD). p38 inhibitors were administered to HFHC-fed wild-type mice for disease treatment.
NASH was established and compared between hepatocyte-specific p38α knockout (p38α<sup>ΔHep</sup>), macrophage-specific p38α knockout (p38α<sup>ΔMΦ</sup>) and wild-type (p38α<sup>fl/fl</sup>) mice fed with high-fat diet (HFD), high-fat/high-cholesterol diet (HFHC), or methionine-and choline-deficient diet (MCD). p38 inhibitors were administered to HFHC-fed wild-type mice for disease treatment.
NASH was established and compared between hepatocyte-specific p38α knockout (p38α<sup>ΔHep</sup>), macrophage-specific p38α knockout (p38α<sup>ΔMΦ</sup>) and wild-type (p38α<sup>fl/fl</sup>) mice fed with high-fat diet (HFD), high-fat/high-cholesterol diet (HFHC), or methionine-and choline-deficient diet (MCD). p38 inhibitors were administered to HFHC-fed wild-type mice for disease treatment.
NASH was established and compared between hepatocyte-specific p38α knockout (p38α<sup>ΔHep</sup>), macrophage-specific p38α knockout (p38α<sup>ΔMΦ</sup>) and wild-type (p38α<sup>fl/fl</sup>) mice fed with high-fat diet (HFD), high-fat/high-cholesterol diet (HFHC), or methionine-and choline-deficient diet (MCD). p38 inhibitors were administered to HFHC-fed wild-type mice for disease treatment.
NASH was established and compared between hepatocyte-specific p38α knockout (p38α<sup>ΔHep</sup>), macrophage-specific p38α knockout (p38α<sup>ΔMΦ</sup>) and wild-type (p38α<sup>fl/fl</sup>) mice fed with high-fat diet (HFD), high-fat/high-cholesterol diet (HFHC), or methionine-and choline-deficient diet (MCD). p38 inhibitors were administered to HFHC-fed wild-type mice for disease treatment.
MTP-493 G/T polymorphism may impact NASH by modulating postprandial lipemia and lipoprotein metabolism; homozygous GG carriers have a more atherogenic postprandial lipid profile than the other genotypes, independently of adipokines and insulin resistance.
MTP-493 G/T polymorphism may impact NASH by modulating postprandial lipemia and lipoprotein metabolism; homozygous GG carriers have a more atherogenic postprandial lipid profile than the other genotypes, independently of adipokines and insulin resistance.
CYP2E1 enzyme is related to nonalcoholic steatohepatitis (NASH) due to its ability for reactive oxygen species production, which can be influenced by polymorphisms in the gene.
Cytokeratin-18 fragments increased significantly postprandially in both groups but more consistently in patients with NASH; their increase was predicted by postprandial adiponectin and FFA responses.
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily, and has been identified as a novel mediator of fatty liver disease (FLD).
MTP-493G/T polymorphism, dietary habits, adipokines and postprandial triglyceride-rich lipoproteins, high-density lipoprotein cholesterol (HDL-C) and oxidized low-density lipoprotein (oxLDL) responses to an oral fat load, were cross-sectionally correlated to oral glucose tolerance test- and frequently sampled intravenous glucose tolerance test-derived Minimal Model indexes of glucose homeostasis in 40 nondiabetic normolipidemic patients with NASH and 40 age-,sex- and body mass index-matched healthy controls.
MTP-493G/T polymorphism, dietary habits, adipokines and postprandial triglyceride-rich lipoproteins, high-density lipoprotein cholesterol (HDL-C) and oxidized low-density lipoprotein (oxLDL) responses to an oral fat load, were cross-sectionally correlated to oral glucose tolerance test- and frequently sampled intravenous glucose tolerance test-derived Minimal Model indexes of glucose homeostasis in 40 nondiabetic normolipidemic patients with NASH and 40 age-,sex- and body mass index-matched healthy controls.
HIG2 could be detected in atherosclerotic arteries and fatty liver disease, suggesting that this ubiquitously inducible HIF-1 target gene may play an important functional role in diseases associated with pathological lipid accumulation.
VEGF levels were significantly elevated in patients with simple steatosis and borderline significantly elevated in NASH patients compared to the serum levels of healthy control subjects.