Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In two separate experiments, using different strains, broiler chicks were reared on either a commercial-type chick mash (control) or a fatty liver and kidney syndrome (FLKS)-inducing diet. In Expt a, chicks were killed on day 29 and in Expt b, on day 32. Body-weights and liver weights were measured, and values from those given the control ration used to construct a hepatomegaly index by employing a variant of linear discriminant analysis. Application of the index to FLKS birds revealed a statistically significant bimodal distribution of liver size. The birds with enlarged livers (high index) also possessed metabolic abnormalities in that 6-phosphofructokinase (EC 2.7.1.11; PFK-1) activity (measured at low substrate concentration) was depressed despite the presence of normal, or even slightly elevated fructose 2,6-bisphosphate concentration. This indicates the presence of an uncharacterized regulatory mechanism for PFK-1 in FLKS-susceptible birds.
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PMID:Biotin deficiency and susceptibility to fatty liver and kidney syndrome in broiler chicks: reduced 6-phosphofructokinase (EC 2.7.1.11) activity but normal fructose 2,6-bisphosphate content in birds with hepatomegaly. 293 68

Akt is critical in insulin-induced metabolism of glucose and lipids. To investigate functions induced by hepatic Akt activation, a constitutively active Akt, NH(2)-terminally myristoylation signal-attached Akt (myr-Akt), was overexpressed in the liver by injecting its adenovirus into mice. Hepatic myr-Akt overexpression resulted in a markedly hypoglycemic, hypoinsulinemic, and hypertriglyceridemic phenotype with fatty liver and hepatomegaly. To elucidate the sterol regulatory element binding protein (SREBP)-1c contribution to these phenotypic features, myr-Akt adenovirus was injected into SREBP-1 knockout mice. myr-Akt overexpression induced hypoglycemia and hepatomegaly with triglyceride accumulation in SREBP-1 knockout mice to a degree similar to that in normal mice, whereas myr-Akt-induced hypertriglyceridemia in knockout mice was milder than that in normal mice. The myr-Akt-induced changes in glucokinase, phosphofructokinase, glucose-6-phosphatase, and PEPCK expressions were not affected by knocking out SREBP-1, whereas stearoyl-CoA desaturase 1 induction was completely inhibited in knockout mice. Constitutively active SREBP-1-overexpressing mice had fatty livers without hepatomegaly, hypoglycemia, or hypertriglyceridemia. Hepatic acetyl-CoA carboxylase, fatty acid synthase, stearoyl-CoA desaturase 1, and glucose-6-phosphate dehydrogenase expressions were significantly increased by overexpressing SREBP-1, whereas glucokinase, phospho-fructokinase, glucose-6-phosphatase, and PEPCK expressions were not or only slightly affected. Thus, SREBP-1 is not absolutely necessary for the hepatic Akt-mediated hypoglycemic effect. In contrast, myr-Akt-induced hypertriglyceridemia and hepatic triglyceride accumulation are mediated by both Akt-induced SREBP-1 expression and a mechanism involving fatty acid synthesis independent of SREBP-1.
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PMID:Hepatic Akt activation induces marked hypoglycemia, hepatomegaly, and hypertriglyceridemia with sterol regulatory element binding protein involvement. 1463 50

The light exposure of parenteral nutritive solutions generates peroxides such as H(2)O(2) and ascorbylperoxide [2,3-diketo-4-hydoxyperoxyl-5,6-dihydroxyhexanoic acid]. This absence of photoprotection is associated with higher plasma triacylglycerol (TG) concentration in premature infants and oxidative stress and H(2)O(2)-independent hepatic steatosis in animals. We hypothesized that ascorbylperoxide is the active agent leading to high TG. The aim was to investigate the role of ascorbylperoxide in glucose and lipid metabolism in an animal model of neonatal parenteral nutrition. Three-day-old guinea pigs received through a catheter in the jugular solutions containing dextrose plus 0, 90, 225, or 450 microM ascorbylperoxide. After 4 days, blood and liver were sampled and treated for determinations of TG, cholesterol, markers of oxidative stress (redox potential of glutathione and F(2alpha)-isoprostane), and activities and protein levels of acetyl-CoA carboxylase (ACC), glucokinase, and phosphofructokinase (PFK). Ascorbylperoxide concentration was measured in urine on the last day. Data were compared by analysis of variance (p < 0.05). Plasma TG and cholesterol and hepatic PFK activity increased (200% of control), whereas ACC activity decreased (66% of control) in the function of the amount of ascorbylperoxide infused. Both markers of oxidative stress were higher in animals receiving the highest amounts of ascorbylperoxide. The logarithmic relations between urinary ascorbylperoxide and plasma TG (r(2) = 0.69) and hepatic PFK activity (r(2) = 0.26) were positive, whereas they were negative with ACC activity (r(2) = 0.50). In conclusion, ascorbylperoxide contaminating parenteral nutrition stimulates glycolysis, allowing higher availability of substrates for lipid synthesis. The logarithmic relation between urinary ascorbylperoxide and plasma TG suggests a very low efficient concentration.
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PMID:Ascorbylperoxide contaminating parenteral nutrition perturbs the lipid metabolism in newborn guinea pig. 2037 99