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hypertriglyceridemia/phosphatase

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Curcumin inhibits hepatic protein-tyrosine phosphatase 1B and prevents hypertriglyceridemia and hepatic steatosis in fructose-fed rats.

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High consumption of dietary fructose is an important contributory factor in the development of hepatic steatosis in insulin or leptin resistance. We investigated the effects of curcumin on fructose-induced hypertriglyceridemia and liver steatosis and explored its preventive mechanisms in rats.

Hepatic oxidative stress promotes insulin-STAT-5 signaling and obesity by inactivating protein tyrosine phosphatase N2.

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Hepatic insulin resistance is a key contributor to the pathogenesis of obesity and type 2 diabetes (T2D). Paradoxically, the development of insulin resistance in the liver is not universal, but pathway selective, such that insulin fails to suppress gluconeogenesis but promotes lipogenesis,
In liver, glucose-6-phosphatase catalyzes the hydrolysis of glucose-6-phosphate (G6P) to glucose and inorganic phosphate, the final step in the gluconeogenic and glycogenolytic pathways. Mutations in the glucose-6-phosphatase catalytic subunit (G6Pase) give rise to glycogen storage disease (GSD)

Combined deficiency of glucose-6-phosphatase and fructose-1, 6-diphosphatase. Studies of glucagon secretion and fuel utilization.

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An adult woman with hypoglycemia, hyperlactatemia, hyperuricemia, hypertriglyceridemia, hyperketonemia and inability to make new glucose from galactose, fructose, glycerol and alanine was found to have no hepatic glucose-6-phosphatase and deficient fructose-1,6-diphosphatase. Nonautonomous
OBJECTIVE Hepatic dysfunction, due to parenteral nutrition, may become severe and lead to cirrhosis and hepatic failure, especially in newborns and infants. This study aimed to evaluate the association between the exclusive use of total parenteral nutrition (TPN) and changes in the hepatic profile,

[Low-dose fish oil in primary hypertriglyceridemia. A randomized placebo-controlled study].

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In a double-blind, randomized, placebo-controlled trial, we prospectively investigated the effects of two low doses of fish oil (10.5 and 5.25 g daily) in capsule form in patients with primary hypertriglyceridemia. During a 6 weeks' therapy with 10.5 g fish oil, serum triglycerides decreased by a

An ANGPTL4-ceramide-protein kinase Cζ axis mediates chronic glucocorticoid exposure-induced hepatic steatosis and hypertriglyceridemia in mice.

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Chronic or excess glucocorticoid exposure causes lipid disorders such as hypertriglyceridemia and hepatic steatosis. Angptl4 (angiopoietin-like 4), a primary target gene of the glucocorticoid receptor in hepatocytes and adipocytes, is required for hypertriglyceridemia and hepatic steatosis induced

Influence of chenodeoxycholic acid on serum triglycerides in patients with primary hypertriglyceridemia.

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Administration of chenodeoxycholic acid (CDCA) to patients with primary hypertriglyceridemia caused the diminution of serum triglyceride concentrations of 54.31% and 46.04% at dosages of 500 mg/day and of 250 mg/day, respectively. Results after 1 month of treatment with 250 mg/day are not
BACKGROUND Establishing animal models with metabolic disorders similar to human metabolic syndrome (MS) is important. In terms of eliciting a full array of MS, we have previously shown that Wistar rats are more responsive to sucrose water drinking than are C57BL/6J mice. This study was aimed at

Association of the acid phosphatase (ACP1) gene with triglyceride levels in obese women.

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The acid phosphatase (ACP1) locus codes for a low molecular weight protein tyrosine phosphatase (LMPTP) that is found ubiquitously in human tissues. The *A allele of the ACP1 gene is associated with lower total enzymatic activity than the *B and *C alleles. An association between the *A allele and
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

Serum liver enzyme activities in healthy Miniature Schnauzers with and without hypertriglyceridemia.

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OBJECTIVE To determine whether hypertriglyceridemia in healthy Miniature Schnauzers is associated with high serum liver enzyme activities. METHODS Cross-sectional study. METHODS 65 Miniature Schnauzers with serum triglyceride concentrations within the reference range (group 1), 20 Miniature

Clinical Consequences of Hypertriglyceridemia-Associated Proteinuria in Miniature Schnauzers.

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BACKGROUND Primary hypertriglyceridemia is a common condition in older Miniature Schnauzers that recently has been associated with proteinuria and underlying glomerular pathology, particularly glomerular lipid thromboemboli. Consequences of glomerular disease can include hypertension, thromboembolic

Protein-tyrosine phosphatase 1B as new activator for hepatic lipogenesis via sterol regulatory element-binding protein-1 gene expression.

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Like hyperglycemia, postprandial (diet-induced) hypertriglyceridemia is thought to play crucial roles in the pathogenesis of insulin resistant/metabolic syndrome. Sterol regulatory element-binding protein-1 (SREBP-1) is a key transcription factor to induce postprandial hypertriglyceridemia. We found
A novel animal model of insulin resistance, the fructose-fed Syrian golden hamster has been previously documented to exhibit considerable hepatic very-low-density lipoprotein (VLDL) overproduction concomitant with the development of whole body insulin resistance. Here, we investigated whether
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