galactosamine/fedme

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The role of osteopontin in d-galactosamine-induced liver injury in genetically obese mice.

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Various epidemiological studies have shown that obesity increases the risk of liver disease, but the precise mechanisms through which this occurs are poorly understood. In the present study, we hypothesized that osteopontin (OPN), an extracellular matrix and proinflammatory cytokine, has an

Targeted expression of uncoupling protein 2 to mouse liver increases the susceptibility to lipopolysaccharide/galactosamine-induced acute liver injury.

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Normal hepatocytes do not express endogenous uncoupling protein 2 (UCP2) in adult liver, although Kupffer cells do, and it is strikingly induced in hepatocytes in steatotic liver and obese conditions. However, the direct link of UCP2 with the pathogenic development of liver diseases and liver injury

Genetic determinants of lipopolysaccharide and D-galactosamine-mediated hepatocellular apoptosis and lethality.

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Lipopolysaccharide and D-galactosamine induced lethality and apoptotic liver injury is dependent upon endogenously produced TNF-alpha. Unlike the response to high dose lipopolysaccharide alone, death in this model is a direct result of hepatocyte apoptosis. In a series of recent studies, we have

Hepatoprotective effects of AdipoRon against d-galactosamine-induced liver injury in mice.

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Adiponectin is an antidiabetic and antiatherogenic adipokine, which plays distinct roles in the balance of energy homoeostasis. As an insulin sensitizing hormone, adiponectin exerts multiple biological effects by the specific receptors (AdipoR1 and AdipoR2), through activation of AMP-activated

Adiponectin protects LPS-induced liver injury through modulation of TNF-alpha in KK-Ay obese mice.

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Adiponectin, an adipocytokine, has been identified in adipose tissue, and its receptors are widely distributed in many tissues, including the liver. The present study was performed to clarify the role of adiponectin in lipopolysaccharide (LPS)-induced liver injury using KK-Ay obese mice. We analyzed

Phenotypic switching of adipose tissue macrophages with obesity is generated by spatiotemporal differences in macrophage subtypes.

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OBJECTIVE To establish the mechanism of the phenotypic switch of adipose tissue macrophages (ATMs) from an alternatively activated (M2a) to a classically activated (M1) phenotype with obesity. METHODS ATMs from lean and obese (high-fat diet-fed) C57Bl/6 mice were analyzed by a combination of flow

Ambient air pollution exaggerates adipose inflammation and insulin resistance in a mouse model of diet-induced obesity.

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BACKGROUND There is a strong link between urbanization and type 2 diabetes mellitus. Although a multitude of mechanisms have been proposed, there are no studies evaluating the impact of ambient air pollutants and the propensity to develop type 2 diabetes mellitus. We hypothesized that exposure to

GALNT2 expression is reduced in patients with Type 2 diabetes: possible role of hyperglycemia.

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Impaired insulin action plays a major role in the pathogenesis of type 2 diabetes, a chronic metabolic disorder which imposes a tremendous burden to morbidity and mortality worldwide. Unraveling the molecular mechanisms underlying insulin resistance would improve setting up preventive and treatment

Reversal of type 2 diabetes in mice by products of malaria parasites. II. Role of inositol phosphoglycans (IPGs).

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We have previously shown that infection with Plasmodium yoelii malaria or injection of extracts from malaria-parasitized red cells induces hypoglycemia in normal mice and normalizes the hyperglycemia in mice made moderately diabetic with streptozotocin. Inositol phosphoglycans (IPGs) are released

Effect of glycomacropeptide fractions on cholecystokinin and food intake.

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Glycomacropeptide (GMP) is the hydrophilic 64-amino acid C-terminal glycopeptide released into cheese whey when kappa-casein is cleaved by chymosin. GMP exists as a mixture of different glycoforms due to the carbohydrates sialic acid (N-acetylneuraminic acid, NeuNAc), galactose (Gal), galactosamine

Experimental studies of transplantation and regeneration of endocrine pancreatic cells.

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Replacement of destroyed B-cells with new "healthy" ones appears to be the most physiological approach to treatment of insulin-dependent (type 1) diabetes. This could be achieved either by transplantation of isolated islets or pancreatic segments or by stimulation of the replicatory activity in the

Effects of sodium fusidate in animal models of insulin-dependent diabetes mellitus and septic shock.

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We have evaluated the effects of the novel immunosuppressant sodium fusidate (fusidin) in the non-obese diabetic (NOD) mouse and in D-galactosamine (D-Gal)-presensitized BALB/c mice challenged with the bacterial superantigen, Staphylococcus aureus enterotoxin B (SEB) or with the endotoxin,

Telmisartan improves insulin resistance and modulates adipose tissue macrophage polarization in high-fat-fed mice.

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Diet-induced obesity is reported to induce a phenotypic switch in adipose tissue macrophages from an antiinflammatory M2 state to a proinflammatory M1 state. Telmisartan, an angiotensin II type 1 receptor blocker and a peroxisome proliferator-activated receptor-γ agonist, reportedly has more

Glycomacropeptide is a prebiotic that reduces Desulfovibrio bacteria, increases cecal short-chain fatty acids, and is anti-inflammatory in mice.

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Glycomacropeptide (GMP) is a 64-amino acid (AA) glycophosphopeptide with application to the nutritional management of phenylketonuria (PKU), obesity, and inflammatory bowel disease (IBD). GMP is a putative prebiotic based on extensive glycosylation with sialic acid, galactose, and galactosamine. Our

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