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glutamate dehydrogenase/nutukimas

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The Amplifying Pathway of the β-Cell Contributes to Diet-induced Obesity.

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Efficient energy storage in adipose tissues requires optimal function of the insulin-producing β-cell, whereas its dysfunction promotes diabetes. The associated paradox related to β-cell efficiency is that excessive accumulation of fat in adipose tissue predisposes for type 2 diabetes. Insulin

Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice.

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Pancreatic beta cell (β) dysfunction is an outcome of malnutrition. We assessed the role of the amplifying pathway (AMP PATH) in β cells in malnourished obese mice. C57Bl-6 mice were fed a control (C) or a low-protein diet (R). The groups were then fed a high-fat diet (CH and RH). AMP PATH
Low-protein diet impairs insulin secretion in response to nutrients and may induce several metabolic disorders including diabetes, obesity, and cardiovascular disease. In the present study, the influence of leucine supplementation on glutamate dehydrogenase (GDH) expression and glucose-induced

Amino acid metabolism enzyme activities in the obese Zucker rat.

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Hepatic serine dehydratase activity was significantly lower in the obese Zucker rats. In both skeletal muscle and kidney adenylate deaminase showed a lower activity in the obese animals. In the small intestine the activity of glutamate dehydrogenase was increased while that of glutamine synthetase

Brown and white adipose tissue adaptive enzymatic changes on amino acid metabolism in persistent dietary-obese rats.

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The objective was to determine the effects of persistent obesity on amino acid enzymes in white (WAT) and brown (BAT) adipose tissues. Dietary obesity was induced by feeding a cafeteria diet ad libitum for 3 months, then it was removed and the obese animals received the same diet as controls for 5
Glucose homeostasis is determined by insulin secretion from the ß-cells in pancreatic islets and by glucose uptake in skeletal muscle and other insulin target tissues. While glutamate dehydrogenase (GDH) senses mitochondrial energy supply and regulates insulin secretion, its role in the muscle has

Oxidative stress and altered lipid homeostasis in the programming of offspring fatty liver by maternal obesity.

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Changes in the maternal nutritional environment during fetal development can influence offspring's metabolic risk in later life. Animal models have demonstrated that offspring of diet-induced obese dams develop metabolic complications, including nonalcoholic fatty liver disease. In this study we
The proteome of liver biopsies from human obese (O) subjects has been compared to those of nonobese (NO) subjects using two-dimensional gel electrophoresis (2-DE). Differentially represented proteins were identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass
Non-alcoholic fatty liver disease is known as determining part of human obesity. The impact of body weight (BW) gain on liver metabolism has not been extensively investigated yet.To investigate hepatic alterations caused by increasing BW in ponies and

Impaired FAD-glycerophosphate dehydrogenase activity in islet and liver homogenates of fa/fa rats.

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The mitochondrial FAD-linked enzyme glycerophosphate dehydrogenase plays a key role in the pancreatic B-cell glucose sensing device. In the present study, the activity of this enzyme was examined in islets of fa/fa rats in which inherited diabetes mellitus is associated with obesity, hyperinsulinism

Adipose tissue proteomes of intrauterine growth-restricted piglets artificially reared on a high-protein neonatal formula.

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The eventuality that adipose tissues adapt to neonatal nutrition in a way that may program later adiposity or obesity in adulthood is receiving increasing attention in neonatology. This study assessed the immediate effects of a high-protein neonatal formula on proteome profiles of adipose tissues in

Metabolic adaptations in the liver of born long-distance running mice.

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OBJECTIVE Long-distance runners have increased needs of energy supply. To unravel genetically based mechanisms required for efficient energy supply, we have analyzed hepatic metabolism of mice characterized by the inborn capacity to perform as long-distance runners. METHODS The mouse model had been
OBJECTIVE Intrauterine growth restriction (IUGR) has been shown to induce the programming of metabolic disturbances and obesity, associated with hypothalamic derangements. The present study aimed at investigating the effects of IUGR on the protein and metabolite profiles of the hypothalamus of adult
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in humans, and ranges from steatosis to non-alcoholic steatohepatitis (NASH), the latter with risk of progression to cirrhosis. The Göttingen Minipig has been used in studies of obesity and diabetes, but liver

The Relevance of the UPS in Fatty Liver Graft Preservation: A New Approach for IGL-1 and HTK Solutions.

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The 26S proteasome is the central proteolytic machinery of the ubiquitin proteasome system (UPS), which is involved in the degradation of ubiquitinated protein substrates. Recently, UPS inhibition has been shown to be a key factor in fatty liver graft preservation during organ cold storage using
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