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glutamine/offita

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Bls 1 frá 258 niðurstöður
OBJECTIVE Diet-induced obesity (DIO) is associated with insulin resistance in liver and muscle, but not in adipose tissue. Mice with fat-specific disruption of the gene encoding the insulin receptor are protected against DIO and glucose intolerance. In cell culture, glutamine induces insulin

Dysregulation of the glutamine transporter Slc38a3 (SNAT3) and ammoniagenic enzymes in obese, glucose-intolerant mice.

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OBJECTIVE Uric acid nephrolithiasis is prevalent among patients with type 2 diabetes and metabolic syndrome; it is correlated with an acidic urine and lower urinary ammonium excretion and is likely associated with insulin resistance. Insulin stimulates ammoniagenesis in renal cell lines via
OBJECTIVE Given the important role of the beta2-adrenoceptor (beta2-AR) in lipid mobilization and the lack of studies in Southern European countries, the aim of this study was to investigate the role of the glutamine 27 glutamic acid (Gln27Glu) beta2-AR polymorphism in the susceptibility to obesity
BACKGROUND The single-nucleotide polymorphism (SNP), rs1042714 or glutamine 27 glutamic acid (Gln27Glu), in the adrenoceptor β2 surface (ADRB2) gene has previously been examined for association with obesity with inconclusive results. The objective of this study was to determine whether the ADRB2
OBJECTIVE Accumulation of lipids in non-adipose tissues particularly the liver is a feature of tissue insulin resistance. Hepatic glycogen depletion reflects counter glucoregulation in an insulin-resistant state and/or obesity. The effect of l-glutamine on fructose-induced increased hepatic lipid
Obesity is a risk factor for heart failure through a set of hemodynamic and hormonal adaptations, but its contribution at the molecular level is not clearly known. Therefore, we investigated the kinetic cardiac transcriptome and metabolome in the Spontaneous Hypertensive Heart Failure (SHHF) rat.

Oral supplementation with L-glutamine alters gut microbiota of obese and overweight adults: A pilot study.

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OBJECTIVE The aim of this study was to determine whether oral supplementation with L-glutamine (GLN) modifies the gut microbiota composition in overweight and obese adults. METHODS Thirty-three overweight and obese adults, ages between 23 and 59 y and body mass index between 25.03 and 47.12 kg/m(2),

Glutamine Metabolism in Macrophages: A Novel Target for Obesity/Type 2 Diabetes.

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Obesity is a nutritional disorder resulting from a chronic imbalance between energy intake and expenditure. This disease is characterized by inflammation in multiple cell types, including macrophages. M1 macrophage responses are correlated with the progression of obesity or diabetes; therefore,
This study investigated whether glutamine (GLN) pretreatment can enhance circulating endothelial progenitor cells (EPCs) and attenuate inflammatory reaction in high-fat diet-induced obese mice with limb ischemia. Mice were assigned to a normal control (NC), high-fat control (HC), limb ischemia (HI),

Use of Glucose, Glutamine and Fatty Acids for Trophoblast Respiration in Lean, Obese and Gestational Diabetic Women.

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Maternal obesity and gestational diabetes (GDM) are associated with adverse outcomes particularly with a male fetus. The composition and amount of substrate supplied to the placenta is altered in these conditions. We hypothesized that there are sexually dimorphic differences in
High-fat diet-induced obesity can lead to hepatic insulin resistance (IR) and alter glucose metabolism. The decreased protein expression involved in the PI3K-Akt pathway may enhance hepatic glycogenolysis and gluconeogenesis. Obesity-associated glucose dysregulation and IR are risk factors for the

Arginine and glutamine availability and macrophage functions in the obese insulin-resistant Zucker rat.

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Increased susceptibility to infections in obese patients may be related to decreased availability of arginine and glutamine, which may affect immune cell functions. Our aim was to evaluate the in vitro effects of these amino acids on the function of macrophages from obese insulin-resistant Zucker

Roux-en-Y gastric bypass alters small intestine glutamine transport in the obese Zucker rat.

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The metabolic effects of Roux-en-Y gastric bypass (RYGB) are caused by postsurgical changes in gastrointestinal anatomy affecting gut function. Glutamine is a critical gut nutrient implicated in regulating glucose metabolism as a substrate for intestinal gluconeogenesis. The present study examines
BACKGROUND Incretin hormones, such as glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in meal-related insulin secretion. We previously demonstrated that glutamine is a potent stimulus of GLP-1 secretion in vitro. OBJECTIVE Our objective

Glutamine supplementation favors weight loss in nondieting obese female patients. A pilot study.

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Glutamine supplementation improves insulin sensitivity in critically ill patients, and prevents obesity in animals fed a high-fat diet. We hypothesized that glutamine supplementation favors weight loss in humans. Obese and overweight female patients (n=6) were enrolled in a pilot, cross-over study.
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