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uridine/obesidad

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Assessment of postprandial hepatic glycogen synthesis from uridine diphosphoglucose kinetics in obese and lean non-diabetic subjects.

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BACKGROUND Obese patients are frequently characterized by insulin resistance and decreased insulin-mediated glycogen synthesis in skeletal muscle. Whether they also have impaired postprandial hepatic glycogen synthesis remains unknown. OBJECTIVE To determine whether postprandial hepatic glycogen

Adipocyte Xbp1s overexpression drives uridine production and reduces obesity.

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OBJECTIVE The spliced transcription factor Xbp1 (Xbp1s), a transducer of the unfolded protein response (UPR), regulates lipolysis. Lipolysis is stimulated by fasting when uridine synthesis is also activated in adipocytes. METHODS Here we have examined the regulatory role Xbp1s in stimulation of

Postprandial Uridine Physiology Is Altered by Obesity.

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Hypothalamic UDP Increases in Obesity and Promotes Feeding via P2Y6-Dependent Activation of AgRP Neurons.

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Activation of orexigenic AgRP-expressing neurons in the arcuate nucleus of the hypothalamus potently promotes feeding, thus defining new regulators of AgRP neuron activity could uncover potential novel targets for obesity treatment. Here, we demonstrate that AgRP neurons express the purinergic

Obstetric Obesity is Associated with Neonatal Hyperbilirubinemia with High Prevalence in Native Hawaiians and Pacific Island Women.

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Obesity and pregnancy both place the liver under metabolic stress, but interactions between obstetric obesity and bilirubin metabolism have not been studied. We determined associations between obesity, maternal/neonatal bilirubin levels, and uridine 5'diphosphate-glucuronosyltransferase 1A1 (UGT1A1)

Inhibition of P2Y6 Signaling in AgRP Neurons Reduces Food Intake and Improves Systemic Insulin Sensitivity in Obesity.

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Uridine-diphosphate (UDP) and its receptor P2Y6 have recently been identified as regulators of AgRP neurons. UDP promotes feeding via activation of P2Y6 receptors on AgRP neurons, and hypothalamic UDP concentrations are increased in obesity. However, it remained unresolved whether inhibition of P2Y6

Uridine monophosphate synthetase enables eukaryotic de novo NAD+ biosynthesis from quinolinic acid.

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NAD+ biosynthesis is an attractive and promising therapeutic target for influencing health span and obesity-related phenotypes as well as tumor growth. Full and effective use of this target for therapeutic benefit requires a complete understanding of NAD+ biosynthetic pathways. Here, we report a
BACKGROUND Sex steroids are involved in the regulation of pubertal cortical bone expansion in males. In vitro studies have indicated that the enzyme uridine diphosphate glucuronosyltransferase (UGT) 2B7 has the capacity to glucuronidate sex steroids and their metabolites. OBJECTIVE Our objective was

Glucose metabolites in blood and adipose tissue of obese diabetic and non-diabetic subjects.

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1. Glucose 6-phosphate, fructose 6-phosphate, fructose diphosphate, glycerol phosphate and uridine diphosphate glucose have been measured in human adipose tissue and blood from obese subjects under fed and fasting conditions and in obese diabetic and non-diabetic subjects before and after an oral

Uridine dynamic administration affects circadian variations in lipid metabolisms in the liver of high-fat-diet-fed mice.

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Carbohydrate and lipid metabolism in the liver has been reported to follow a certain circadian rhythm. Moreover, uridine supplementation also affected glucose and lipid homeostasis in previous studies; however, the mechanisms remain unclear. Therefore, this study was conducted to investigate whether

Comparison of plasma nucleotide metabolites and amino acids pattern in patients with binge eating disorder and obesity

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Binge eating disorder (BED) increasingly affects population, but the mechanisms of the disease and its biomarkers are not well characterized. Recently, plasma purines, pyrimidines, amino acid and nicotinamide metabolites profiling attracted attention in studies on pathology and biomarkers of mental

Species Differences in Stereoselective Pharmacokinetics of HSG4112, A New Anti-Obesity Agent.

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HSG4112, a racemic drug, is a new anti-obesity agent. In this study, the stereoselective pharmacokinetics of HSG4112 were investigated in rats and dogs, and the underlying mechanism was investigated. The plasma concentrations of HSG4112(S) and HSG4112(R) were quantitated in plasma from rats and
Genetically obese Zucker rats exhibit symptoms similar to those of obese patients with insulin-resistance or Type II diabetes; therefore, they have been used as a genetic model to study obesity, as well as a pharmacological model for the discovery of new drugs for the treatment of Type II diabetes

Metabolomics Associated with Genome-Wide Association Study Related to the Basal Metabolic Rate in Overweight/Obese Korean Women.

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A previous genome-wide association study (GWAS) on obese/overweight Korean women reported five new genetic loci associated with the basal metabolic rate (BMR) and body mass index (BMI), NRG3, OR8U8, BCL2L2-PABPN1, PABPN1, and SLC22A17. This metabolite GWAS (mGWAS)

Coordinate induction of Na(+)-dependent transport systems and Na+,K(+)-ATPase in the liver of obese Zucker rats.

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Solute uptake into liver plasma membrane vesicles from either lean or obese Zucker rats was monitored. D-Glucose and L-leucine uptakes at physiological concentrations of the substrate were not different in lean and obese Zucker rats. In agreement with a previous report (Ruiz et al. (1991) Biochem.
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