cresol/obesity

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[Excretion of phenol and p-cresol in the urine in fasting obese individuals and in persons treated with total enteral nutrition].

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In the literature it is maintained that phenol and p-cresol are produced in humans in the gut by bacteria from dietary protein. Both substances are absorbed from the small intestine and excreted in the urine. If the urinary output of phenol and p-cresol depends really on the dietary protein intake

Gender-specific metabolomic profiling of obesity in leptin-deficient ob/ob mice by 1H NMR spectroscopy.

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Despite the numerous metabolic studies on obesity, gender bias in obesity has rarely been investigated. Here, we report the metabolomic analysis of obesity by using leptin-deficient ob/ob mice based on the gender. Metabolomic analyses of urine and serum from ob/ob mice compared with those from

Effects of uremic toxin p-cresol on proliferation, apoptosis, differentiation, and glucose uptake in 3T3-L1 cells.

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Malnutrition is a common feature seen in chronic dialysis patients, and the survival rate of obese patients receiving such treatment is higher than that of lean patients. Irrespective of obesity or diabetes, dialysis patients commonly have insulin resistance, and the leading cause of death is

Metabolomic alternations of follicular fluid of obese women undergoing in-vitro fertilization treatment.

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Obesity exerts negative effects on the metabolic homeostasis of cells in various tissues, but how it influences ovum metabolism is not fully understood. Previous studies demonstrate that oocyte genes that regulate oxidative stress, lipid metabolism, and inflammation are highly expressed in obese

Untargeted metabolomics approach (UPLC-Q-TOF-MS) explores the biomarkers of serum and urine in overweight/obese young men.

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OBJECTIVE Obesity is linked to metabolic diseases characterized by insulin resistance, such as diabetes and cardiovascular disease. In this study, we investigated the metabolic disorders of uncomplicated obesity to identify early alterations in biological systems. METHODS Metabolic differences

Uremic Toxins Activates Na/K-ATPase Oxidant Amplification Loop Causing Phenotypic Changes in Adipocytes in In Vitro Models.

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BACKGROUND Oxidant stress plays a key role in the development of chronic kidney disease (CKD). Experimental CKD leads to accumulation of uremic toxins (UT) in the circulation resulting in increased ROS production, which in turn, is known to activate the Na/K-ATPase/ROS amplification loop. Studies in

Microbial-Derived Metabolites Reflect an Altered Intestinal Microbiota during Catch-Up Growth in Undernourished Neonatal Mice.

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Protein-energy undernutrition during early development confers a lifelong increased risk of obesity-related metabolic disease. Mechanisms by which metabolic abnormalities persist despite catch-up growth are poorly understood. We sought to determine whether abnormal metabolomic and intestinal

Microbial Fermentation of Dietary Protein: An Important Factor in Diet⁻Microbe⁻Host Interaction.

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Protein fermentation by gut microbiota contributes significantly to the metabolite pool in the large intestine and may contribute to host amino acid balance. However, we have a limited understanding of the role that proteolytic metabolites have, both in the gut and in systemic circulation. A review

Metabolite profiling identifies candidate markers reflecting the clinical adaptations associated with Roux-en-Y gastric bypass surgery.

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BACKGROUND Roux-en-Y gastric bypass (RYGB) surgery is associated with weight loss, improved insulin sensitivity and glucose homeostasis, and a reduction in co-morbidities such as diabetes and coronary heart disease. To generate further insight into the numerous metabolic adaptations associated with

The ability of human intestinal anaerobes to metabolize different oligosaccharides: Novel means for microbiota modulation?

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Prebiotic oligosaccharides are known to have significant impacts on gut microbiota and are thus widely used to program healthy microbiota composition and activity from infants to the elderly. Bifidobacteria and lactobacilli are among the major target microorganisms of oligosaccharides, but the

Ursodeoxycholic acid improves liver function via phenylalanine/tyrosine pathway and microbiome remodelling in patients with liver dysfunction.

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Ursodeoxycholic acid (UDCA) is a metabolic by-product of intestinal bacteria, showing hepatoprotective effects. However, its underlying molecular mechanisms remain unclear. The purpose of this study was to elucidate the action mechanisms underlying the protective effects of UDCA and vitamin E

The gut microbiota and its relationship with chronic kidney disease.

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Chronic kidney disease (CKD) is a worldwide health problem, because it is one of the most common complications of metabolic diseases including obesity and type 2 diabetes. Patients with CKD also develop other comorbidities, such as hypertension, hyperlipidemias, liver and cardiovascular diseases,

Effect of dietary supplementation of (-)-epigallocatechin gallate on gut microbiota and biomarkers of colonic fermentation in rats.

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Alterations in gut microbiota composition offer insights that may be relevant for several chronic conditions, including obesity. This study aimed to evaluate the effect of (-)-epigallocatechin gallate (EGCG) on the modulation of gut microbiota and biomarkers of colonic fermentation end-products in

The gut microbiota metabolite indole alleviates liver inflammation in mice.

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The gut microbiota regulates key hepatic functions, notably through the production of bacterial metabolites that are transported via the portal circulation. We evaluated the effects of metabolites produced by the gut microbiota from aromatic amino acids (phenylacetate, benzoate, p-cresol, and

Development of Biomarkers for Inhibition of SLC6A19 (B⁰AT1)-A Potential Target to Treat Metabolic Disorders.

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Recent studies have established that dietary protein restriction improves metabolic health and glucose homeostasis. SLC6A19 (B⁰AT1) is the major neutral amino acid transporter in the intestine and carries out the bulk of amino acid absorption from the diet. Mice lacking SLC6A19 show signs of protein

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