Abundance of Gut Microbiota, Concentration of Short-Chain Fatty Acids, and Inflammatory Markers Associated with Elevated Body Fat, Overweight, and Obesity in Female Adolescents.

BACKGROUND AND AIMS: Overweight is ever more prevalent in the pediatric population, and this cardiometabolic factor can be associated with inflammatory markers, gut microbiota composition, and short-chain fatty acid (SCFA) concentrations. The aim of this study is to evaluate to what extent the abundance of gut microbiota phyla, SCFA concentrations, and inflammatory markers are associated with elevated body fat percentage (BF%), overweight, and obesity in female adolescents. METHODS: An experimental and comparative study was conducted with 96 girls 14 to 19 years old. They were divided into 3 groups: G1-eutrophic (EUT) and adequate BF%; G2-EUT and high BF%; and G3-overweight (OW) or obese (OB) and high BF%. Waist circumference (WC), waist to height ratio (WtHR), and neck circumference (NC) were analyzed as indicators of central visceral adiposity. The BF% was evaluated by DEXA equipment. A food frequency questionnaire was used to evaluate the main types of food consumed in a week. The abundance of the Firmicutes, Bacteroidetes, and Proteobacteria phyla was measured by real-time polymerase chain reaction (RT-qPCR), and the SFCA concentrations (acetic, butyric, and propionic) were determined by high-performance liquid chromatography (HPLC). The inflammatory markers leptin, tumor necrosis factor-alpha, interleukin-6, and high-sensitivity C-reactive protein (hs-CRP) were assessed. RESULTS: Female adolescents in groups G2 and G3 had greater central visceral adiposity and leptin concentration than those in group G1. No association was found between gut microbiota phyla abundance and SFCA concentrations in any of the groups. WC and frequency of consumption of oily and fatty foods were associated with Firmicutes abundance and SFCA concentrations. Girls with high WC also had the greatest leptin (p < 0.001) and hs-CRP (p = 0.035) concentrations. CONCLUSIONS: Inflammatory markers showed association with increased BMI and high BF% in female adolescents. The abundance of Firmicutes was associated with WC and NC, but not with BMI classification or BF%. Specifically, WC and the consumption of oils and fats showed correlation with SCFA concentrations. Different anthropometric indicators, such as NC and WC, should be incorporated into the clinical evaluation of the nutritional status of individuals in the adolescent population.

Intensive liquid feeding of dairy calves with a medium crude protein milk replacer: Effects on performance, rumen, and blood parameters.

The objective of this study was to evaluate the effects of different liquid-feeding systems using a medium crude protein milk replacer on performance, rumen, and blood parameters. Thirty newborn Holstein calves were blocked according to birth weight and date of birth, and randomly distributed to different liquid-feeding systems: conventional (4 L/d), intensive (8 L/d), or step-up/step-down (wk 1, 4 L/d; wk 2 to 6, 8 L/d; wk 7 and 8, 4 L/d). The commercial milk replacer (12.5% solids, 20.2% crude protein, 15.6% fat) was fed twice daily (0700 and 1700 h) until calves were weaned, at 8 wk of age. Calves were individually housed in wood hutches, with free access to water and starter concentrate, and to hay only after weaning. They were followed through 10 wk of age. Milk replacer and starter intake were inversely affected by feeding system. After weaning, starter intake and hay intake were similar among feeding systems. Total dry matter intake was higher during the liquid-feeding period for calves on the intensive system compared to calves on the conventional system, but conventional feeding resulted in the highest dry matter intake after weaning. Feed efficiency was similar among feeding systems before and after weaning. Average body weight and daily gain were not affected by feeding system before or after weaning. During liquid feeding, diarrhea occurrence was lower for calves on the conventional system; however, when calves on the step-up/step-down system were fed lower volumes of liquid feed, diarrhea occurrence was similar to that of calves on the conventional system. Plasma concentrations of ß-hydroxybutyrate were higher for calves on the conventional system, reflecting starter intake. Rumen pH, short-chain fatty acids, and N-NH3 were not affected by feeding system. Feeding higher volumes of milk replacer with a medium crude protein content had no beneficial effect on the performance of calves up to 10 wk of age.

Agavins reverse the metabolic disorders in overweight mice through the increment of short chain fatty acids and hormones.

In this study, the effects of agavins (branched fructans) along with a diet shift on metabolic parameters, short chain fatty acid (SCFA) production and gastrointestinal hormones in overweight mice were established. Male C57BL/6 mice were fed with a standard (ST) or high fat (HF) diet over the course of 5 weeks, with the objective to induce overweightness in the animals, followed by a diet shift (HF_ST) and a diet shift with agavins (HF_ST + A) or inulin (HF_ST + O) for 5 additional weeks. After the first 5 weeks, the HF group showed a 30% body weight gain and an increase in glucose, triglyceride and cholesterol concentrations of 9%, 79% and 38% respectively when compared to the ST group (P < 0.05). Only the overweight mice that received agavins or inulin in their diets reversed the metabolic disorders induced by consumption of the HF diet, reaching the values very close to those of the ST group (P < 0.05). Furthermore, the consumption of agavins or inulin led to higher SCFA concentrations in the gut and modulated hormones such as GLP-1 and leptin involved in food intake regulation (P < 0.05). These findings demonstrate that a change of diet and fructan consumption such as agavins is a good alternative to increase weight loss and to improve the metabolic disorders associated with being overweight.

Reduction of serum carnitine concentrations during anticonvulsant therapy with phenobarbital, valproic acid, phenytoin, and carbamazepine in children.

We determined four carnitine constituents (total and free carnitine and short- and long-chain fatty acid carnitine esters) in serum from 471 patients treated for convulsions with phenobarbital, valproic acid, phenytoin, and/or carbamazepine. The 471 patients were in eight treatment groups; four were treated with monotherapy and four with polytherapy. The means of all four carnitine constituents were significantly reduced in all treatment groups (except for free carnitine in four groups). Total carnitine was reduced by 23% to 48%, free carnitine by 9% to 45%, short-chain fatty acid carnitine by 46% to 64%, and long-chain fatty acid carnitine by 6% to 29%. Patient frequency of reduction for total carnitine was 20% of all patients (10% for free carnitine), 23% of patients receiving valproate (9% for free carnitine), 36% of those receiving phenobarbital (21% for free carnitine), 12% of those receiving phenytoin (8% for free carnitine), and 8% of those receiving carbamazepine (1% for free carnitine). Only for phenobarbital was there an inverse correlation between the serum concentration of the drug and that of carnitine concentration. One patient receiving carbamazepine had a 59% reduction in the total and a 65% reduction in the free carnitine concentration and a fivefold increase in long-chain fatty acid carnitine, values similar to those seen in neonatal lethal carnitine palmitoyl transferase II deficiency. It remains to be determined whether a reduction in serum carnitine values in patients receiving anticonvulsant therapy is of clinical consequence, whether the reduction is present in some patients before the start of therapy, when and by what mechanism carnitine levels may become reduced during therapy, and whether the reduction exists in the solid tissues of these patients.

[Hepatic encephalopathy]. / Encefalopatia hepática.

This is a review of basic concepts on the etiopathogeny and treatment of hepatic encephalopathy focusing in more detail on the role of amino acids and neurotransmitters in precipitating the neurological picture.

Jamaican vomiting sickness. Biochemical investigation of two cases.

We identified methylenecyclopropylacetic acid, a known metabolite of hypoglycin A, in the urine of two patients with Jamaican vomiting sickness. Excretion of unusual dicarboxylic acids such as 2-ethylmalonic, 2-methylsuccinic, glutaric, adipic and dicarboxylic acids with eight and 10 carbon chains were also detected in both patients. The amounts of these dicarboxylic acids were 70 to 1000 times higher than normal. These metabolites have also been identified in urine of hypoglycin-treated rats. This evidence links hypoglycin A to Jamaican vomiting sickness as its causative agent. Urinary excretion of short-chain fatty acids was also increased up to 300 times higher than normal. These results indicate that, despite their clinical and histologic similarities, the cause and biochemical mechanisms of Jamaican vomiting sickness differ distinctly from those of Reye's syndrome in which these abnormal urinary metabolites are not appreciably increased.

Jamaican vomiting sickness: biochemical investigation of two cases

We identified methylenecyclopropylacetic acid, a known metabolite of hypoglycin A, in the urine of two patients with Jamaican vomiting sickness. Excretion of unusual dicarboxylic acids such as 2-ethylmalonic, 2-methylsuccinic, glutaric, adipic and dicarboxylic acids with eight and 10 carbon chains were also detected in both patients. The amounts of these dicarboxylic acids were 70 to 1000 times higher than normal. These metabolities have also been identified in urine of hypoglycin-treated rats. This evidence links hypoglycin A to Jamaican vomiting sickness as its causative agent. Urinary excretion of short-chain fatty acids was also increased up to 300 times higher than normal. These results indicate that, despite their clinical and histological similarities, the cause and biochemical mechanisms of Jamaican vomiting sickness differ distinctly from those of Reye's syndrome in which these abnormal urinary metabolities are not appreciably increased.(AU)