Association of cagA+ Helicobacter pylori strains with high urease activity and dyspepsia in Mexican adults. / Asociación de cepas de Helicobater pylori cagA+ con alta actividad de ureasa y dispepsia en adultos mexicanos.

INTRODUCTION AND AIMS: Helicobacter pylori (H. pylori) is associated with a higher risk of peptic ulcer and gastric cancer. The sole presence of the bacterium is not a determinant of clinical outcome, but rather the interaction of strain type and host factors determines the risk of disease. Our aim was to study the association between bacterial load, strain type, and gastric symptoms in H. pylori-positive subjects. MATERIALS AND METHODS: In a community survey, a diagnostic 13C-urea breath test for H. pylori was performed on 302 volunteers that were not taking antibiotics, antacids, or proton pump inhibitors one month prior to the test. The breath test produced 25 H. pylori-positive subjects, between 25-74 years of age, who then took a gastric symptoms survey and were tested for the presence of the cagA genotype in gastric juice, using the Entero-test®. Bacterial load was determined as a measure of urease activity, utilizing the delta over baseline value, obtained in the 13C-urea breath test. RESULTS: A total of 48% of the H. pylori-positive subjects were cagA+. A positive association was found between cagA status and high gastric urease activity (P<.0001) and the latter was significantly associated with the presence of symptoms (P<.0001). CONCLUSION: Gastric urease activity was strongly associated with dyspeptic symptoms and cagA+ H. pylori. Elevated 13C-delta over baseline values could be used as indicators of a higher risk for gastric disease.

Dietary conjugated linoleic acid and its effect on immune response in pigs infected with the porcine reproductive and respiratory syndrome virus.

The aim of this study was to evaluate the effects of dietary conjugated linoleic acid (CLA) on immune response in pigs infected with porcine reproductive and respiratory syndrome virus (PRRSV). A total of 18 pigs 4 weeks of age were allocated to 3 treatments, 6 per treatment: 0% CLA, 1% CLA, and 2% CLA. Serum IL-1ß, IL-6 and TNF-α; lymphocyte proliferation; and IL-2, IFN-γ, IL-10, IL-4 and IL-12 in PBMCs were evaluated. NF-κB, COX2, iNOS and PPAR-γ mRNA were also evaluated. No differences were observed among treatment groups in most of the in vivo cytokine profiles; only TNF-α production was increased in infected pigs in the CLA-supplemented groups. The cytokine profile in vitro was not affected by CLA supplementation. CLA decreased the proliferation of PBMCs stimulated with PRRSVs. Inflammation mediators and PPAR-γ were not affected by CLA in infected pigs. CLA did not improve the immune response of PRRSV infected pigs.

Body composition prediction equations based on deuterium oxide dilution method in Mexican children: a national study.

BACKGROUND/OBJECTIVES: Obesity and undernutrition co-exist in many regions of Mexico. However, accurate assessments are difficult because epidemiological data on body composition are not available. The aim of this study was to facilitate assessments of body composition in Mexican school children of different geographical regions and ethnicity by developing equations for bioelectrical impedance and anthropometry based on deuterium oxide dilution. SUBJECTS/METHODS: We evaluated 336 subjects (143 belonged to six major indigenous groups) from Northern, Central and Southern Mexico. We measured height (Ht), weight (Wt), tricipital skinfold (Tricp-SKF) and resistance (R) based on a bioimpedance analysis (BIA). Fat-free mass (FFM) and fat mass (FM) were estimated from measurements of total body water with the deuterium dilution technique. RESULTS: The final BIA equation was FFM (kg)=0.661 × Ht²/R+0.200 × Wt-0.320. The R² was 0.96; the square root of the mean square error (SRMSE) was 1.39 kg. The final anthropometric equation was FM (kg)=-1.067 × sex+0.458 × Tricp-SKF+0.263 × Wt-5.407. The R² was 0.91; SRMSE was 1.60 kg. The BIA equation had a bias of 0.095 kg and precision of 1.43 kg. The anthropometric equation had a bias of 0.047 kg and precision of 1.58 kg. CONCLUSIONS: We validated two equations for evaluating body composition in Mexican indigenous and non-indigenous children and youth from three main regions of the country. These equations provided reliable estimates and will promote a better understanding of both obesity and undernutrition.

[Improvement of insulin sensitivity after an intensive lifestyle program for youth's weight management in the primary care]. / Mejora en la sensibilidad a la insulina con un programa intensivo de cambio en el estilo de vida para control de obesidad en niños y adolescentes en el primer nivel de atención.

The aim of this study was to evaluate an intensive lifestyle intervention for weight management among youth in a primary care setting on insulin sensibility, compared to a control group. The study included 42 youths 9-17 years old (n=23 intensive lifestyle intervention, n=19 control group) who completed a randomized trial for weight management in a primary care setting which included an oral glucose tolerance test. The intensive lifestyle intervention included monthly consultations with the primary care physician, nutrition counseling with a registered dietitian (weekly first 3 months and then monthly) and 12 group sessions in a behavioral change protocol. The control group attended monthly consultations with the primary care physician. Insulin sensitivity was estimated by the Insulin Sensitivity Index ISI(0,120) at baseline and 6 months posttreatment. At 6 months, the mean +/- DE, increase in insulin sensitivity was greater in the intensive lifestyle intervention than the control group (+46.8 +/- 56 vs. +5.6 +/- 47, between-group difference 41.2 [CI 95%, 8.5, 73.9], p = 0.01): Sixty five percent of youths on the intensive lifestyle intervention increased insulin sensitivity over 9 units vs. 32% in the control group (p=0.03). This study shows preliminary evidence that an intensive lifestyle intervention program can be an alternative model to improve insulin sensitivity among youths in the primary care setting.

Conjugated linoleic acid is a potent naturally occurring ligand and activator of PPARalpha.

We have previously shown that a mixture of dietary conjugated derivatives of linoleic acid (conjugated linoleic acid, CLA) induces peroxisome proliferator-responsive enzymes and modulates hepatic lipid metabolism in vivo. The present studies demonstrate that CLA is a high affinity ligand and activator of peroxisome proliferator-activated receptor alpha (PPARalpha) and induces accumulation of PPAR-responsive mRNAs in a rat hepatoma cell line. Using a scintillation proximity assay (SPA), CLA isomers were shown to be ligands for human PPARalpha with a rank order of potency of (9Z,11E)>(10E,12Z)>(9E,11E)> furan-CLA (IC(50) values from 140 nm to 400 nm). Levels of acyl-CoA oxidase (ACO), liver fatty acid-binding protein (L-FABP), and cytochrome P450IVA1 (CYP4A1) mRNA were induced by CLA in FaO hepatoma cells. Even though linoleate and CLA were incorporated into lipids of hepatoma cells to the same extent, linoleate had little or no effect on ACO, CYP4A1, or L-FABP mRNA. In agreement with its binding potency, (9Z,11E)-CLA was the most efficacious PPARalpha activator in the mouse PPARalpha-GAL4(UAS)(5)-CAT reporter system. These data indicate that CLA is a ligand and activator of PPARalpha and its effects on lipid metabolism may be attributed to transcriptional events associated with this nuclear receptor. Also, (9Z,11E)-CLA is one of the most avid fatty acids yet described as a PPARalpha ligand.

Conjugated linoleic acid activates peroxisome proliferator-activated receptor alpha and beta subtypes but does not induce hepatic peroxisome proliferation in Sprague-Dawley rats.

Since conjugated linoleic acid (CLA) has structural and physiological characteristics similar to peroxisome proliferators, we hypothesized that CLA would activate peroxisome proliferator-activated receptor (PPAR). We compared the effects of dietary CLA (0.0, 0.5, 1.0 and 1.5% by weight) with a peroxisome proliferator (0.01% Wy-14,643) in female and male Sprague-Dawley (SD) rats. Dietary CLA had little effect on body weight, liver weight, and hepatic peroxisome proliferation, compared to male rats fed Wy-14,643 diet. Lipid content in livers from rats fed 1.5% CLA and Wy-14,643 diets was increased (P < 0.01) when compared to rats fed control diets regardless of gender. Hepatic acyl-CoA oxidase (ACO) mRNA levels were increased 3-fold in male rats fed 1.5% CLA diet compared to rats fed control diets while Wy-14,643 supported approximately 30-fold ACO mRNA accumulation. A similar response was observed for liver fatty acid-binding protein (L-FABP) mRNA. The effect of dietary treatments on hepatic PPAR-responsive genes in female rats was weaker than in male rats. The (9Z,11E)-CLA isomer activated PPAR alpha in transfected cells to a similar extent as Wy-14,643, whereas the furan-CLA metabolite was comparable to bezafibrate on activating PPAR beta. These data suggest that while CLA was able to activate PPARs it is not a peroxisome proliferator in SD rats.

Species differences in the metabolism and regulation of gene expression by conjugated linoleic acid.

Conjugated linoleic acid (CLA) inhibits carcinogenesis and atherosclerotic plaque formation and delays the onset of diabetes in experimental animals. Whereas a plethora of data has demonstrated beneficial effects in rodent models, little work has been done to determine the role of dietary CLA in human health. The ability of CLA to modulate lipid metabolism appears to be a pivotal mechanism of CLA's beneficial effects in mice and rats. In particular, dietary CLA induces the expression of genes dependent in part on the transcription factor, peroxisome proliferator-activated receptor (PPAR). Furthermore, several CLA isomers are high-affinity ligands and activators for PPAR alpha. Within various rodent species and strains, dietary CLA exerts varying potencies; therefore, the differences in species' sensitivities are of great importance when trying to extrapolate the rodent data to be relevant in humans. This review presents the latest findings of the ability of CLA to alter lipid metabolism and gene expression in several different strains of mice and rats and speculates on the implications of these findings for human health.

Comparison of dose-response relationships for induction of lipid metabolizing and growth regulatory genes by peroxisome proliferators in rat liver.

The regulation of gene expression via the peroxisome proliferator-activated receptor (PPAR) is believed to be critical in the effects of peroxisome proliferators on lipid metabolism and possibly in hepatocarcinogenesis. The involvement of PPAR in the peroxisome proliferator-mediated induction of fatty acid metabolizing genes such as acyl-CoA oxidase (ACO), fatty acid-binding protein (FABP), and cytochrome P450IVA1 (CYP4A1) has been clearly demonstrated. However, the induction by peroxisome proliferators of important growth regulatory genes such as c-myc has not been investigated extensively. In these studies we examined the dose-response relationships for the induction of mRNA for the PPAR-regulated and lipid metabolizing genes ACO, FABP, and CYP4A1 and compared them to the immediate early gene c-myc. Liver mRNA from rats fed various amounts of the peroxisome proliferator Wy14,643 for 13 weeks was utilized. The lipid metabolism and growth regulatory genes were induced by subchronic administration of Wy14,643 but to varying degrees and with different sensitivities. The lowest dose that resulted in a significant change in ACO and FABP expression was 10 ppm. The mRNA for CYP4A1 and c-myc was significantly affected at the lowest dose examined (5 ppm). Also, the maximal induction ranged from 10(5)-fold (CYP4A1) to less than 10-fold (FABP) relative to vehicle-treated animals. The accumulation of mRNA for ACO, FABP, and CYP4A1, but not c-myc, showed typical receptor-mediated dose-response relationships. The effects on gene expression were compared to rates of hepatic cell proliferation, a pertinent marker of tumor promotion and hepatocarcinogenesis. Surprisingly, ACO mRNA showed an excellent correlation (r2 = 0.9) while c-myc mRNA exhibited a poor correlation (r2 = 0.3) with cell proliferation in rat liver. Although the differences between the dose-response relationships of ACO and c-myc mRNA accumulation may suggest immediate early genes are not controlled by PPAR, evidence from PPARalpha null mice support this receptor in both lipid metabolism and growth regulatory genes. This study shows the complexity of responses mediated by peroxisome proliferators, with ACO being a good marker of PPAR-mediated events as well as cell proliferation, while c-myc, a known growth regulatory gene, was induced by Wy14,643 partially via PPAR but did not correlate well with cell proliferation.

Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat.

Conjugated linoleic acid (CLA) is a naturally occurring fatty acid which has anti-carcinogenic and anti-atherogenic properties. CLA activates PPAR alpha in liver, and shares functional similarities to ligands of PPAR gamma, the thiazolidinediones, which are potent insulin sensitizers. We provide the first evidence that CLA is able to normalize impaired glucose tolerance and improve hyperinsulinemia in the pre-diabetic ZDF rat. Additionally, dietary CLA increased steady state levels of aP2 mRNA in adipose tissue of fatty ZDF rats compared to controls, consistent with activation of PPAR gamma. The insulin sensitizing effects of CLA are due, at least in part, to activation of PPAR gamma since increasing levels of CLA induced a dose-dependent transactivation of PPAR gamma in CV-1 cells cotransfected with PPAR gamma and PPRE X 3-luciferase reporter construct. CLA effects on glucose tolerance and glucose homeostasis indicate that dietary CLA may prove to be an important therapy for the prevention and treatment of NIDDM.