n-3 polyunsaturated fatty acids in the regulation of adipose tissue browning and thermogenesis in obesity: Potential relationship with gut microbiota.

BACKGROUND: Obesity is a worldwide public health problem characterized by fat tissue accumulation, favouring adipose tissue and metabolic alterations. Increasing energy expenditure (EE) through brown adipose tissue activation and white adipose tissue (WAT) browning has gained relevance as a therapeutic approach. Different bioactive compounds, such as n-3 polyunsaturated fatty acids (PUFA), have been shown to induce those thermogenic effects. This process is regulated by the gut microbiota as well. Nevertheless, obesity is characterized by gut microbiota dysbiosis, which can be restored by weight loss and n-3 PUFA intake, among other factors. Knowledge gap: However, the role of the gut microbiota on the n-3 PUFA effect in inducing thermogenesis in obesity has not been fully elucidated. OBJECTIVE: This review aims to elucidate the potential implications of this interrelation on WAT browning adiposw sittue (BAT), BAT activity, and EE regulation in obesity models.

Amoxicillin treatment modifies the composition of Bifidobacterium species in infant intestinal microbiota.

OBJECTIVES: Amoxicillin is a beta-lactam antibiotic largely used in childhood. However only few studies described its impact on composition of children gut microbiota, in particular on Bifidobacterium populations considered as beneficial microorganisms. In this study, the impact on faecal Bifidobacterium species of a seven-day amoxicillin treatment was quantitatively and qualitatively assessed in infants during an episode of acute respiratory infection. METHODS: Faecal samples from 31 infants were obtained on day 0 (just before amoxicillin therapy) and on day 7 (the end of therapy). Total DNA was extracted and bifidobacteria were quantified using real-time PCR. Predominant Bifidobacterium species were then identified using specific PCR-TTGE. RESULTS: Bifidobacteria concentrations were not significantly altered by amoxicillin compared to the healthy group. However, amoxicillin treatment induced a complete disappearance of Bifidobacterium adolescentis species (occurrence rate of 0% versus 36.4% in healthy group, P < 0.001), a significant decrease in the occurrence rate of Bifidobacterium bifidum (23% versus 54.5% in healthy group, P < 0.05), but did not affect Bifidobacterium longum (93.5% versus 100% in healthy group) and Bifidobacterium pseudocatenulatum/B. catenulatum (about 55% in both groups). The number of Bifidobacterium species per microbiota significantly decreased from 2.5 +/- 1 for healthy group to 1.8 +/- 0.9 for treated infants (P < 0.05). CONCLUSIONS: This study showed that a 7 day amoxicillin treatment did not alter the counts of Bifidobacterium. However amoxicillin can have an impact by changing the microbiota at the species level and decreased the diversity of this population.

Systematic review: are probiotics useful in controlling gastric colonization by Helicobacter pylori?

Helicobacter pylori is a highly prevalent pathogen considered as an aetiological factor for gastroduodenal ulcers, and a risk factor for gastric adenocarcinoma and lymphoma in humans. Most subjects colonized by this micro-organism are asymptomatic and remain untreated. In symptomatic patients, the antibiotic treatment has a high cost and is not 100% effective because of resistance to antibiotics and to moderate patient compliance. This review discusses the role of probiotics as alternative solutions to assist in the control of H. pylori colonization in at-risk populations. The evidence that some strains of Lactobacillus and Bifidobacterium are able to inhibit H. pylori growth through the release of bacteriocins or organic acids, and may also decrease its adhesion to epithelial cells, is reviewed. In addition, probiotics have a possible role in the stabilization of the gastric barrier function and the decrease of mucosal inflammation. Other aspects that are considered are the contribution of probiotics to the healing of the gastric mucosa linked to their antioxidant and anti-inflammatory properties. Clinical trials in colonized adults and children are reviewed, and suggest that probiotics do not eradicate H. pylori but maintain lower levels of this pathogen in the stomach; in combination with antibiotics, probiotics may increase eradication rate and/or decrease adverse effects. Papers suggesting similar effects on H. pylori by foodstuffs such as berry juice and some milk proteins are quoted. Regular intake of these and other dietary products might constitute a low-cost, large-scale alternative solution applicable for populations at-risk for H. pylori colonization.

Induction of apoptosis by transiently transfected metabolically stable wt p53 in transformed cell lines.

Biochemical and functional properties of wild-type (wt) and mutant p53 were studied under the same cellular environment by transient transfection. Exogenous wt p53 expressed in transformed cell lines was found to be as metabolically stable as mutant p53. Yet only mutant p53 bound to hsp70 whereas wt p53 did not, suggesting that the metabolic stability of p53 does not depend on its ability to form complexes with hsp70. The wt protein was expressed essentially in the nucleus, while mutant p53 showed both nuclear and cytoplasmic expression, as determined by immunofluorescence staining with PAb122. In addition, staining with PAb1801 revealed a number of strongly fluorescent cell fragments in cultures transfected by wt p53. Morphological features of apoptosis were observed in these cultures. Quantitative analysis by flow cytometry confirmed that only the cell population expressing wt p53 had a significant amount of cell debris. Thus, transient expression of a metabolically stable wt, but not mutant, p53 induces cell death by apoptosis. The present study demonstrates a model system to investigate the functional domains of p53 in the induction of apoptosis.

Prebiotic ingestion does not improve gastrointestinal barrier function in burn patients.

Prebiotics increase intestinal levels of health-promoting bacteria implicated in decreasing pathogen colonization, stimulating immune functions and stabilizing gut barrier functions, parameters which are altered in burn patients. We propose that regular intake of a prebiotic, oligofructose (OF), might help to improve the altered gastrointestinal (GI) permeability observed in burn patients. A randomized, double-blind, controlled clinical trial was carried out in 41 burn patients (mean burn surface area=17.1+/-8.2%) who ingested daily 6 g of oligofructose (OF group) or sucrose as placebo (Control group) during 15 days. Gastrointestinal permeability to sucrose and lactulose/mannitol (L/M) was evaluated on days 1 (before treatment) 3, 7, 14 and 21. A permeability test was also performed in 18 healthy subjects as controls. Thirty-one patients completed the protocol (dropout rate=24.4%). Healthy subjects had a basal sucrose excretion of 21.3 mg (14.0-32.5 mg) and a basal L/M ratio of 0.017% (0.009-0.022%). Sucrose excretion increased 5-fold and L/M ratio 4.4-fold in burn patients on day 1 and these high levels of marker excretion decreased significantly throughout the study (p=0.016 and 0.000001, respectively). No differences between the OF and Control groups were observed for sucrose excretion or L/M ratio. In conclusion, the normalization of gastrointestinal permeability is not accelerated by prebiotic intake.

Is the negative prognostic value of high oestrogen receptor (ER) levels in postmenopausal breast cancer patients due to a modified ER gene product?

Recently, it was found that, among post menopausal breast cancer patients receiving no adjuvant therapy, the highest oestrogen receptor (ER) levels (ER++) as opposed to the intermediate ER levels (ER+) indicated a poorer prognosis in terms of recurrence-free survival (Thorpe et al. Eur J Cancer 1993, 29A, 971-977). In the present study, we confirm, in a series of 218 node negative, postmenopausal patients in whom ER was determined using a one-dose saturating method, that ER+ tumours have a more negative effect on disease-free survival (DFS) than ER+ tumours (P = 0.02). In another series of 87 ER positive, postmenopausal patients, we found a significant correlation (P = 0.04) between the ER level and ER+R ratio (ER protein/ER-specific mRNA): the higher the ER level, the more numerous the high ER+R ratio cases (ER+R > 1.5), reflecting an imbalance between the ER protein level and ER-specific mRNA. From these results, we hypothesise that high ER levels related to a high ER+R ratio suggest the presence of a modified ER gene product.

Human estrogen receptor messenger RNA variants in both normal and tumor breast tissues.

By using the PCR-SSCP technique we characterized various ER-specific RNA species present in a series of primary breast cancers, as well as in cell lines established from breast carcinomas and in mammary gland tissues from healthy specimens. A series of six truncated messenger RNAs generated by alternative splicing was characterized. These RNAs correspond to specific deletions of one (exons 2-7, except exon 6) or two (exons 3 + 4) exons. All these RNA variants are observed in each one of the analyzed RNAs, regardless of origin. In addition, the relative amount of these different variants in ER + tumors is comparable to that measured in ER - tumors and healthy mammary gland tissues. This data suggests that tumor progression is not related to the emergence of any of the ER mRNA variants.

Effect of Lactobacillus ingestion on the gastrointestinal mucosal barrier alterations induced by indometacin in humans.

BACKGROUND: Chronic nonsteroidal anti-inflammatory drug (NSAID) ingestion strongly affects the gastrointestinal mucosa as a first stage before ulceration. Some Lactobacillus strains may stabilize the mucosal barrier by increasing mucin expression, reducing bacterial overgrowth, stimulating mucosal immunity and synthetizing antioxidant substances; these events are altered in NSAID-associated gastroenteropathy. AIM: To determine whether ingestion of the probiotic Lactobacillus GG (LGG) protects the gastrointestinal mucosa against indometacin-induced alterations of permeability. SUBJECTS AND METHODS: Four gastrointestinal permeability tests were carried out in random order in 16 healthy volunteers: (i) basal; (ii) after indometacin; (iii) after 5 days of living LGG ingestion before indometacin administration; (iv) after 5 days of heat-killed LGG ingestion before indometacin administration. RESULTS: Indometacin significantly increased basal sucrose urinary excretion (29.6 mg [17.1-42.1] vs. 108.5 mg [68.2-148.7], P=0.0030) (means [95% CI]) and lactulose/mannitol urinary excretion (1.03% [0.73-1. 32] vs. 2.93% [1.96-3.90], P=0.00012). Heat-killed LGG did not modify the indometacin-induced increase of gastrointestinal permeability, while live bacteria significantly reduced the alteration of gastric (47.8 mg [31.1-64.6], P=0.012) but not intestinal permeability induced by NSAID. CONCLUSIONS: Regular ingestion of LGG protects the integrity of the gastric mucosal barrier against indometacin, but has no effect at the intestinal level.

Basement membrane and connective tissue proteins in intestinal mucosa of patients with coeliac disease.

AIMS: Gluten ingestion in coeliac disease is associated with alterations of the intestinal mucosa, especially the expansion of the lamina propria. Antiendomysium and antireticulin antibodies may result from interactions between gliadin and extracellular matrix components. By behaving as autoantigens, connective tissue proteins could initiate mucosal damage. This study evaluates changes in the distribution of laminin, type IV collagen, and fibronectin in the mucosa of patients with coeliac disease in an attempt to explain the alterations of mucosal morphology. METHODS: Intestinal biopsies were obtained from patients with coeliac disease on admission and while on a gluten free diet. The distribution of type IV collagen, laminin, fibronectin, and alpha-smooth muscle actin was evaluated by immunofluorescence and by immunogold labelling and electron microscopy. RESULTS: In patients with coeliac disease, the intensity of type IV collagen, laminin, and fibronectin immunofluorescent staining was decreased and less well defined than in controls, with frequent breaches in the basement membrane; fibronectin staining was weak in the distal third of the elongated crypts and absent under the flat surface. The distribution of smooth muscle fibre in the distal lamina propria of flat mucosae was altered. The distribution of these proteins was normal as assessed by immunoelectron microscopy. CONCLUSIONS: The intensity of staining of some components of the basement membrane is decreased in coeliac disease and the distribution of smooth muscle fibres is altered. These changes may result from interactions between gliadin and components of the extracellular matrix and may play a role in the genesis of mucosal lesions and in the damage to the epithelium.

Loss of the metal binding properties of metallothionein induced by hydrogen peroxide and free radicals.

The relationship between the metal-binding properties of metallothionein (MT) and its ability to interact with peroxides and free radicals was explored in vitro. The binding of 109Cd to MT and the thiol density of the protein were determined after incubation of a purified Zn/Cd-metallothionein preparation with either hydrogen peroxide alone, or with a number of free radical generating systems. Exposure of MT to H2O2, whether in the presence or absence of Fe2+, resulted in the progressive loss of the thiol residues of the protein and led to a parallel decrease of its 109Cd-binding capacity. These changes correlated with r values of 0.999 (P = 0.001) and 0.998 (P = 0.001), in the absence and presence of iron, respectively. The effects of H2O2, alone or plus Fe2+, on MT were completely prevented by catalase, but totally unaffected by superoxide dismutase or desferrioxamine. Exposure of MT to xanthine/xanthine oxidase also led to thiol oxidation and to a concomitant loss of the Cd-binding properties. In this system, both changes correlated with an r of 0.993 (P = 0.001) and were completely inhibited by superoxide dismutase. Exposure of MT to the peroxyl radical generator, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH), resulted in the progressive loss of its the metal-binding properties and its thiol residues, both changes correlating with an r of 0.986 (P = 0.002). The ability of MT to bind 109Cd, lost as a result of its prior exposure to either H2O2 alone, H2O2 plus Fe2+, xanthine/xanthine oxidase, or to AAPH was, in all cases, completely recovered after incubation of the modified protein with dithiothreitol. These results indicate that H2O2 alone, and/or the oxygen-derived species, superoxide anion and peroxyl radicals, can all directly interact in vitro with MT to modify the protein oxidatively, and suggest that, under in vivo conditions, these species may be implicated as modifying factors of the metal-binding capacity of metallothionein.

Effect of acute cigarette smoking, alone or with alcohol, on gastric barrier function in healthy volunteers.

BACKGROUND: Smoking is a risk factor for gastroduodenal ulcer and gastric adenocarcinoma. However, the pathophysiological mechanisms induced by acute cigarette smoking in the human gastric mucosa are poorly understood. AIM: To evaluate the effect of acute cigarette smoking, alone or with alcohol, on the gastric permeability to sucrose, a specific marker of mucosal damage in the stomach. SUBJECTS AND METHODS: Twenty healthy volunteers (8 smokers/12 non-smokers) were studied. Each fasted subject ingested 500 ml of a 20% sucrose solution and the amount of sucrose excreted in a 5-hour urine collection was measured by gas chromatography Four sucrose permeability tests were carried out: 1. basal, 2. while smoking 5 cigarettes, 3. after drinking 50 ml of a 40 degrees alcoholic beverage, 4. a combination of 2+3. RESULTS: Sucrose excretion increased after alcohol ingestion (40.5 +/- 6.0 mg vs 143.1 +/- 28.9 mg, p = 0.002), but was not modified by acute cigarette smoking (34.4 +/- 5.9 mg). When alcohol and cigarettes were simultaneously consumed, the increase in alcohol-induced sucrose excretion was significantly reduced (73.1 +/- 16.6 mg, p = 0.03). Basal sucrose excretion was similar in smokers and non-smokers. However, in acute cigarette smoking, a decrease in sucrose excretion was observed in smokers (p = 0.02) but not in non-smokers. CONCLUSIONS: These results indicate that acute cigarette smoking may tighten the gastric mucosa in habitual smokers and this is associated with a smaller increase of gastric permeability induced by alcohol.

Gastric permeability is not increased in children colonized by CagA-positive strains of Helicobacter pylori.

BACKGROUND: Sucrose permeability has been used as a marker to detect gastric lesions in children. As CagA status of Helicobacter pylori is an important factor in determining the evolution of the gastric lesion, CagA-positive strains being more frequently associated with severe mucosal lesions, the aim of this study was to determine the prevalence of CagA-positive strains in Helicobacter pylori-colonized children and to evaluate whether the sucrose permeability test might discriminate between colonization by CagA-positive or negative strains. PATIENTS AND METHODS: A series of 38 children (11.1+/-3.6 years) who required upper endoscopy for diagnostic purposes were included in the study. Endoscopy was carried out after the sucrose permeability test, and gastric biopsies were obtained for histologic examination, Helicobacter pylori detection by Giemsa staining and CLO-test, and determination of CagA status of the colonizing Helicobacter pylori strains by polymerase chain reaction. RESULTS: Helicobacter pylori was detected in 26 subjects (68.4%) and of these, 16 (61.5%) were colonized by CagA-positive strains. The intensity of the histologic findings was significantly associated with the presence of Helicobacter pylori and with CagA status of the infecting strains (chi2=21.2, p=0.0017). However no significant difference in the urinary excretion of sucrose between children not colonized and children with CagA- negative or positive strains was observed (0.027% [0.012-0.035%]; 0.027% [0.016-0.047%] and 0.026% [0.016-0.038], median [range], respectively; Kruskal-Wallis analysis of variance F=0.75, p=0.69). CONCLUSIONS: These results indicate that in Chile, about 60% of the Helicobacter pylori infected children are colonized by CagA-positive strains, in association with more intense lesions of the gastric mucosa, but that gastric permeability to sucrose does not discriminate between colonization by CagA-negative and positive strains of Helicobacter pylori.

I-R hybrid dysgenesis in Drosophila melanogaster. Use of in situ hybridization to show the association of I factor DNA with induced sex-linked recessive lethals.

The purpose of this paper is the genetic visualization by in situ hybridization of 130 sex-linked recessive lethals plus a non-lethal induced by I-R dysgenesis. This collection of lethals involves inducer strains which differ in the position of the I elements on the X chromosomes. The I-R interaction was strong. Our previous results have shown that about 30% of the induced recessive lethals are associated with cytologically visible chromosomal rearrangements. (1) The rearrangements induced by I-R-type hybrid dysgenesis often exhibit homology with the I factor at the level of one or both junction points, depending on the types of chromosome rearrangements. These results suggest that the chromosome rearrangements arise directly from the transposition of I elements. However, the breakpoints of some types of cytologically non-visible deficiencies and of 2 small cytologically visible deficiencies do not present detectable homology with the I factor. (2) The majority of rearrangements do not involve the I elements already present on the paternal X chromosome. (3) The hybridization signal distributions on the X chromosome are not uniform. They present peaks of various heights which may correspond to specific anchoring areas of copies of I in the course of integration. (4) The data presented here agree with the literature with respect to the mean number of copies of I per X chromosome and to the excess of copies of I at locus 1A. Two rearrangement formation mechanisms are envisaged: crossing-over and 'target' exchanges.

Combined overexpression of c-erbB-2 protein and epidermal growth factor receptor (EGF-R) could be predictive of early and long-term outcome in human breast cancer: a pilot study.

In order to determine the prognostic value of c-erbB-2 protein and Epidermal Growth Factor Receptor (EGF-R), we used an immunohistochemical procedure with specific antibodies on paraffin-embedded material from a series of 73 operable breast cancer carcinomas. c-erbB-2 protein (c-erbB-2 score > 1) was overexpressed in 10/73 cases (14%) and EGF-R (EGF-R ratio > 1) in 42/73 cases (58%). c-erbB-2 overexpression was correlated with tumour size (P < 0.02) and lymph-node involvement (P = 0.05) whereas EGF-R overexpression did not correlate with any of the variables tested. The relative risk of relapse was respectively 1 vs 4.5 (P = 0.001) for patients with a negative (0-1) or positive (> 1) c-erbB-2 score and 1 vs 3 for patients with an EGF-R ratio < or = 1 and > 1 (P = 0.03). Moreover, c-erbB-2 protein overexpression is more specifically an early factor of poor prognosis whereas EGF-R overexpression is a long-term factor of poor prognosis. Patients with an early good prognosis (c-erbB-2 score = 0-1) are found to relapse with time when EGF-R is overexpressed. In a multivariate analysis including axillary lymph-node status, histological grade, tumour size, ER status, c-erbB-2 score, EGF-ratio and hormonal treatment, c-erbB-2 overexpression was the most powerful parameter (P = 0.001) followed by EGF-R overexpression (P = 0.02). We concluded that, in our series, the combined determination of c-erbB-2 protein and EGF-R appeared to be a prognostic indicator whereby both early and long term prognosis could be determined in breast cancer patients.

Review article: intestinal barrier dysfunction and central nervous system disorders--a controversial association.

BACKGROUND: Central nervous system (CNS) development and physiopathology are greatly affected by environmental stimuli. The intestinal barrier restricts the entrance of toxins, pathogens, and antigens while modulating the expression of various neuroactive compounds. The existence of a rich gut-to-brain communication raises the possibility that intestinal barrier alterations may take part in the pathophysiology of CNS disorders. AIM: To review evidence associating intestinal barrier dysfunction with the development of CNS disorders. METHODS: Literature search was conducted on PubMed using the following terms: intestinal barrier, intestinal permeability, central nervous system, mental disorders, schizophrenia, autism, stress, anxiety, depression, and neurodegeneration. RESULTS: Clinical and animal model studies of the association between intestinal barrier and schizophrenia, autism spectrum disorders, neurodegenerative diseases or depression were reviewed. The majority of reports concentrated on schizophrenia and autism spectrum disorders. About half of these described increased intestinal permeability/mucosal damage in patients compared with healthy controls, with up to 43% of children with autism spectrum disorders and up to 35% of schizophrenia patients displaying abnormally high urinary excretion of the sugars used as permeability markers. However, another substantial group of studies did not find such differences. In autism spectrum disorders, some reports show that the use of diets such as the gluten-free casein-free diet may contribute to the normalisation of lactulose/mannitol ratio, but to date there is no adequately controlled study showing improvement in behavioural symptoms following these dietary interventions. CONCLUSIONS: Evidence of altered intestinal permeability in individuals suffering from CNS disorders is limited and cannot be regarded as proven. Moreover the efficacy of targeting gut barrier in the management of neurological and behavioural aspects of CNS disorders has not yet been established, and needs further investigation.

Pilot study: alterations of intestinal microbiota in obese humans are not associated with colonic inflammation or disturbances of barrier function.

BACKGROUND: Obesity is associated with low-grade inflammation contributing to insulin-resistance. Gut barrier alterations, described in animal models of obesity, probably favour inflammation. This has not been hitherto described in obese humans. AIM: To evaluate gut permeability in asymptomatic obese and its association with plasma (C-reactive protein (CRP), arachidonate/eicosapentaenoate ratio) and faecal (calprotectin and leptin) markers of inflammation and microbiota alterations. METHODS: A total of 13 obese (age: 33.9 ± 11.5 years; BMI: 35.9 ± 5.0 kg/m²) and 11 control subjects (age: 30.3 ± 8.1 years; BMI: 23.5 ± 2.4 kg/m²) were recruited. Gut permeability was assessed by the lactulose-mannitol-sucralose test, plasma fatty acids by gas chromatography, faecal calprotectin and leptin by Elisa and faecal microbiota by G+C profiling. RESULTS: C-reactive protein was increased in the obese subjects (P = 0.01), but neither the plasma arachidonate/eicosapentaenoate ratio, the faecal levels of calprotectin and leptin, nor the gut permeability were altered. The faecal microbiota was altered in the obese (P = 0.0002), with predominance of bacterial populations having a lower G+C content and decreased concentrations of high G+C populations. CONCLUSIONS: Asymptomatic obese individuals with systemic low-grade inflammation do not have evidence of colonic inflammation or gut barrier alteration; however, the biodiversity of their intestinal microbiota is affected.

Prevalencia de hipolactasia en escolares de la Región Metropolitana / Prevalence of hypolactasia in chilean schoolchildren from Santiago city

adult primary hypolactasia results from the genetically programmed decrease of intestinal lactase after weaning. It is estimated that about 75% of the adult population in the world is hypolactasic. Aim: To determine the prevalence of hypolactasia in school children in the Metropolitan Area and its relation to the consumption of dairy products and calcium. Subjects and methods: A cross-sectional study was performed in 326 schoolchildren aged 7 to 18 years belonging to 6 educational establishments from different socioeconomic levels in Santiago. A lactose hydrogen breath test was performed in each subject and gastrointestinal symptoms were registered during the test. A survey of dairy product consumption was carried out to determine calcium intake. Results: Hypolactasia was detected in 42.3% of the subjects and those had a higher prevalence of gastrointestinal symptoms compared to the lactase-persistent subjects (81.9% vs. 70.2%, P = 0.019). In addition, digestive symptoms were also more severe in the hipolactasic children (p <0.00000). Calcium intake from dairy sources was 492.5 ± 22.5 mg/d, with no differences according to the hipolactasic/lactase-persistent status of the subjects or their socioeconomic stratum. This intake covers only 37.9 ± 1.7% of the recommended intakes of calcium. Conclusions: a high percentage of hypolactasia and low dietary intake of calcium from dairy origin was detected in the school population evaluated. These data are important to develop new strategies to increase the consumption of calcium-containing foodstuffs and improve bone health in the population.

La hipolactasia primaria del adulto resulta de la disminución genéticamente programada de la lactasa intestinal después del destete. Se estima que alrededor del 75% de la población adulta en el mundo presentaría es hipolactásica. Objetivo: Determinar la prevalencia de hipolactasia en escolares de la Región Metropolitana y su relación con el consumo de productos lácteos y de calcio. Sujetos y métodos: Se realizó un estudio transversal en una muestra de 326 escolares de 7 a 18 años pertenecientes a 6 establecimientos educacionales de distintos niveles socioeconómicos en Santiago. A cada sujeto se les realizó una prueba de hidrógeno en aire espirado (HBT) con lactosa y se registró la aparición de sintomatología digestiva durante la prueba. También se realizó una encuesta de tendencia de consumo de productos lácteos para determinar la ingesta de calcio. Resultados: 42.3% de los escolares eran hipolactásicos y presentaron una mayor prevalencia de sintomatología digestiva comparado con aquellos sujetos lactasa-persistente(81.9% vs. 70.2%; p=0.019); dicha sintomatología, además, fué más intensa en los hipolactásicos(p<0.00). La ingesta de calcio de origen lácteo fue de 492.5±22.5 mg/día, sin diferencias según el estado hipolactásico/lactasa-persistente o el nivel socioeconómico de los sujetos. Dicha ingesta cubre sólo el 37.9±1.7% de los aportes recomendados de calcio. Conclusiones: la población de escolares estudiada se caracteriza por tener un porcentaje de hipolactasia alta y aportes dietarios de calcio de origen lácteo bajos. Estos datos son de importancia para desarrollar programas destinados a aumentar el consumo de calcio para mejorar la salud ósea de la población.

Functional fermented milk products.

Fermented foods have been used since prehistoric times. Their number, variety and geographic origin are considerable, and different substrates and agents including bacteria, yeasts and moulds have been used in their preparation. In the last few decades the scientific approach to the study of the participating microorganisms and the resulting products have provided a better understanding of their biological importance. Among the many health-related properties of fermented foods, effects on blood pressure have been described after casein hydrolysis by lactic acid bacteria. Peptides with antimicrobial activity, mainly against Gram-negative bacteria, and derived from casein have also been identified. This could explain, at least in part, the antidiarrheal effects of fermented products including those on traveler's diarrhea and against colonization by Helicobacter pylori. One of the best known advantages of fermented milk products is their capacity to improve lactose tolerance in hypolactasic subjects. With the growing prevalence of allergies and inflammatory bowel diseases, considerable interest has been focused on the effects of lactic acid bacteria in these conditions; there is evidence that these agents are associated with improvements in allergy; no such evidence exists for Crohn's disease or ulcerative colitis. A cholesterol-lowering capacity has also been described for some microorganisms. Not all the fermenting microorganisms have probiotic capacities as the latter are strain-specific.

Paraventricular-coerulear interactions: role in hypertension induced by prenatal undernutrition in the rat.

Rats submitted to fetal growth retardation by in utero malnutrition develop hypertension when adult, showing increased hypothalamic mRNA expression for corticotropin-releasing hormone (CRH) and increased central noradrenergic activity. As hypothalamic CRH serves as an excitatory neurotransmitter within the locus coeruleus (LC) and coerulear norepinephrine plays a similar role within the paraventricular nucleus (PVN) of the hypothalamus, we studied, in both normal and prenatally undernourished 40-day-old anesthetized rats, the effects of intra-LC microinjection of CRH and intra-PVN microinjection of the alpha(1)-adrenoceptor antagonist prazosin on multiunit neuronal activity recorded simultaneously from the two nuclei, as well as the effects on systolic pressure. Undernutrition was induced during fetal life by restricting the diet of pregnant mothers to 10 g daily, whereas mothers of control rats received the same diet ad libitum. At day 40 of postnatal life: (i) undernourished rats showed increased neuronal activity in the PVN and LC, as well as increased systolic pressure; (ii) intra-LC CRH stimulated LC and PVN neurons and increased systolic pressure only in normal rats; (iii) intra-PVN prazosin decreased LC and PVN neuronal activity and systolic pressure only in undernourished rats; and (iv) in normal rats, prazosin prevented the stimulatory effect of CRH only in PVN activity; in undernourished rats, prazosin allowed CRH to regain its stimulatory effects. The results point to the existence of an excitatory PVN-LC closed loop, which seems to be hyperactive in prenatally undernourished rats as a consequence of fetal programming; this loop could be responsible, in part, for the hypertension developed by these animals.

[Effect of a dry boldo extract on oro-cecal intestinal transit in healthy volunteers]. / Effecto de un extracto seco de boldo sobre el tránsito intestinal oro-cecal en voluntarios sanos.

BACKGROUND: Boldo (Peumus boldus Molina) is a widely used medicinal plant. However, its physiological effects are not well known. Recent studies in animals showed that certain components of boldo relax smooth muscle and prolong intestinal transit. AIM: To assess the effects of a dry boldo extract on oro cecal transit time in normal humans. SUBJECTS AND METHODS: Twelve volunteers received 2.5 g of a dry boldo extract or a placebo (glucose) during two successive periods of four days. On the fourth day, 20 g of lactulose were administered and breath hydrogen was collected every 15 min. Oro cecal transit time was defined as the time in which breath hydrogen increased by 20 ppm over the fasting level. RESULTS: Oro cecal transit time was larger after dry boldo extract administration, compared to placebo (112.5 +/- 15.4 and 87 +/- 11.8 min respectively, paired t p < 0.05). CONCLUSIONS: Dry boldo extract prolongs oro cecal transit time, a possible explanation for its medicinal use.