Biomedical subjects

J A Martínez

Publications and source records attributed to J A Martínez.

At least 19 recordsLinked to original sources

PubMed2006

Differences in short-term metabolic responses to a lipid load in lean (resistant) vs obese (susceptible) young male subjects with habitual high-fat consumption.

OBJECTIVE: To determine the role of macronutrients oxidation ability in the postprandial response to a high lipid load in the mechanisms conferring resistance or susceptibility to obesity. SUBJECTS AND DESIGN: Nine lean and nine obese young male subjects with habitual similar high-fat intake (>40 % of energy) and comparable physical activity were selected and categorized as 'resistant', those who remained lean (body mass index (BMI) <25 kg/m2), and 'susceptible', those who were obese (BMI>30 kg/m2). Fasting blood samples were taken for the evaluation of blood metabolic and hormonal variables. Resting metabolic rate (RMR) and substrates oxidation were measured by indirect calorimetry, in the fasting state and every 30 min for 3 h after a rich lipid meal (fat 94.7%) supplied to cover the 50% of the volunteers energy requirements. The study was performed at the Metabolic Unit of the University of Navarra. RESULTS: Fasting RMR and lipid oxidation were higher in obese-susceptible subjects. However, similar values were found in both groups after adjustment for fat mass and free fat mass. The cumulative postprandial fat oxidation was also similar in both groups (despite having different tissue metabolic activity), whereas cumulative carbohydrate oxidation was lower in the obese-susceptible group. The thermic effect of food (% of dietary induced thermogenesis) was lower (P<0.05) in the susceptible-obese subjects. The energy and fat balance were more positive in the obesity-susceptible individuals after the high fat load, who also showed higher fasting homeostatic model assessment index, low-density lipoprotein-cholesterol and triacylglyceride levels, hyperleptinemia and hypoadiponectinemia. CONCLUSION: Lean-resistant individuals came closer to achieving fat balance than obese-susceptible subjects. These metabolic and hormonal differences are probably genetically determined.

Area Under Curve↗

PubMed2006

The nucleus tractus solitari (NTS) participates in peripheral ghrelin glucostatic hunger signalling mediated by insulin.

Three extrahypothalamic areas, the nucleus of the tractus solitari (NTS), the central nucleus of the amygdala (CeA) and the dorsal raphe nucleus (DRN), all potentially involved in peripheral ghrelin signalling of appetite control mediated by the glucose levels were examined. Thus, a specific anti-ghrelin antibody (AGA) was intravenously administered in order to remove the ghrelin signalling and then, subsequently, 4-h food intake, plasma glucose levels and the brain c-fos expression in the NTS, CeA and DRN were assessed. Food intake significantly decreased when the AGA was administered. NTS c-Fos expression was significantly augmented by insulin, while it was significantly decreased by the AGA. These results suggest that the NTS is a part of the ghrelin pathway that regulates the orexigenic signalling cascade, which may be triggered by a drop in blood glucose levels mediated by insulin.

Amygdala↗

PubMed2006

Effects of eicosapentaenoic acid (EPA) on adiponectin gene expression and secretion in primary cultured rat adipocytes.

Adiponectin, a hormone produced by adipocytes, is involved in glucose metabolism and insulin sensitivity. The production of this adipokine is impaired in obesity and insulin resistance. Eicosapentaenoic acid (EPA) is a dietary n-3 polyunsaturated fatty acid that improves insulin sensitivity in several models of obesity and diabetes, which has been suggested to be related to adiponectin induction. An increase in adiponectin production has been also associated with an up-regulation of the transcriptional factor PPARgamma. The aim of this trial was to evaluate the direct effects of EPA on adiponectin gene expression and protein secretion in isolated rat adipocytes as well as to explore the potential mechanisms involved. A comparative study with troglitazone, a PPARgamma agonist, was also performed. For these purposes, primary rat adipocytes were cultured with EPA (100 and 200 microM) and with troglitazone (10 microM) for 96 hours. Both EPA and troglitazone improved glucose utilization by adipocytes. As expected, troglitazone enhanced adiponectin secretion and increased PPARgamma gene expression. However, EPA significantly decreased adiponectin gene expression and protein secretion and reduced PPARy mRNA levels, suggesting that the inhibition of adiponectin by EPA is likely to be secondary to the down-regulation of this adipogenic transcription factor. Moreover, these results suggest that other mechanisms different from the direct stimulation of adiponectin by the fatty acid are underlying the insulin-sensitizing properties observed after EPA treatment in vivo.

Adipocytes↗

PubMed2006

Diferential gene expression and adiposity reduction induced by ascorbic acid supplementation in a cafeteria model of obesity.

Obesity is considered as an inflammatory disease, in which free radical-induced oxidative stress and excessive intake of macronutrients exacerbate their symptoms. In this context, we assessed in rats the possible preventive effect of the supplementation with an antioxidant molecule, ascorbic acid, in order to reduce the adiposity induced by the intake of a high-fat diet. For this purpose, during 56 days, three groups of male Wistar rats were fed on: a) standard pelleted diet, b) Cafeteria diet, c) ascorbate-supplemented (750 mg/kg of body weight) Cafeteria diet. At the end of the experimental period, microarray analysis was used to identify genes transcriptionally induced or repressed by both experimental dietary models (Cafeteria diet supplemented or not with ascorbic acid) in subcutaneous adipose tissue. Dietary ascorbic acid was able to protect against high fat diet effects, reducing the increase of body weight, total body fat and enlargement of different adipose depots induced by the Cafeteria diet without affecting food intake. An association analysis accurately and differentially allowed the detection of gene expression changes related with adiposity and insulin resistance. The genes that more strongly correlated with body fat and HOMA insulin resistance index were involved in adipocyte differentiation, lipid and glucocorticoid metabolism, cell cycle regulation, as well as in several insulin-induced processes. Some other transcripts are regulated by the vitamin C-mediated reduction of adiposity, such as genes that participate in glucocorticoid metabolism, adipogenesis, pentose phosphate pathway, or tricarboxylic acid cycle. This strategy was able to link variations in adipose tissue gene expression with markers of diet-induced obesity in rats, such as insulin resistance and body fat content.

Animals↗

PubMed2006

Usefulness of teicoplanin for preventing methicillin-resistant Staphylococcus aureus infections in orthopedic surgery.

In order to gather more data on the use of teicoplanin for reducing MRSA infections in high-risk populations, the present study was conducted. At a hospital in Barcelona, Spain, there was a high prevalence of MRSA infections among patients who underwent surgery for femoral neck fracture during the first 5 months of 2002 (period A) when cefuroxime was the antibiotic prophylaxis. During the following 12 months (period B) 600 mg of teicoplanin was added to cefuroxime. The rates of overall and MRSA infection during period A were 5.07 and 2.73%, respectively. Pulsed-field gel electrophoresis demonstrated there was no clonal relationship among MRSA strains. No nasal carriers of MRSA were detected among health workers. During period B the rates of overall and MRSA infection were 2.36 and 0.19%, respectively. Both rates were statistically significantly lower than those in period A (p<0.05). These results suggest teicoplanin may be useful in patients undergoing orthopedic surgery when the prevalence of MRSA is high.

Aged, 80 and over↗

PubMed2006

Prospective evaluation of procalcitonin in adults with non-neutropenic fever after allogeneic hematopoietic stem cell transplantation.

The aim of this study was to analyze whether procalcitonin (PCT) is a diagnostic marker of infectious diseases during the non-neutropenic period in patients who have received an allogeneic hematopoietic stem cell transplant (HSCT). We included 65 patients in whom an allogeneic HSCT was performed in a 2-year period (April 2002-July 2004). PCT levels were monitored in every febrile episode by an immunoluminometric assay. Febrile episodes were classified according to the final diagnosis in: fever of unknown origin, microbiologically or clinically documented infection and non-infectious fever. Fifty-two febrile episodes in the non-neutropenic period were included in the study. Out of these 52, 26 had an infectious etiology: 11 fulfilled criteria for probable or proven invasive aspergillosis (IA), three were classified as possible invasive fungal infection (IFI) and 12 episodes were caused by other infections. Mean values of PCT on the first day of admission were: 8.0 (+/- 4.9) in probable-proven IA (P = 0.013, Kruskall-Wallis), 4.5 (+/- 3.4) in possible IFI and 1.5 (+/- 0.9) in infections other than IFI. Therefore, we could conclude that during the non-neutropenic phases of allogeneic HSCT, a high PCT value is associated significantly with IA.

Adult↗

PubMed2006

Treatment of acute post-surgical infection of joint arthroplasty.

The best antibiotic regimen for acute prosthetic joint infection, treated without removal of the implant, has not been well-defined. This study describes the use of a protocol based on oral rifampicin combinations to treat 47 cases that were followed prospectively for a 2-year period. The regimen used most commonly was levofloxacin 500 mg/24 h plus rifampicin 600 mg/24 h for a mean duration of 2.7 +/- 1 months. The cure rate was 76.9%, and the only independent risk-factor associated with treatment failure was infection caused by methicillin-resistant Staphylococcus aureus or Enterococcus spp. (OR 17.6, p 0.003). Overall, the results suggested that use of oral antibiotics, including rifampicin, for 2-3 months was a good treatment option.

Acute Disease↗

PubMed2005

Serum and gene expression levels of leptin and adiponectin in rats susceptible or resistant to diet-induced obesity.

The aim of the present study was to identify the role of leptin and adiponectin in the development of resistance or susceptibility to diet-induced obesity in rats. For this purpose, male Wistar rats were fed with standard laboratory diet (control group) or cafeteria diet. After 15 days, two groups of rats with different response respect to the cafeteria diet were identified, and were assigned as diet-induced obesity (DIO) and diet resistant (DR) rats. The high-fat diet induced a very significant increase in both body and fat mass weight in DIO group. However, DR rats, gained even less weight than control-fed animals. Food intake was increased in cafeteria-fed rats (both DIO and DR) in comparison to control group; but hyperphagia was higher in DIO rats. In addition, feed efficiency (the ratio of weight gained to calories consumed) was significantly decreased in DR as compared to DIO rats. Regarding leptin, a significant increase in both adipose tissue gene expression and serum levels was observed in DIO rats in comparison with other groups (control and DR). A significant increase in both adiponectin circulating levels and adipose tissue mRNA expression was also observed in DIO animals as compared with the other groups. These data suggest that the susceptibility to obesity of DIO rats might be secondary, at least in part, to an earlier development of leptin resistance, which could lead to alterations in food intake (hyperphagia) and energetic metabolism. However, neither changes in leptin or adiponectin seem to be involved in the adaptive mechanisms that confer resistance to high fat intake.

Adipose Tissue↗

PubMed2005

Ectopic UCP1 gene expression in HepG2 cells affects ATP production.

The UCP1 is an uncoupling protein located in the inner mitochondrial membrane of brown adipocytes, which has a well-documented role in diet-induced thermogenesis. The current study assessed whether UCP1 transfected liver cells demand more fuel substrates in the oxidative phosphorylation processes. Therefore, the purpose of this experiment was to achieve an ectopic expression of UCP1 in HepG2 cells to significantly decrease the production of ATP. The UCP1 gene was transferred into the hepatic cells by using a calcium phosphate precipitation protocol. The efficiency of the transfection was tested, 48 hours later, by bioluminescence of luciferase previously transfected, while the expression of mRNA of UCP1 was demonstrated by RT-PCR. In addition, measuring the production of ATP by using a bioluminescence procedure assessed the functionality of this protein. Transfected liver cells with UCP1 showed a decrease of 23% in ATP production in comparison with control cells without expression of UCP1 (2.23 vs. 2.90 RLU/pg protein, p=0.015). In conclusion, the ectopic expression of UCP1 decreased the production of ATP, possibly uncoupling the oxidative phosphorylation, which could be a novel approach for understanding thermogenic processes and eventually for energy metabolism and body weight management.

Adenosine Triphosphate↗

PubMed2005

Inflammation and conjugated linoleic acid: mechanisms of action and implications for human health.

Data from a number of studies and trials have shown that different conjugated linoleic acids (CLA's) may produce beneficial effects on cancer, atherosclerosis, hypertension, diabetes and changes in body composition. Despite the increasing knowledge about CLA's implications on health, the mechanism of action of these fatty acids is not completely understood. Moreover, human studies indicate that some of these beneficial effects are considerably less evident than anticipated from mice studies, while the efficacy and safety of dietary supplements containing CLA have been questioned in some intervention trials. Recently, it has been suggested that the anti-carcinogenic and anti-atherosclerosis effects of CLA's stem from its anti-inflammatory properties. Because inflammatory responses are associated with the pathophysiology of many diseases, including obesity and the metabolic syndrome, the investigation in this area is of growing interest in recent years.

Anti-Inflammatory Agents↗

PubMed2005

Lower mortality among patients with community-acquired pneumonia treated with a macrolide plus a beta-lactam agent versus a beta-lactam agent alone.

A cohort of 1,391 patients with community-acquired pneumonia of unknown etiology, atypical pneumonia, Legionella pneumophila pneumonia, viral pneumonia, or pneumococcal pneumonia was studied according to a standard protocol to analyse whether the addition of a macrolide to beta-lactam empirical treatment decreases mortality rates. Patients admitted to the intensive care unit were excluded. Severity was assessed using the PORT score. An etiological diagnosis was achieved in 498 (35.8%) patients (292 infections due to Streptococcus pneumoniae). Treatment was chosen by the attending physician according to his/her own criteria: beta-lactam agent in 270 and beta-lactam agent plus a macrolide in 918 cases. The mortality rate was 13.3% in the group treated with a beta-lactam agent alone and 6.9% in the group treated with a beta-lactam agent plus a macrolide (p=0.001). The percentage of PORT-group V patients was 32.6% in the group treated with a beta-lactam agent alone compared to 25.7% in the group who received a beta-lactam agent plus a macrolide (p=0.02). After controlling for PORT score, the odds of fatal outcome was two times higher in patients treated with a beta-lactam agent alone than in those treated with a beta-lactam agent plus a macrolide (adjusted OR = 2, 95%CI 1.24-3.23). The results suggest that the addition of a macrolide to an initial beta-lactam-based antibiotic regimen is associated with lower mortality in patients with community-acquired pneumonia, independent of severity of infection, thus supporting the recommendation of a beta-lactam-agent plus a macrolide as empirical therapy.

Amoxicillin-Potassium Clavulanate Combination↗

PubMed2005

Bacteremia and septic shock after solid-organ transplantation.

BACKGROUND: Bacteremia and septic shock remain important causes of morbidity and mortality after solid-organ transplantation. The aim of this study was to assess the characteristics and risk factors for mortality among patients with bloodstream infections and shock. METHODS: From January 1991 to December 2000, all episodes of bloodstream infection were prospectively examined, considering bacteremia or fungemia as significant according to the CDC criteria. Septic shock was diagnosed in a patient with systemic inflammatory response syndrome and persistent dysfunction of at least one organ caused by hypoperfusion despite hemodynamic support. RESULTS: There were 466 episodes of bacteremia in 382 patients, with 66 of them developing septic shock. Risk factors for developing shock were age >50 (P = .006), liver transplant (P = .029), nosocomial infection (P = .034), pulmonary focus (P = .0001), P. aeruginosa infection (P = .001), and polymicrobial etiology (P = .039). On multivariate analysis, only age, nosocomial infection, and pulmonary source were significant. Among 66 shock patients, bacteremia was due to gram-negative bacteria in 53%, gram-positive bacteria in 24%, fungal in 7.5%, and polymicrobial in 12% of patients. The most frequent source was the lung (26%). Empiric antimicrobial therapy was correctly chosen in 79%; however, 36 patients died (54%), including 27 despite correct therapy. Urinary tract infections had less mortality than other foci. CONCLUSIONS: Risk factors for developing septic shock in bacteremia were age more than 50 years, nosocomial acquisition, and pulmonary focus. Despite adequate empiric antibiotic therapy, the mortality remained high.

Bacteremia↗

PubMed2005

Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight.

Obesity, hyperglycemia, and insulin resistance have been associated to an oxidative mitochondrial dysfunction. The aim of this research was to evaluate the relation between carbohydrate metabolism and mitochondrial oxidation, as affected by the weight status and the weight loss induced by a calorie-restricted diet. Lean control men (BMI<25 kg/m2, n = 6) and obese men (BMI>30 kg/m2, n = 14), who were characterized as insulin resistant (n = 6) or insulin sensitive (n = 8) based on HOMA index values, participated in the trial. Plasma insulin levels and mitochondrial oxidation estimated by the 2-keto(1-13C)isocaproate breath test, were measured after ingestion of a test meal during 3 h. Obese subjects repeated the breath test protocol after a 10-week caloric restriction diet to lose weight. Postprandial insulin secretion tended to be marginally higher (P = 0.059) in both obese groups than in controls, while the rate of postprandial mitochondrial oxidation was markedly decreased (P = 0.019) in the obese subjects as compared with lean individuals. The nutritionally induced weight loss produced a rise in the postprandial oxidative process in volunteers initially considered as insulin resistant (P = 0.036), while no statistical differences in the insulin-sensitive obese (P = 0.241) were found. Interestingly, the percentage of oxidized tracer was inversely related to postprandial insulin secretion (r = -0.56; P = 0.001). In conclusion, these results support the hypothetized relation between carbohydrate metabolism and mitochondrial oxidation at a postprandial state in obese subjects, raising interest about mitochondria stimulation as a target in the therapy of obesity.

Adult↗

PubMed2005

No evidence of association between the serotonin 2A receptor--1438G/A promoter polymorphism and childhood obesity in a Spanish population: A case-parent study and a matched case-control study.

Serotonin has been related to feeding behaviour and body weight control through its suppressive effect on appetite. Conflicting results have been published in the literature regarding the association between the - 1438 G/A promoter polymorphism of the 5HT2A gene with obesity-related variables. The aim of this study was to assess the association between the--1438 G/A polymorphism of the 5HT2A gene with childhood obesity in a Spanish population. A total of 136 cases aged 6-16 years with BMI above the 97th percentile of the Spanish BMI reference data for age and gender were matched by gender and age (+/- 6 months) with 136 controls. Additionally, 43 obese children and their parents were selected for a family-based association study (case-parent study). Genotyping was carried out by polymerase chain reaction and restriction enzyme analysis. Conditional logistic regression and transmission/disequilibrium test were used to assess genotype-obesity association. In the matched case-control study, the crude and adjusted odds ratios for the association between 5HT2A--1438 G/A genotypes were nonsignificant. Likewise, no association is suggested by the case-parent study. In conclusion, it is unlikely that the--1438 G/A polymorphism of 5HT2A gene may influence obesity in a Spanish children population.

Alleles↗

PubMed2005

Does weight loss prognosis depend on genetic make-up?

The prevalence of obesity is rising throughout the world. Indeed, obesity has reached epidemic proportions in many developed and transition countries. Obesity is a complex disease with multifactorial origin, which in many cases appears as a polygenic condition affected by environmental factors. Treatment or prevention of obesity is necessary to reverse or avoid the onset of type 2 diabetes and other obesity-related diseases. Weight loss is a complex trait that depends on many environmental, behavioural and genetic influences. An effective programme for the management of overweight and obesity must take into account all of these factors. Individual responses to weight loss interventions vary widely and reliable predictors of successful slimming are poorly understood. The individual genetic make-up participating in energy expenditure regulation, appetite control, lipid metabolism and adipogenesis, have been reported to affect the risk of treatment failure in some subjects. In addition, the genotype could also help to predict the changes in lipid profile, cardiovascular risk factors and insulin sensitivity in response to weight loss. Herein, the current evidence from human studies that support the existence of a genetic component and the participation of different polymorphisms in the prognosis of weight loss induced by interventions leading to a negative energy balance are reviewed.

Energy Metabolism↗

PubMed2005

Is the combination of pyrazinamide plus rifampicin safe for treating latent tuberculosis infection in persons not infected by the human immunodeficiency virus?

SETTING: Nine public health care centres in four Spanish cities. OBJECTIVE: To evaluate the efficacy and safety of 2 months of rifampicin (R) plus pyrazinamide (Z) therapy (2RZ) compared with a 6-month course of isoniazid therapy (6H) for treating latent tuberculosis infection (LTBI). DESIGN: Multicentered, randomised, comparative and prospective trial conducted in HIV-seronegative contacts of infectious pulmonary TB cases. RESULTS: Of 352 individuals, 199 received 6H and 153 2RZ; 73% of contacts receiving 6H and 71% receiving 2RZ completed treatment (P = 0.73). Treatment interruption due to hepatotoxicity (ALT/AST > 5 times upper limit of normal) was observed in 10% of contacts in the 2RZ group and in 2.5% of the 6H group (P = 0.007). This higher than expected rate of hepatotoxicity in the 2RZ arm led to premature termination of the study. Severe or fatal liver injury was not detected. Liver function tests normalised after discontinuation of treatment. We conclude that the use of RZ should only be considered when other regimens are unsuitable and intensive monitoring of liver function is feasible.

Adolescent↗

PubMed2005

[Comparison between two methods to estimate physical activity in obese women: accelerometry and self-administered questionnaire].

The aims of this study were to describe a female obese population according to their food intake and physical activity, and to compare two methods to estimate physical activity (PA). The study included a nutritional interview where a detailed dietary history was done, an initial clinical day in which measurements of body composition and basal metabolic rate (BMR) were carried out and an estimation of PA by means of a triaxial accelerometer and a PA questionnaire. The group of volunteers showed a mean BMI of 37.15 kg/m2, a waist/hip ratio of 0.82 and a mean body fat mass of 43.34%. The average of BMR was 1720 Kcal/d and the CRNP of 0.79. The total caloric intake was 3344 Kcal/d with a energy-distribution of 43.1% Carbohydrates, 16.4% Proteins, 40.3% Lipids. Weight and BMI showed a positive correlation (p < 0.05) with the sedentary index (SI). Also, weight presented a positive correlation with the heart rate (p < 0.05). The estimates of PA derived from the questionnaire showed a positive correlation with the triaxial accelerometer (p < 0.01); and this one, revealed a negative correlation with the SI (p < 0.01). Anthropometric, metabolic and food intake variables are comparable to the results found in obese women from similar socioeconomic background. The estimates of PA according to the questionnaire were significantly correlated to the results of the triaxial accelerometer, thus confirming the validity of the questionnaire to assess PA in an obese population.

Acceleration↗

PubMed2004

Gene expression changes in rat white adipose tissue after a high-fat diet determined by differential display.

The differences in gene expression pattern of visceral white adipose tissue between control and high-fat-fed rats were compared using the mRNA differential display methodology. The results, confirmed by Northern blot, showed eight genes upregulated: adiponectin, fibrillin-1, transferrin, Y-box binding protein-1, IgE receptor beta chain (FcRIbeta), alpha-1 haemoglobin, and ribosomal proteins S10 and L7 and four genes downregulated: caveolin-2, lactate dehydrogenase-A, mitochondrial 16S rRNA, and mitochondrial cytochrome oxidase subunit I/serine tRNA. Two of these genes have been already related to obesity (adiponectin and caveolin-2) while the others are known to participate in metabolic, signalling or transcription regulation pathways that can be relevant in energy (lipid and/or carbohydrate) metabolism.

Adipose Tissue↗