Hospital Universitari Joan Tarragona

Tarragona, Spain

Hospital Universitari Joan Tarragona

Tarragona, Spain
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Auguet T.,Rovira i Virgili University | Auguet T.,Hospital Universitari Joan Tarragona | Terra X.,Rovira i Virgili University | Porras J.A.,Hospital Universitari Joan Tarragona | And 9 more authors.
Clinical Biochemistry | Year: 2013

Objectives: The few studies on the physiopathological role of visfatin in morbid obesity and the related metabolic diseases have led us to examine visfatin levels and its liver gene expression in morbidly obese women with non-alcoholic fatty liver disease (NAFLD). Design and methods: We examined the circulating levels of visfatin by ELISA in serum samples from 95 morbidly obese women (MO) (BMI>40kg/m2) who underwent bariatric surgery and 38 normal weight control women (BMI<25kg/m2). We analysed visfatin liver and adipose tissue mRNA expression by RT-PCR. We evaluated the circulating levels and gene expression of adiponectin, resistin, RBP4, TNFα, IL6 and CRP. Results: Serum visfatin was significantly higher in MO compared with controls, and also in MO with NAFLD was significantly higher than MO with normal liver. We found that NAFLD diabetic patients presented similar serum visfatin levels than non-diabetic. Serum visfatin correlated with IL6 (r = 0.496; p<0.001) and CRP levels (r = 0.241; p = 0.049).Liver visfatin expression was significantly higher in MO compared to controls and was also significantly higher in MO with NAFLD than in MO with normal liver. Visfatin liver expression correlated positively with resistin (r = 0.436, p = 0.018) and TNFα expression (r = 0.328, p = 0.028).Visfatin expression in adipose tissues was similar among the MO groups analysed. Conclusion: Serum visfatin and its liver expression are higher in MO women with NAFLD, irrespective of the presence of diabetes. Serum visfatin and its liver expression correlate positively with pro-inflammatory factors. These findings suggest that visfatin may be a molecule related with fat inflammation in morbid obesity and fatty liver disease. © 2012 The Canadian Society of Clinical Chemists.


Auguet T.,Hospital Universitari Joan Tarragona | Auguet T.,Grup Of Recerca En Medicina Aplicada Hospital Joan Xxiii | Quintero Y.,Grup Of Recerca En Medicina Aplicada Hospital Joan Xxiii | Terra X.,Grup Of Recerca En Medicina Aplicada Hospital Joan Xxiii | And 12 more authors.
Obesity | Year: 2011

Because the role of lipocalin 2 (LCN2) in morbid obesity is still not well defined, the aim of this study was to evaluate the circulating levels and the expression of LCN2 in visceral (VAT) and subcutaneous adipose tissue (SAT) in severely obese (SO) women. We also analyzed its relationship with inflammatory cytokines in the same subjects. The study comprised 90 white women, 39 of whom were lean controls (BMI 25kg/m 2) and 51 SO (BMI 40kg/m 2). Both circulating and adipose tissue levels of LCN2 were quantified by enzyme-linked immunosorbent assays. LCN2 mRNA levels from VAT and SAT were assessed by real-time reverse transcriptase-PCR (n = 60). LCN2 serum levels were significantly higher in the SO women than in the lean controls (P = 0.042), and were found to be strongly correlated with tumor necrosis factor receptor I (TNFR1) circulating levels. In the SO cohort, LCN2 serum levels were also associated with higher BMI values, but not with the homeostasis model assessments of insulin resistance (HOMA2-IR). LCN2 mRNA expression was markedly higher in SO women than in lean women in both VAT (P = 0.043) and SAT (P = 0.031). In SAT, LCN2 was negatively correlated with adiponectin and adiponectin receptor-2 expression, and positively with interleukin-6 (IL-6) expression. A strong positive correlation was also found between LCN2 expression and the mean diameter of adipocytes in VAT. Our results revealed that the circulating level of LCN2 is associated with obesity and BMI. LCN2 mRNA is over-expressed in adipose tissue from SO subjects. Finally, the expression of LCN2 is strongly related to an expression profile of proinflammatory cytokines but not to insulin resistance in nondiabetic SO women. © 2011 The Obesity Society.


Terra X.,Rovira i Virgili University | Auguet T.,Rovira i Virgili University | Auguet T.,Hospital Universitari Joan Tarragona | Guiu-Jurado E.,Rovira i Virgili University | And 11 more authors.
Obesity Surgery | Year: 2013

Background: Different studies have evaluated changes in adipo/cytokine levels after bariatric surgery and have given conflicting results. The adipo/cytokines, leptin and chemerin, and the orexigenic hormone, ghrelin, have been shown to play a role in the regulation of metabolism and appetite. The aims of our study were to test the levels of these molecules after bariatric surgery and to compare the results between Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy. Methods: We analysed circulating levels of chemerin, ghrelin and leptin in 30 morbidly obese women (body mass index of >40 kg/m 2). Subjects were studied at three time points: baseline (before the surgery started), and after 6 and 12 months. Results: After surgery, chemerin (baseline, 95.03 ± 23.79; after 12 months, 76.80 ± 21.51; p = 0.034) and leptin levels (baseline, 248.17 ± 89.16; after 12 months, 63.85 ± 33.48; p < 0.001) were significantly lower than their baseline levels, whereas ghrelin was higher (baseline, 0.87 ± 0.38; after 12 months, 1.08 ± 0.31; p = 0.010). Fasting glucose, insulin and homeostasis model assessment of insulin resistance levels were markedly lower postoperatively. High-density lipoprotein levels moderately increased and triglyceride levels sharply decreased. There were no differences between the types of bariatric surgery in terms of weight reduction, general metabolic state or adipo/cytokine levels after surgery. Conclusions: Our study demonstrates a marked decrease in fasting leptin and chemerin levels, and an increase in ghrelin levels, after bariatric surgery-induced weight loss, independently of the type of surgery performed. Further studies are needed on the interrelation between the changes in the circulating levels of these molecules and the efficacy of the bariatric surgery procedures to induce the beneficial metabolic changes and to sustain body weight loss. © 2013 Springer Science+Business Media New York.


Auguet T.,Rovira i Virgili University | Auguet T.,Hospital Universitari Joan Tarragona | Terra X.,Rovira i Virgili University | Hernandez M.,Hospital Sant Joan Of Reus | And 11 more authors.
Obesity | Year: 2014

Objective Recent studies report the effect of bariatric surgery on glycaemia control and prevention of type-2-diabetes in obese patients. This study is about the pathophysiological mechanisms associated to these changes. Design and Methods Circulating levels of receptors of tumor necrosis factor (TNF-RI, TNF-RII), visfatin, high molecular weight (HMW) adiponectin, and C reactive protein (CRP) in 30 morbidly obese women (body mass index, BMI>40 kg/m2) and 60 normal-weight controls (BMI>25 kg/m2) were analyzed. Morbidly obese were studied at three time-points: before surgery (baseline), and 6 and 12 months after. Results After surgery, the levels of TNF-RI, TNF-RII, visfatin, and CRP were significantly lower than its baseline levels, whereas HMW adiponectin was higher. Fasting glucose, insulin, and homeostasis model assessment of insulin resistance (HOMA2-IR) levels were markedly lower postoperatively. High density lipoproteins (HDL) moderately increased, and triglyceride levels had sharply decreased. The study of the predictive value of variables indicated that preoperative levels of TNF-RI and visfatin correlated positively with levels of glucose, insulin, glycosylated hemoglobin A1c, and HOMA2-IR postoperatively, whereas adiponectin levels correlated negatively. Baseline CRP levels negatively linked to HDL and TNF-RII positively to triglyceride. Conclusions The preoperative profile with high levels of proinflammatory adipocytokines is linked to smaller improvements in glucose homeostasis and lipid factors. The use of a range of biomarkers may predict the level of metabolic changes following bariatric surgery. Copyright © 2013 The Obesity Society.


Berlanga A.,Rovira i Virgili University | Guiu-Jurado E.,Rovira i Virgili University | Porras J.A.,Rovira i Virgili University | Porras J.A.,Hospital Universitari Joan Tarragona | And 2 more authors.
Clinical and Experimental Gastroenterology | Year: 2014

Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological change characterized by the accumulation of triglycerides in hepatocytes and has frequently been associated with obesity, type 2 diabetes mellitus, hyperlipidemia, and insulin resistance. It is an increasingly recognized condition that has become the most common liver disorder in developed countries, affecting over one-third of the population and is associated with increased cardiovascular- and liver-related mortality. NAFLD is a spectrum of disorders, beginning as simple steatosis. In about 15% of all NAFLD cases, simple steatosis can evolve into non-alcoholic steatohepatitis, a medley of inflammation, hepatocellular injury, and fibrosis, often resulting in cirrhosis and even hepatocellular cancer. However, the molecular mechanism underlying NAFLD progression is not completely understood. Its pathogenesis has often been interpreted by the "double-hit" hypothesis. The primary insult or the "first hit" includes lipid accumulation in the liver, followed by a "second hit" in which proinflammatory mediators induce inflammation, hepatocellular injury, and fibrosis. Nowadays, a more complex model suggests that fatty acids (FAs) and their metabolites may be the true lipotoxic agents that contribute to NAFLD progression; a multiple parallel hits hypothesis has also been suggested. In NAFLD patients, insulin resistance leads to hepatic steatosis via multiple mechanisms. Despite the excess hepatic accumulation of FAs in NAFLD, it has been described that not only de novo FA synthesis is increased, but FAs are also taken up from the serum. Furthermore, a decrease in mitochondrial FA oxidation and secretion of very-low-density lipoproteins has been reported. This review discusses the molecular mechanisms that underlie the pathophysiological changes of hepatic lipid metabolism that contribute to NAFLD. © 2014 Berlanga et al.


PubMed | Rovira i Virgili University and Hospital Universitari Joan Tarragona
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2015

The purpose of this work was to evaluate the expression of fatty acid metabolism-related genes in human adipose tissue from moderately obese women. We used qRT-PCR and Western Blot to analyze visceral (VAT) and subcutaneous (SAT) adipose tissue mRNA expression involved in de novo fatty acid synthesis (ACC1, FAS), fatty acid oxidation (PPAR, PPAR) and inflammation (IL6, TNF), in normal weight control women (BMI < 25 kg/m, n = 35) and moderately obese women (BMI 30-38 kg/m, n = 55). In SAT, ACC1, FAS and PPAR mRNA expression were significantly decreased in moderately obese women compared to controls. The downregulation reported in SAT was more pronounced when BMI increased. In VAT, lipogenic-related genes and PPAR were similar in both groups. Only PPAR gene expression was significantly increased in moderately obese women. As far as inflammation is concerned, TNF and IL6 were significantly increased in moderate obesity in both tissues. Our results indicate that there is a progressive downregulation in lipogenesis in SAT as BMI increases, which suggests that SAT decreases the synthesis of fatty acid de novo during the development of obesity, whereas in VAT lipogenesis remains active regardless of the degree of obesity.


PubMed | Rovira i Virgili University and Hospital Universitari Joan Tarragona
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2016

Recent reports suggest a role for the Patatin-like phospholipase domain-containing protein 3 (PNPLA3) in the pathology of non-alcoholic fatty liver disease (NAFLD). Lipid deposition in the liver seems to be a critical process in the pathogenesis of NAFLD. The aim of the present work was to evaluate the association between the liver PNPLA3 expression, key genes of lipid metabolism, and the presence of NAFLD in morbidly obese women. We used real-time polymerase chain reaction (PCR) analysis to analyze the hepatic expression of PNPLA3 and lipid metabolism-related genes in 55 morbidly obese subjects with normal liver histology (NL, n = 18), simple steatosis (SS, n = 20), and non-alcoholic steatohepatitis (NASH, n = 17). Liver biopsies were collected during bariatric surgery. We observed that liver PNPLA3 expression was increased in NAFLD than in NL. It was also upregulated in SS than in NL. Interestingly, we found that the expression of PNPLA3 was significantly higher in severe than mild SS group. In addition, the expression of the transcription factors LXR, PPAR, and SREBP2 was positively correlated with PNPLA3 liver expression. Regarding rs738409 polymorphism, GG genotype was positive correlated with the presence of NASH. In conclusion, our results show that PNPLA3 could be related to lipid accumulation in liver, mainly in the development and progression of simple steatosis.


PubMed | Rovira i Virgili University and Hospital Universitari Joan Tarragona
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2016

Specific miRNA expression profiles have been shown to be associated with nonalcoholic fatty liver disease (NAFLD). We examined the correlation between the circulating levels and hepatic expression of miR122 and miR33a/b*, the key lipid metabolism-related gene expression and the clinicopathological factors of obese women with NAFLD. We measured miR122 and miR33a/b* expression in liver samples from 62 morbidly obese (MO), 30 moderately obese (ModO), and eight normal-weight controls. MiR122 and miR33a/b* expression was analyzed by qRT-PCR. Additionally, miR122 and miR33b* circulating levels were analyzed in 122 women. Hepatic miR33b* expression was increased in MO compared to ModO and controls, whereas miR122 expression was decreased in the MO group compared to ModO. In obese cohorts, miR33b* expression was increased in nonalcoholic steatohepatitis (NASH). Regarding circulating levels, MO patients with NASH showed higher miR122 levels than MO with simple steatosis (SS). These circulating levels are good predictors of histological features associated with disease severity. MO is associated with altered hepatic miRNA expression. In obese women, higher miR33b* liver expression is associated with NASH. Moreover, multiple correlations between miRNAs and the expression of genes related to lipid metabolism were found, that would suggest a miRNA-host gene circuit. Finally, miR122 circulating levels could be included in a panel of different biomarkers to improve accuracy in the non-invasive diagnosis of NASH.


PubMed | Rovira i Virgili University and Hospital Universitari Joan Tarragona
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2015

Data from recent studies conducted in rodent models and humans suggest that interleukin-17A (IL-17A) plays a role in the induction of inflammation in adipose tissue during obesity. The aim of this study was to assess the gene expression of IL-17A in adipose tissue of morbidly obese patients. We used RT-PCR to evaluate the expression of IL-17A and several adipo/cytokines in the visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) of 10 normal-weight control women (BMI < 25 kg/m2) and 30 morbidly obese women (MO, BMI > 40 kg/m2). We measured serum levels of IL-17A and adipo/cytokines in MO and normal weight women. IL-17A expression was significantly higher in VAT than in SAT in MO patients (p = 0.0127). It was very low in normal-weight controls in both VAT and SAT tissues. We found positive correlations between IL-17A and IL-6, lipocalin-2 and resistin in VAT of MO patients. The circulating level of IL-17A was higher in the normal-weight group than the MO patients (p = 0.032), and it was significantly related to adiponectin and TNFRII levels. In conclusion, IL-17A expression in VAT is increased in morbidly obese women, which suggests a link between obesity and innate immunity in low-grade chronic inflammation in morbidly obese women.

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