Moreno-Aliaga, M. J. (María Jesús)
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- Effects of DHA-Rich n-3 Fatty Acid Supplementation and/or Resistance Training on Body Composition and Cardiometabolic Biomarkers in Overweight and Obese Post-Menopausal Women(2021) Lorente-Cebrian, S. (Silvia); Moreno-Aliaga, M. J. (María Jesús); Félix-Soriano, E. (Elisa); García-Unciti, M.S. (María Soledad); Gonzalez-Muniesa, P. (Pedro); Palacios-Samper, N. (Natalia); Cuervo, M. (Marta); Pérez-Chávez, A. (Adriana); Santos, J. (Javier); Cobo-Díez, M.J. (María José); Martínez-Gayo, A. (Alejandro); Goikoetxea-Galarza, I. (Iñaki)Resistance training (RT) and n-3 polyunsaturated fatty acids (n-3 PUFA) supplementation have emerged as strategies to improve muscle function in older adults. Overweight/obese postmenopausal women (55-70 years) were randomly allocated to one of four experimental groups, receiving placebo (olive oil) or docosahexaenoic acid (DHA)-rich n-3 PUFA supplementation alone or in combination with a supervised RT-program for 16 weeks. At baseline and at end of the trial, body composition, anthropometrical measures, blood pressure and serum glucose and lipid biomarkers were analyzed. Oral glucose tolerance tests (OGTT) and strength tests were also performed. All groups exhibit a similar moderate reduction in body weight and fat mass, but the RT-groups maintained bone mineral content, increased upper limbs lean mass, decreased lower limbs fat mass, and increased muscle strength and quality compared to untrained-groups. The RT-program also improved glucose tolerance (lowering the OGTT incremental area under the curve). The DHA-rich supplementation lowered diastolic blood pressure and circulating triglycerides and increased muscle quality in lower limbs. In conclusion, 16-week RT-program improved segmented body composition, bone mineral content, and glucose tolerance, while the DHA-rich supplement had beneficial effects on cardiovascular health markers in overweight/obese postmenopausal women. No synergistic effects were observed for DHA supplementation and RT-program combination.
- Dietary total antioxidant capacity and obesity in children and adolescents(Informa Healthcare, 2010) Martinez, J.A. (José Alfredo); Martinez-Gonzalez, M.A. (Miguel Ángel); Patiño-García, A. (Ana); Moreno-Aliaga, M. J. (María Jesús); Zulet, M.A. (María Ángeles); Ochoa, M.C. (María Carmen); Azcona-San-Julian, M.C. (María Cristina); Puchau, B. (Blanca); Chueca, M. (María); Oyarzabal, M. (M.); Marti-del-Moral, A. (Amelia)Dietary antioxidant intake has been suggested to protect against oxidative damage and related clinical complications. The aim of this study was to assess the potential relationships between the dietary total antioxidant capacity (TAC) and obesity-related features in children and adolescents. Anthropometric variables from 369 children and adolescents were measured (184 obese and 185 control). A validated food-frequency questionnaire was used to calculate the TAC and the daily nutrient and energy intake. Dietary TAC showed positive associations with fiber, folic acid, magnesium, and vitamins A, C and E. BMI, SDS-BMI and total body fat were inversely associated with dietary TAC only in obese subjects. These data suggest that dietary TAC may be a potential indicator of the risk to develop obesity-related features and could be considered as a useful method in assessing antioxidant intake.
- Vitamin C modulates the interaction between adipocytes and macrophages(Wiley Blackwell, 2011) Martinez, J.A. (José Alfredo); Quintero, P. (Pablo); Garcia-Diaz, D.F. (Diego F.); Moreno-Aliaga, M. J. (María Jesús); Milagro-Yoldi, F.I. (Fermín Ignacio); Campión-Zabalza, J. (Javier)Scope: Increased adiposity is related with monocyte infiltration into the adipose tissue that accentuates inflammation. Antioxidant treatments emerge as approaches to counteract this phenomenon. Methods and results: Cocultures of differentiated 3T3-L1 adipocytes and RAW264.7 macrophages were incubated for 24-72 h with/without 100 nM insulin and/or 200 μM vitamin C (VC). Nitric oxide (NO) secretion (24 h) was measured. Also, expression (24 h) and secretion (72 h) of MCP-1, leptin and apelin were analyzed. NO secretion was significantly inhibited by insulin and VC only in cocultures. MCP-1 expression/secretion was enhanced in cocultures. Insulin incubation reduced MCP-1 expression in both cultures and VC only in controls. Both treatments inhibited MCP-1 secretion in cocultures. Apelin gene expression was induced in cocultures. Insulin induced apelin mRNA expression, but VC inhibited its expression in cocultures under insulin treatment. Apelin secretion was notably induced by insulin and inhibited by VC in cocultures. Leptin expression was decreased in coculture, while presented no effects by VC. Conclusion: VC importantly modulates the established pro-inflammatory state in the interaction between adipocytes and macrophages.
- Some cyclin-dependent kinase inhibitors-related genes are regulated by vitamin C in a model of diet-induced obesity(Pharmaceutical Society of Japan, 2009) Martinez, J.A. (José Alfredo); Boque, N. (Noemi); Moreno-Aliaga, M. J. (María Jesús); Milagro-Yoldi, F.I. (Fermín Ignacio); Campión-Zabalza, J. (Javier)The aim of this research was to investigate differential gene expression of cyclin-dependent kinase inhibitors (CKIs) in white adipose tissue (WAT) and liver from high-fat fed male Wistar rats with or without vitamin C (VC) supplementation (750 mg/kg of body weight). After 56 d of experimentation, animals fed on a cafeteria diet increased significantly body weights and total body fat. Reverse transcription-polymerase chain reaction (RT-PCR) studies showed that cafeteria diet decreased p21 and p57 mRNA expression in subcutaneous WAT and increased p21 mRNA in liver. Overall, these data provide new information about the role of high fat intake on mRNA levels of several CKIs with implications in adipogenesis, cell metabolism and weight homeostasis. Interestingly, VC supplementation partially prevented diet-induced adiposity and increased p27 mRNA in liver without any changes in the other tissues and genes analyzed. Thus, hepatic mRNA changes induced by ascorbic acid indicate a possible role of these genes in diet-induced oxidative stress processes.
- Decreased cardiotrophin-1 levels are associated with a lower risk of developing the metabolic syndrome in overweight/obese children after a weight loss program(Elsevier, 2013) Martinez, J.A. (José Alfredo); Moreno-Aliaga, M. J. (María Jesús); Azcona-San-Julian, M.C. (María Cristina); Garcia-Calzon, S. (Sonia); Rendo-Urteaga, T. (Tara); Bustos, M. (Matilde); Chueca, M. (María); Oyarzabal, M. (M.); Martinez-Anso, E. (Eduardo); Marti-del-Moral, A. (Amelia)Objective: Cardiotrophin-1 (CT-1) shares some similarities with other cytokines, and participates in the control of energy metabolism. Higher circulating levels are observed in obese humans, but little information is gathered in weight loss (WL) programs. Therefore, we aimed to investigate the association of serum CT-1 levels with metabolic variables and the risk of developing metabolic syndrome (MetS) after a WL program in overweight/obese children. Subjects and Methods: Forty-four overweight/obese children (mean age 11.5 yr; 50% males) undergoing a 10-week WL program were enrolled. Subjects were dichotomized at the median of Body Mass Index-Standard Deviation Score (BMI-SDS) change, as high and low responders after intervention. Results: CT-1 levels were significantly reduced (-48 fmol/mL, p=0.043) in the high responder group after the WL program. They had significantly lower body weight (-3.7 kg, p<0.001), body fat mass (-8%, p<0.001), BMI-SDS (-0.78, p<0.001) and waist circumference (-5.4 cm, p<0.001), and a significant improvement in lipid and glucose profiles (p<0.05). Interestingly, decreased CT-1 levels significantly predicted changes in total cholesterol (41%) and LDL-cholesterol (28%). Moreover, in our participants the lower the CT-1 levels, the higher the reduction in MetS risk components, after the 10- week intervention, (p-ANCOVA=0.040, p-trend=0.024). Conclusion: We showed, for the first time, a reduction in serum CT-1 levels after a WL program and this decrease in CT-1 was strongly associated with a reduction in cholesterol levels and in MetS risk factors in overweight/obese children. Our findings may suggest that CT-1 could be an indirect marker for the diagnosis of MetS in this population.
- A Fermented Food Product Containing Lactic Acid Bacteria Protects ZDF Rats from the Development of Type 2 Diabetes(MDPI AG, 2019) Moreno-Aliaga, M. J. (María Jesús); Encío, I. (Ignacio); Araña, M. (Miriam); Oneca, M. (María); Cabello-Olmo, M. (Miriam); Barajas, M. (Miguel); Díaz, J.V. (Jesús Vicente); Guruceaga, E. (Elizabeth); Torre, P. (Paloma); Sainz, N. (Neira)Type 2 diabetes (T2D) is a complex metabolic disease, which involves a maintained hyperglycemia due to the development of an insulin resistance process. Among multiple risk factors, host intestinal microbiota has received increasing attention in T2D etiology and progression. In the present study, we have explored the effect of long-term supplementation with a non-dairy fermented food product (FFP) in Zucker Diabetic and Fatty (ZDF) rats T2D model. The supplementation with FFP induced an improvement in glucose homeostasis according to the results obtained from fasting blood glucose levels, glucose tolerance test, and pancreatic function. Importantly, a significantly reduced intestinal glucose absorption was found in the FFP-treated rats. Supplemented animals also showed a greater survival suggesting a better health status as a result of the FFP intake. Some dissimilarities have been observed in the gut microbiota population between control and FFP-treated rats, and interestingly a tendency for better cardiometabolic markers values was appreciated in this group. However, no significant differences were observed in body weight, body composition, or food intake between groups. These findings suggest that FFP induced gut microbiota modifications in ZDF rats that improved glucose metabolism and protected from T2D development.
- DNA hybridization arrays: a powerful technology for nutritional and obesity research.(Cambridge University Press, 2001) Martinez, J.A. (José Alfredo); Moreno-Aliaga, M. J. (María Jesús); Garcia-Foncillas, J. (Jesús); Marti-del-Moral, A. (Amelia)
- Cardiotrophin-1 is a key regulator of glucose and lipid metabolism(Elsevier, 2011) Martinez, J.A. (José Alfredo); Gimenez, I. (I.); Moreno-Aliaga, M. J. (María Jesús); Perez-Echarri, N. (Nerea); Viollet, B. (Benoit); Larequi-García, E. (Eduardo); Prieto, J. (Jesús); Gil-Bea, F.J. (Francisco J.); Marcos, B. (Beatriz); Bustos, M. (Matilde)Cardiotrophin-1 (CT-1) is a member of the gp130 family of cytokines. We observed that ct-1(-/-) mice develop mature-onset obesity, insulin resistance, and hypercholesterolemia despite reduced calorie intake. Decreased energy expenditure preceded and accompanied the development of obesity. Acute treatment with rCT-1 decreased blood glucose in an insulin-independent manner and increased insulin-stimulated AKT phosphorylation in muscle. These changes were associated with stimulation of fatty acid oxidation, an effect that was absent in AMPKα2(-/-) mice. Chronic rCT-1 treatment reduced food intake, enhanced energy expenditure, and induced white adipose tissue remodeling characterized by upregulation of genes implicated in the control of lipolysis, fatty acid oxidation, and mitochondrial biogenesis and genes typifying brown fat phenotype. Moreover, rCT-1 reduced body weight and corrected insulin resistance in ob/ob and in high-fat-fed obese mice. We conclude that CT-1 is a master regulator of fat and glucose metabolism with potential applications for treatment of obesity and insulin resistance.
- Genetics of obesity.(Cambridge University Press, 2007) Martinez, J.A. (José Alfredo); Enriquez, L. (Luis); Moreno-Aliaga, M. J. (María Jesús); Marti-del-Moral, A. (Amelia)OBJECTIVE: The aim was to review and update advances in genetics of obesity. DESIGN: Analysis and interpretation of recent investigations about regulating the energy balance as well as about gene-nutrient interactions and current nutri-genomic research methods. BACKGROUND AND MAIN STATEMENTS: Obesity results from a long-term positive energy balance. However, its rising prevalence in developed and developing societies must reflect lifestyle changes, since genetic susceptibility remains stable over many generations. Like most complex diseases, obesity derives from a failure of adequate homoeostasis within the physiological system controlling body weight. The identification of genes that are involved in syndromic, monogenic and polygenic obesity has seriously improved our knowledge of body weight regulation. This disorder may arise from a deregulation at the genetic level (e.g. gene transcription or altered protein function) or environmental exposure (e.g. diet, physical activity, etc.). CONCLUSIONS: In practice, obesity involves the interaction between genetic and environmental factors.
- Effects of Maresin 1 (MaR1) on Colonic Inflammation and Gut Dysbiosis in Diet-Induced Obese Mice(2020) León, I.C. (Irene C.); Escoté-Miró, X. (Xavier); Moreno-Aliaga, M. J. (María Jesús); Guruceaga, E. (Elizabeth); Vázquez, S. (Sergio); Sainz, N. (Neira)The aim of this study was to characterize the effects of Maresin 1 (MaR1), a DHA-derived pro-resolving lipid mediator, on obesity-related colonic inflammation and gut dysbiosis in diet-induced obese (DIO) mice. In colonic mucosa of DIO mice, the MaR1 treatment decreased the expression of inflammatory genes, such as Tnf-α and Il-1β. As expected, the DIO mice exhibited significant changes in gut microbiota composition at the phylum, genus, and species levels, with a trend to a higher Firmicutes/Bacteroidetes ratio. Deferribacteres and Synergistetes also increased in the DIO animals. In contrast, these animals exhibited a significant decrease in the content of Cyanobacteria and Actinobacteria. Treatment with MaR1 was not able to reverse the dysbiosis caused by obesity on the most abundant phyla. However, the MaR1 treatment increased the content of P. xylanivorans, which have been considered to be a promising probiotic with healthy effects on gut inflammation. Finally, a positive association was found between the Deferribacteres and Il-1β expression, suggesting that the increase in Deferribacteres observed in obesity could contribute to the overexpression of inflammatory cytokines in the colonic mucosa. In conclusion, MaR1 administration ameliorates the inflammatory state in the colonic mucosa and partially compensates changes on gut microbiota caused by obesity.