Atención farmacéutica domiciliaria a pacientes frágiles en Gipuzkoa / Pharmaceutical home care for frail patients in Gipuzkoa

Introducción: la asistencia sanitaria a domicilio es una de las estrategias que impulsan las administraciones para pacientes pluripatológicos que viven en sus domicilios y que debido a su grado de discapacidad o vulnerabilidad no pueden desplazarse a los centros sanitarios. Este estudio consiste en pilotar la Atención Farmacéutica Domiciliaria (AFD) ofreciendo respuestas individualizadas a los pacientes en sus domicilios, dentro del equipo multidisciplinar de atención a los pacientes frágiles de la Fundación Hurkoa.Material y métodos: se convocó a todas las farmacias de los municipios de Irún y Azkoitia a una formación. Los pacientes incluidos en el Plan Integral de Atención a la Fragilidad de la Fundación Hurkoa, que requerían ayuda con la gestión de la medicación y aceptaron incluir a un farmacéutico en el equipo multidisciplinar de cuidados, seleccionaron su farmacia comunitaria. Los farmacéuticos de dichas farmacias realizaron una revisión del botiquín junto con la revisión de la medicación. Resultados: en la revisión del botiquín se detectaron medicamentos caducados o no utilizados y se retiraron entre 2 y 3 medicamentos a todos los pacientes. En la revisión de la medicación se detectaron al menos un Problema Relacionado con la Medicación (PRM) en todos los pacientes del estudio. En la evaluación de la satisfacción el 100 % de los pacientes refirieron un grado de satisfacción alto con el programa. Discusión: el presente estudio refuerza la importancia de la inclusión del farmacéutico comunitario en el equipo multidisciplinar de AFD, ofreciendo respuestas individualizadas a cada paciente, mejorando la gestión de su medicación y así consiguiendo mejoras significativas en la calidad de vida. (AU)

Confirmación de los compromisos de una Farmacia Amigable / Confirmation of the commitments of a Friendly Pharmacy

INTRODUCCIÓN: La farmacia se encuentra en pleno proceso de trasformación. Dada su accesibilidad y cercanía con la atención primaria, una de las vías de desarrollo de la farmacia comunitaria debería ser la profundización en aspectos sociales. OBJETIVOS: Confirmar si las personas mayores que acuden a las farmacias siguen pensando que los compromisos anteriormente definidos son los que deben definir a la Farmacia Amigable (FA). MATERIAL Y MÉTODOS: Se realizó un grupo focal con personas mayores en San Sebastián. Se contactó con los individuos responsables de tres organizaciones relacionadas con las personas mayores. Se grabó y analizó siguiendo el método de análisis de contenido dirigido. RESULTADOS: Se confirmaron los 15 compromisos ya publicados que definen una FA. CONCLUSIONES: Confirmados los compromisos que definen una FA desde el Colegio Oficial de Farmacéuticos de Gipuzkoa se pretende que la red de farmacias sea más cercana, accesible y que esté cada vez más inmersa en el ámbito social

INTRODUCTION: The community pharmacy is in a process of transformation. Due to its accessibility and proximity with primary care, one of the development paths should be the deepening in social aspects. OBJECTIVE: Confirm if the elderly people who go to the pharmacies still think that the commitments that define the Friendly Pharmacy are the ones previously identified. MATERIAL AND METHODS: A focus group was carried out with elderly people. An invitation to participate was elaborated and the responsible people for three organizations related to elderly people were contacted. It was recorded and analyzed as a directed content analysis method. RESULTS: It has been possible to verify that, in a general way, the participants confirmed the data obtained in the previous work. CONCLUSIONS: The commitments aimed at developing a closer, more accessible pharmacy network and increasingly involved in the social field, are confirmed

Cost-effectiveness of professional pharmacy services in community pharmacy: a systematic review.

INTRODUCTION: The aim was to determine whether professional pharmacy services (PPS) provided to ambulatory patients attending community pharmacy are cost-effective compared with usual care (UC). Areas covered: MEDLINE, Web of Knowledge, Scopus, Cochrane Library and Centre for Reviews and Dissemination databases were searched, and the risk of bias of randomized controlled trials, and the methodological quality of economic evaluations was assessed. A total of 17 economic evaluations of 13 studies were included. Seven studies were classified as high-, three as medium- and three as low-quality. PPS were more effective and less costly than UC in four studies; seven studies concluded that PPS were more effective and more costly and two studies concluded that the service was as effective as the UC, with higher and lower costs. Expert commentary: Although the uncertainty was variable among the studies, a general trend towards the cost-effectiveness of PPS was observed. Decision makers are encouraged to consider the feasibility of implementing PPS.

Epigenetic patterns of two gene promoters (TNF-alpha and PON) in stroke considering obesity condition and dietary intake

Some causal bases of stroke remain unclear, but the nutritional effects on the epigenetic regulation of different genes may be involved. The aim was to assess the impact of epigenetic processes of human tumor necrosis factor (TNF-alfa) and paraoxonase (PON) promoters in the susceptibility to stroke when considering body composition and dietary intake. Twenty-four patients (12 non-stroke/12 stroke) were matched by sex (12 male/12 female), age (mean 70 ± 12 years old), and BMI (12 normal-weight/12 obese; mean 28.1 ± 6.7 kg/m2). Blood cell DNA was isolated and DNA methylation levels of TNF-alfa (-186 to +349 bp) and PON (-231 to +250 bp) promoters were analyzed by the Sequenom EpiTYPER approach. Histone modifications (H3K9ac and H3K4me3) were analyzed also by chromatin immunoprecipitation in a region of TNF-α (-297 to -185). Total TNF-α promoter methylation was lower in stroke patients (p < 0.001) and showed no interaction with body composition (p = 0.807). TNF-α and PON total methylation levels correlated each other (r = 0.44; p = 0.031), especially in stroke patients (r = 0.72; p = 0.008). The +309 CpG methylation site from TNF-α promoter was related to body weight (p = 0.027) and the region containing three CpGs (from −170 to -162 bp) to the percentage of lipid intake and dietary indexes (p < 0.05) in non-stroke patients. The methylation of PON +15 and +241 CpGs was related to body weight (p = 0.021), waist circumference (p = 0.020), and energy intake (p = 0.018), whereas +214 was associated to the quality of the diet (p < 0.05) in non-stroke patients. When comparing stroke vs non-stroke patients regarding the histone modifications analyzed at TNF-α promoter, no changes were found, although a significant association was identified between circulating TNF-alfa level and H3K9ac with H3K4me3. TNF-alfa and PON promoter methylation levels could be involved in the susceptibility to stroke and obesity outcome, respectively. The dietary intake and body composition may influence this epigenetic regulation in non-stroke patients

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Pre-treatment circulating leptin/ghrelin ratio as a non-invasive marker to identify patients likely to regain the lost weight after an energy restriction treatment.

BACKGROUND: Leptin and ghrelin appear to play a role in weight regain after a successful weight loss. The pre-treatment plasma levels of leptin/ghrelin ratio (L/G) could have power to predict this clinically relevant issue in the obesity treatment. OBJECTIVE: To evaluate the ability of the L/G as a non-invasive tool for the early discrimination of obese patients who are more likely to regain weight after an energy restriction program (regainers) from those who maintain the lost weight (non-regainers). SUBJECTS AND METHODS: Fasting leptin and ghrelin levels were evaluated in 88 overweight/obese patients who followed an 8-week hypocaloric diet program and were categorized as regainers (≥10 % weight-lost regain) and non-regainers (<10 % weight-lost regain) 6 months (32 weeks) after finishing the dietary treatment. A receiver operating characteristic (ROC) curve analysis was employed to evaluate the diagnostic value of the L/G ratio and to establish a cut-off point to differentiate regainers from non-regainers. RESULTS: Regainers showed a statistically higher baseline (week 0) and after treatment (week 8) L/G ratio than non-regainers. The baseline L/G ratio was associated with an increased risk for weight regain (odds ratio 1.051; p = 0.008). Using the area under the ROC curve (AUC), the L/G ratio significantly identified female (AUC = 0.69; p = 0.040) and male regainers (AUC = 0.68; p = 0.030). The maximum combination of sensitivity and specificity was shown at the cut-off point of 26.0 for women and 9.5 for men. CONCLUSIONS: The pre-intervention fasting leptin/ghrelin ratio could be a useful non-invasive approach to personalize obesity therapy and avoid unsuccessful treatment outcomes.

Epigenetic patterns of two gene promoters (TNF-α and PON) in stroke considering obesity condition and dietary intake.

Some causal bases of stroke remain unclear, but the nutritional effects on the epigenetic regulation of different genes may be involved. The aim was to assess the impact of epigenetic processes of human tumor necrosis factor (TNF-α) and paraoxonase (PON) promoters in the susceptibility to stroke when considering body composition and dietary intake. Twenty-four patients (12 non-stroke/12 stroke) were matched by sex (12 male/12 female), age (mean 70 ± 12 years old), and BMI (12 normal-weight/12 obese; mean 28.1 ± 6.7 kg/m(2)). Blood cell DNA was isolated and DNA methylation levels of TNF-α (-186 to +349 bp) and PON (-231 to +250 bp) promoters were analyzed by the Sequenom EpiTYPER approach. Histone modifications (H3K9ac and H3K4me3) were analyzed also by chromatin immunoprecipitation in a region of TNF-α (-297 to -185). Total TNF-α promoter methylation was lower in stroke patients (p < 0.001) and showed no interaction with body composition (p = 0.807). TNF-α and PON total methylation levels correlated each other (r = 0.44; p = 0.031), especially in stroke patients (r = 0.72; p = 0.008). The +309 CpG methylation site from TNF-α promoter was related to body weight (p = 0.027) and the region containing three CpGs (from -170 to -162 bp) to the percentage of lipid intake and dietary indexes (p < 0.05) in non-stroke patients. The methylation of PON +15 and +241 CpGs was related to body weight (p = 0.021), waist circumference (p = 0.020), and energy intake (p = 0.018), whereas +214 was associated to the quality of the diet (p < 0.05) in non-stroke patients. When comparing stroke vs non-stroke patients regarding the histone modifications analyzed at TNF-α promoter, no changes were found, although a significant association was identified between circulating TNF-α level and H3K9ac with H3K4me3. TNF-α and PON promoter methylation levels could be involved in the susceptibility to stroke and obesity outcome, respectively. The dietary intake and body composition may influence this epigenetic regulation in non-stroke patients.

Obesity and metabolic syndrome: potential benefit from specific nutritional components.

The prevalence of metabolic syndrome (MetS) manifestations is rapidly increasing worldwide, and is becoming an important health problem. Actually, MetS includes a combination of clinical complications such as obesity (central adiposity), insulin resistance, glucose intolerance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. All these alterations predispose individuals to type 2 diabetes and cardiovascular disease inducing earlier mortality rates among people. In general terms, it is difficult for patients to follow a standard long-term diet/exercise regime that would improve or alleviate MetS symptoms. Thus, the investigation of food components that may deal with the MetS features is an important field for ameliorate and facilitate MetS dietary-based therapies. Currently antioxidants are of great interest due to the described association between obesity, cardiovascular alterations and oxidative stress. On the other hand, high MUFA and PUFA diets are being also considered due to their potential benefits on hypertension, insulin resistance and triglyceride levels. Mineral composition of the diet is also relevant since high potassium intake may improve hypertension and high calcium consumption may promote lipid oxidation. Thus, although nutritional supplements are at the peak of dietetic therapies, the consumption of some specific foods (legumes, fatty fish, vegetables and fruits, etc) with bioactive components within an energy-restricted diet is a promising approach to manage MetS manifestations. Therefore, the present review focuses on some of the most important food components currently investigated to improve and make easier the nutritional MetS treatment.

High fat diet-induced obesity modifies the methylation pattern of leptin promoter in rats.

Leptin is an adipokine involved in body weight and food intake regulation whose promoter region presents CpG islands that could be subject to dynamic methylation. This methylation process could be affected by environmental (e.g. diet) or endogenous (e.g., adipocyte differentiation, inflammation, hypoxia) factors, and could influence adipocyte leptin gene expression. The aim of this article was to study whether a high-energy diet may affect leptin gene promoter methylation in rats. A group of eleven male Wistar rats were assigned into two dietary groups, one fed on a control diet for 11 weeks and the other on a high-fat cafeteria diet. Rats fed a high-energy diet become overweight and hyperleptinemic as compared to the controls. DNA isolated from retroperitoneal adipocytes was treated with bisulfite and a distal portion of leptin promoter (from -694 to -372 bp) including 13 CpG sites was amplified by PCR and sequenced. The studied promoter portion was slightly more methylated in the cafeteria-fed animals, which was statistically significant (p < 0.05) for one of the CpG sites (located at the position -443). In obese rats, such methylation was associated to lower circulating leptin levels, suggesting that this position could be important in the regulation of leptin gene expression, probably by being a target sequence of different transcription factors. Our findings reveal, for the first time, that leptin methylation pattern can be influenced by diet-induced obesity, and suggest that epigenetic mechanisms could be involved in obesity by regulating the expression of important epiobesigenic genes.

La obesidad inducida por dieta alta en grasas modifica el patrón de metilación del promotor de la leptina en la rata / High fat diet-induced obesity modifies the methylation pattern of leptin promoter in rats

Leptin is an adipokine involved in body weight and food intake regulation whosepromoter region presents CpG islands that could be subject to dynamic methylation.This methylation process could be affected by environmental (e.g. diet) or endogenous(e.g., adipocyte differentiation, inflammation, hypoxia) factors, and could influenceadipocyte leptin gene expression. The aim of this article was to study whether ahigh-energy diet may affect leptin gene promoter methylation in rats. A group ofeleven male Wistar rats were assigned into two dietary groups, one fed on a controldiet for 11 weeks and the other on a high-fat cafeteria diet. Rats fed a high-energy dietbecome overweight and hyperleptinemic as compared to the controls. DNA isolatedfrom retroperitoneal adipocytes was treated with bisulfite and a distal portion of leptinpromoter (from -694 to -372 bp) including 13 CpG sites was amplified by PCRand sequenced. The studied promoter portion was slightly more methylated in thecafeteria-fed animals, which was statistically significant (p<0.05) for one of the CpGsites (located at the position –443). In obese rats, such methylation was associated tolower circulating leptin levels, suggesting that this position could be important in theregulation of leptin gene expression, probably by being a target sequence of differenttranscription factors. Our findings reveal, for the first time, that leptin methylationpattern can be influenced by diet-induced obesity, and suggest that epigenetic mechanismscould be involved in obesity by regulating the expression of important epiobesigenicgenes(AU)

La leptina es una adipoquina implicada en laregulación del peso corporal y la ingesta energéticacuya región promotora presenta islasCpG que podrían ser metiladas dinámicamente.Este proceso de metilación podría verseafectado por factores ambientales, como ladieta, o endógenos, como la diferenciación adipocitaria,inflamación o hipoxia, y podríainfluir en la expresión de leptina por parte delos adipocitos. El objetivo de este artículo esestudiar si una dieta alta en grasa podría afectara la metilación del promotor de la leptina enratas. Un grupo de once ratas Wistar machofue dividido en dos subgrupos, uno alimentadocon dieta control durante 11 semanas y el otrocon dieta alta en grasa (dieta de cafetería). Lasratas alimentadas con la dieta rica en grasa presentaronsobrepeso e hiperleptinemia. El ADNaislado de los adipocitos retroperitoneales fuetratado con bisulfito y una porción distal delpromotor de la leptina (de la base -694 a la -372), conteniendo 13 sitios CpG, fue amplificadapor PCR y secuenciada. Esta región delpromotor apareció ligeramente más metiladaen los animales alimentados con dieta de cafetería,lo cuál fue especialmente significativo (p<0,05) para uno de los sitios CpG (en la posición-443). En las ratas obesas, la metilación seasoció a una disminución de los niveles de leptinacirculante, lo que sugiere que esta posiciónpodría ser importante en la regulación de laexpresión génica de esta adipoquina, probablementepor ser una secuencia diana de diferen-tes factores de transcripción. Nuestros resultados,por primera vez, ponen de manifiesto queel patrón de metilación del promotor de la leptinapuede estar influido por la obesidad inducidapor la dieta, y sugieren que los mecanismosepigenéticos podrían estar implicados enla reciente pandemia de obesidad mediante laregulación de la expresión de importantesgenes epiobesigénicos(AU)

The - 11391 G/A polymorphism of the adiponectin gene promoter is associated with metabolic syndrome traits and the outcome of an energy-restricted diet in obese subjects.

Adiponectin is an adipose tissue-specific hormone that is commonly decreased in obese subjects. Furthermore, single-nucleotide polymorphisms (SNPs) of the adiponectin gene have been associated with metabolic phenotypes. The present study investigated whether the adiponectin gene promoter variant -11391 G/A (rs17300539) could predict the risk of developing traits characterizing the metabolic syndrome (MetS) and the impact of weight management. The -11391 G/A SNP was genotyped in 180 Spanish volunteers (BMI: 31.4+/-3.2 kg/m (2); age: 35+/-5 years). Clinical measurements were determined at baseline, following an 8-week low-calorie diet (LCD), and at 32 and 60 weeks. At baseline, the GG genotype was associated with higher HOMA-IR, insulin and triacylglyceride concentrations than other genotypes (p<0.05) and was also related with a higher risk of insulin resistance (OR: 2.437, p=0.025) and MetS clinical manifestations (OR: 3.236, p=0.003). Following the LCD, the increased risk in GG subjects compared with others disappeared (p>0.05). By 32 weeks after dietary therapy (n=84), GG carriers had recovered the risk of metabolic comorbidities (OR: 2.420, p=0.043). This risk was even more evident after 60 weeks (OR: 2.875, p=0.014). These data show an increased risk of insulin resistance and MetS complications in obese subjects of the -11391 GG genotype. The risk was markedly reduced during an energy-restricted diet, but was not sustained. Carriage of the A allele therefore confers protection from weight regain, and the effect is particularly evident 32-60 weeks after the dietary intervention, when improvement in GG subjects had disappeared.

Sirtuin gene expression in human mononuclear cells is modulated by caloric restriction.

BACKGROUND: Sirtuins may provide novel targets for treating some diseases associated with oxidative stress, such as obesity and its comorbidities. However, there are a few in vivo studies in humans about the potential role of sirtuins as therapeutic targets among obese patients undergoing caloric restriction. Therefore, the aim of this study was to assess if the gene expression of sirtuins is modulated in peripheral blood mononuclear cells (PBMC) by a hypocaloric diet devised to lose weight in humans. MATERIALS AND METHODS: Gene expression of two sirtuins (SIRT1 and SIRT2) in the PBMC of obese subjects (32.3 +/- 5.5 kg m(-2)) before and following an 8-week hypocaloric diet was investigated. NADH-coenzyme Q reductase (NDUFS2) and cytochrome c oxidase assembly protein (COX15) gene expression was selected together with plasma antioxidant power and nitric oxide as markers of antioxidant status. A quantitative real-time polymerase chain reaction approach was performed to assess the nutrigenomics outcome. Moreover, 2-keto[1-(13)C]isocaproate breath test (KICA-BT) parameters were evaluated to study mitochondrial oxidation in vivo. RESULTS: The intervention up-regulated the expression of both sirtuins, being inversely associated with total antioxidant capacity and directly related to nitric oxide, mitochondrial oxidation assessed by the KICA-BT and the expression of the mitochondrial proteins COX15 and NDUFS2. CONCLUSION: SIRT1 and SIRT2 may serve as key regulators for some obesity comorbidities related to antioxidant status, while PBMC could be a model to study the effect of the sirtuin response in obesity therapy.

Specific insulin sensitivity and leptin responses to a nutritional treatment of obesity via a combination of energy restriction and fatty fish intake.

BACKGROUND: Nutritional strategies to treat obesity often influence neuroendocrine factors related to body weight control. The present study aimed to investigate whether the inclusion of three fatty fish servings per week within a hypocaloric diet may have specific healthy effects on insulin and leptin functions. METHODS: Thirty-two subjects (body mass index = 31.6 +/- 3.5 kg m(-2)) aged 36 +/- 7 years, were assigned to a control or fish-based energy-restricted diet over an 8-week period. Anthropometry, body composition, lipid profile, leptin and insulin values were measured at the start and at the end of the dietary intervention. RESULTS: Both experimental diets resulted in a similar mean weight loss (control = 5.3 +/- 2.6% versus fish-based = 5.5 +/- 2.5%; P = 0.783). A significant reduction in insulin resistance, as determined by the homeostatic model assessment index (HOMA-IR = insulin x glucose/22.5), was observed after the fish-based intervention. The change in circulating leptin was higher in the fish-based diet compared to the control group. Sixteen percent of the variability in the change of adjusted-leptin could be explained (P = 0.034) by the HOMA index change and the type of diet. CONCLUSIONS: Three servings a week of fatty fish included in an energy-restricted diet appears to be a valid strategy for specifically improving insulin sensitivity and leptin levels in obese subjects, which could involve a better body weight regulation after a nutritional intervention period.

Energy restriction in obese subjects impact differently two mitochondrial function markers

Excessive fat deposition is the key feature in obesity, which is empowered bycytokines overproduction and stimulation of cell oxidative stress processes, but littleis known about energy availability in the form of ATP and mitochondrial functionin the obese subjects. Thus, the aim of this study was to evaluate the possible changesin energy metabolism after a 8-weeks balanced-hypocaloric diet in obese subjects bymeasuring the ATP-content in leukocytes, by assessing 2-keto[1-13C]isocaproatebreath test (KICA-BT) parameters related to mitochondrial function and by analyzinginflammatory and oxidative stress biomarkers. All the recruited obese subjects(n=19) lost body weight after dieting (-5.55±2.88%). The hypocaloric treatmentinduced a decrease in leptin levels and lipid peroxidation markers. Interestingly, theATP content in blood leukocytes increased (49.9±32.5 vs 36.2±27.9 pmol/mg prot.;p<0.05), while KICA tracer mitochondrial oxidation decreased (30.9±5.9 vs. 33.1±4.5%13C; p<0.05) after weight loss. These results show that two minimally invasivemethods were able to detect changes in mitochondrial function as induced by ahypocaloric diet, which is of great interest in order to understand oxidative processesassociated with weight homeostasis as well as to establish newer anti-obesity therapeutictargets by using mitochondrial function markers in vivo (AU)

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Energy restriction in obese subjects impact differently two mitochondrial function markers.

Excessive fat deposition is the key feature in obesity, which is empowered by cytokines overproduction and stimulation of cell oxidative stress processes, but little is known about energy availability in the form of ATP and mitochondrial function in the obese subjects. Thus, the aim of this study was to evaluate the possible changes in energy metabolism after a 8-weeks balanced-hypocaloric diet in obese subjects by measuring the ATP-content in leukocytes, by assessing 2-keto[1-13C]isocaproate breath test (KICA-BT) parameters related to mitochondrial function and by analyzing inflammatory and oxidative stress biomarkers. All the recruited obese subjects (n = 19) lost body weight after dieting (-5.55 +/- 2.88%). The hypocaloric treatment induced a decrease in leptin levels and lipid peroxidation markers. Interestingly, the ATP content in blood leukocytes increased (49.9 +/- 32.5 vs 36.2 +/- 27.9 pmol/mg prot.; p < 0.05), while KICA tracer mitochondrial oxidation decreased (30.9 +/- 5.9 vs. 33.1 +/- 4.5 % 13C; p < 0.05) after weight loss. These results show that two minimally invasive methods were able to detect changes in mitochondrial function as induced by a hypocaloric diet, which is of great interest in order to understand oxidative processes associated with weight homeostasis as well as to establish newer anti-obesity therapeutic targets by using mitochondrial function markers in vivo.

Implicación de la IL-6 y su polimorfismo -174G>C en el control del peso corporal y en las complicaciones metabólicas asociadas a la obesidad / Role of IL-6 and its -174G>C polymorphism in weight management and in the metabolic comorbidities associated with obesity

La obesidad y sus comorbilidades se han relacionado con un estado proinflamatorio de bajo grado, en el que el tejido adiposo parece estar implicado. De hecho, el adipocito secreta diferentes citoquinas proinflamatorias, como la IL-6, entre otras. En efecto, las concentraciones elevadas de IL-6 se han asociado con elevados índices de masa corporal, con la diabetes mellitus tipo 2, con dislipemias y con la hipertensión arterial. La implicación de la IL-6 en la homeostasis energética está ampliamente documentada, de forma que su posible relación con el desarrollo de obesidad podría estar mediada por las acciones de esta citoquina y en función del polimorfismo -174G>C presente en el genoma.Diferentes investigaciones han señalado la relación del alelo G del gen de la IL-6 con la obesidad, la resistencia a la insulina y diferentes factores de riesgo cardiovascular. Sin embargo, también se han publicado estudios que han asociado estos procesos patológicos con el alelo C de este gen.El presente trabajo revisa los datos publicados recientemente sobre la IL-6 y sus implicaciones fisiopatológicas en la ganancia de peso, con el fin de profundizar en el conocimiento que se dispone del polimorfismo -174G>C en el desarrollo de esta enfermedad, así como de las complicaciones para las cuales la obesidad supone uno de los factores de riesgo más relevantes

Obesity and its comorbidities have been associated with a low grade proinflammatory state, in which the adipose tissue seems to be involved. In fact, this tissue produces different proinflammatory cytokines, such as IL-6 and others.High circulating concentrations of IL-6 have been related to high body mass index, to diabetes mellitus type 2, to lipid abnormalities and to high blood pressure. There are some studies, which reported a relationship between IL-6 and energy metabolism, so this cytokine and its -174G>C gene polymorphism could be factors involved in the development of obesity. Different studies have associated the G allele of the IL-6 gene with obesity, with insulin resistance and with different cardiovascular risk factors. However, other published reports have associated the C allele of this gene to these metabolic disturbances and pathologies.This paper reviews recently published evidences about IL-6 and its physiopathological involvement in obesity and comorbidities, with emphasis on the role of the -174G>C polymorphism in the aetiology of these disturbances, in which obesity is a major risk factor

[Role of IL-6 and its -174G>C polymorphism in weight management and in the metabolic comorbidities associated with obesity]. / Implicación de la IL-6 y su polimorfismo -174G>C en el control del peso corporal y en las complicaciones metabólicas asociadas a la obesidad.

Obesity and its comorbidities have been associated with a low grade proinflammatory state, in which the adipose tissue seems to be involved. In fact, this tissue produces different proinflammatory cytokines, such as IL-6 and others. High circulating concentrations of IL-6 have been related to high body mass index, to diabetes mellitus type 2, to lipid abnormalities and to high blood pressure. There are some studies, which reported a relationship between IL-6 and energy metabolism, so this cytokine and its -174G>C gene polymorphism could be factors involved in the development of obesity. Different studies have associated the G allele of the IL-6 gene with obesity, with insulin resistance and with different cardiovascular risk factors. However, other published reports have associated the C allele of this gene to these metabolic disturbances and pathologies. This paper reviews recently published evidences about IL-6 and its physiopathological involvement in obesity and comorbidities, with emphasis on the role of the -174G>C polymorphism in the aetiology of these disturbances, in which obesity is a major risk factor.