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1.
Nutrients ; 13(1)2021 Jan 12.
Artículo en Inglés | MEDLINE | ID: mdl-33445809

RESUMEN

Consumption of trans fatty acids (TFAs) has been unequivocally linked to several adverse health effects, with the increased risk of cardiovascular disease being one of the most well understood. To reduce TFA-related morbidity and mortality, several countries have imposed voluntary or mandatory measures to minimize the content of industrial TFAs (iTFAs) in the food supply. In 2018, Slovenia introduced a ban on iTFAs on top of preceding voluntary calls to industry to reduce its use of partially hydrogenated oils (PHOs) as the main source of iTFAs. To investigate the consumption of TFAs, data available from the nationally representative dietary survey SI.Menu were analyzed. The survey consisted of two 24-h non-consecutive day recalls from 1248 study participants from three age groups (10-17, 18-64, 65-74 years old), combined with socio-demographic, socio-economic, and lifestyle parameters. The analyses demonstrated that, on average, TFAs accounted for 0.38-0.50% of total energy intake (TEI). However, 13% of adolescents, 29.4% of adults, and 41.8% of the elderly population still consumed more than 0.50% TEI with TFAs. The main sources of TFAs in the diet were naturally present TFAs from butter, meat dishes, and meat products, regardless of the age group. Results indicate that following the reformulation activities, the major sources of TFAs in the diets of the Slovenian population now represent foods which are natural sources of TFAs.


Asunto(s)
Enfermedades Cardiovasculares , Grasas de la Dieta/efectos adversos , Ingestión de Energía , Ácidos Grasos Trans/efectos adversos , Adolescente , Adulto , Anciano , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/etiología , Niño , Femenino , Humanos , Masculino , Persona de Mediana Edad , Factores de Riesgo , Eslovenia/epidemiología
2.
Toxicol Lett ; 339: 23-31, 2021 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-33359558

RESUMEN

Interesterified fat (IF) currently substitutes the hydrogenated vegetable fat (HVF) in processed foods. However, the IF consumption impact on the central nervous system (CNS) has been poorly studied. The current study investigated connections between IF chronic consumption and locomotor impairments in early life period and adulthood of rats and access brain molecular targets related to behavior changes in adulthood offspring. During pregnancy and lactation, female rats received soybean oil (SO) or IF and their male pups received the same maternal supplementation from weaning until adulthood. Pups' motor ability and locomotor activity in adulthood were evaluated. In the adult offspring striatum, dopaminergic targets, glial cell line-derived neurotrophic factor (GDFN) and lipid profile were quantified. Pups from IF supplementation group presented impaired learning concerning complex motor skill and sensorimotor behavior. The same animals showed decreased locomotion in adulthood. Moreover, IF group showed decreased immunoreactivity of all dopaminergic targets evaluated and GDNF, along with important changes in FA composition in striatum. This study shows that the brain modifications induce by IF consumption resulted in impaired motor control in pups and decreased locomotion in adult animals. Other studies about health damages induced by IF consumption may have a contribution from our current outcomes.


Asunto(s)
Encéfalo/metabolismo , Grasas de la Dieta/efectos adversos , Locomoción/fisiología , Actividad Motora/fisiología , Sistema Nervioso/metabolismo , Efectos Tardíos de la Exposición Prenatal/fisiopatología , Ácidos Grasos Trans/efectos adversos , Factores de Edad , Fenómenos Fisiológicos Nutricionales de los Animales , Animales , Grasas de la Dieta/metabolismo , Femenino , Humanos , Fenómenos Fisiologicos Nutricionales Maternos , Modelos Animales , Fenómenos Fisiológicos del Sistema Nervioso , Embarazo , Ratas , Ácidos Grasos Trans/metabolismo
3.
PLoS One ; 15(10): e0235875, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33022003

RESUMEN

The oral lipid tolerance test (OLTT) has been known to assess intestinal fat metabolism and whole-body lipid metabolism, but rodent models for OLTT are not yet established. Differences in OLTT methodology preclude the generation of definitive results, which may cause some confusion about the anti-hypertriglyceridemia effects of the test materials. To standardize and generate more appropriate methodology for the OLTT, we examined the effects of mice strain, dietary lipid sources, fasting period, and gender on lipid-induced hypertriglyceridemia in mice. First, lipid-induced hypertriglyceridemia was more strongly observed in male ddY mice than in C57BL/6N or ICR mice. Second, the administration of olive and soybean oils remarkably represented lipid-induced hypertriglyceridemia. Third, fasting period before the OLTT largely affected the plasma triglyceride elevation. Fasting for 12 h, but less than 48 h, provoked lipid-induced hypertriglyceridemia. Fourth, we explored the suppressive effects of epigallocatechin gallate (EGCG), a green tea polyphenol, on lipid-induced hypertriglyceridemia. The administration of 100 mg/kg of EGCG suppressed lipid-induced hypertriglyceridemia and intestinal lipase activity. Fifth, EGCG-induced suppressive effects were observed after lipid-induced hypertriglyceridemia was observed in male mice, but not in female mice. Lastly, lipid-induced hypertriglyceridemia could be more effectively induced in mice fed a high-fat diet for 1 week before the OLTT. These findings indicate that male ddY mice after 12 h fasting displayed marked lipid-induced hypertriglyceridemia in response to soybean oil. Hence, the defined experiment condition may be a more appropriate OLTT model for evaluating lipid-induced hypertriglyceridemia.


Asunto(s)
Grasas de la Dieta/efectos adversos , Hipertrigliceridemia/sangre , Lípidos/efectos adversos , Té/química , Triglicéridos/sangre , Animales , Hipertrigliceridemia/tratamiento farmacológico , Hipertrigliceridemia/etiología , Lípidos/administración & dosificación , Lípidos/sangre , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Endogámicos ICR , Ratas , Ratas Sprague-Dawley , Ratas Wistar
4.
Nutr Metab Cardiovasc Dis ; 30(10): 1673-1678, 2020 09 24.
Artículo en Inglés | MEDLINE | ID: mdl-32736955

RESUMEN

BACKGROUND AND AIMS: The present study analyzes the relation between diet and all-cause mortality in a cohort of Italian men residing in different regions of Italy. METHODS AND RESULTS: The cohort was established using the members of the Associazione Nazionale Alpini, a voluntary organization that enlists individuals who have served in the Alpine troup; a mountain warfare infantry corps of the Italian Army. For the purpose of these analyses a total of 5049 participants were followed for an average of seven years. At baseline information was collected regarding age, education, life style habits, with special emphasis on diet (with the use of a validated dietary questionnaire), smoking and alcohol use. A total of 190 deaths were ascertained. In multivariate analyses the consumption of a Mediterranean type diet was inversely associated with mortality. Additional findings of relevance include: an inverse association between mortality and intake of vegetable fats and proteins, monounsaturated (MUFA) fats of vegetable origins, starch and folic acid. Positive association were evident between mortality and intake of animal fats, MUFA of animal origins and sugar. CONCLUSIONS: This study, focusing on a homogenous cohort characterized by a varied intake and high intake of monounsaturated fats, confirms the inverse association between a Mediterranean type diet and mortality and points out that the nature of the MUFA may be relevant for their effects on health. In addition, the study confirms that fats of animal origins and dietary sugar are associated with an overall deleterious effect on mortality.


Asunto(s)
Causas de Muerte , Dieta Saludable , Dieta Mediterránea , Conducta Alimentaria , Adulto , Encuestas sobre Dietas , Grasas de la Dieta/efectos adversos , Azúcares de la Dieta/efectos adversos , Humanos , Italia/epidemiología , Masculino , Persona de Mediana Edad , Salud Militar , Factores Protectores , Medición de Riesgo , Factores de Riesgo , Factores Sexuales , Factores de Tiempo , Adulto Joven
5.
PLoS Med ; 17(8): e1003234, 2020 08.
Artículo en Inglés | MEDLINE | ID: mdl-32764760

RESUMEN

BACKGROUND: In common with many other low- and middle-income countries (LMICs), rural to urban migrants in India are at increased risk of obesity, but it is unclear whether this is due to increased energy intake, reduced energy expenditure, or both. Knowing this and the relative contribution of specific dietary and physical activity behaviours to greater adiposity among urban migrants could inform policies for control of the obesity epidemic in India and other urbanising LMICs. In the Indian Migration Study, we previously found that urban migrants had greater prevalence of obesity and diabetes compared with their nonmigrant rural-dwelling siblings. In this study, we investigated the relative contribution of energy intake and expenditure and specific diet and activity behaviours to greater adiposity among urban migrants in India. METHODS AND FINDINGS: The Indian Migration Study was conducted between 2005 and 2007. Factory workers and their spouses from four cities in north, central, and south of India, together with their rural-dwelling siblings, were surveyed. Self-reported data on diet and physical activity was collected using validated questionnaires, and adiposity was estimated from thickness of skinfolds. The association of differences in dietary intake, physical activity, and adiposity between siblings was examined using multivariable linear regression. Data on 2,464 participants (median age 43 years) comprised of 1,232 sibling pairs (urban migrant and their rural-dwelling sibling) of the same sex (31% female) were analysed. Compared with the rural siblings, urban migrants had 18% greater adiposity, 12% (360 calories/day) more energy intake, and 18% (11 kilojoules/kg/day) less energy expenditure (P < 0.001 for all). Energy intake and expenditure were independently associated with increased adiposity of urban siblings, accounting for 4% and 6.5% of adiposity difference between siblings, respectively. Difference in dietary fat/oil (10 g/day), time spent engaged in moderate or vigorous activity (69 minutes/day), and watching television (30 minutes/day) were associated with difference in adiposity between siblings, but no clear association was observed for intake of fruits and vegetables, sugary foods and sweets, cereals, animal and dairy products, and sedentary time. The limitations of this study include a cross-sectional design, systematic differences in premigration characteristics of migrants and nonmigrants, low response rate, and measurement error in estimating diet and activity from questionnaires. CONCLUSIONS: We found that increased energy intake and reduced energy expenditure contributed equally to greater adiposity among urban migrants in India. Policies aimed at controlling the rising prevalence of obesity in India and potentially other urbanising LMICs need to be multicomponent, target both energy intake and expenditure, and focus particularly on behaviours such as dietary fat/oil intake, time spent on watching television, and time spent engaged in moderate or vigorous intensity physical activity.


Asunto(s)
Adiposidad/fisiología , Dieta/tendencias , Ingestión de Energía/fisiología , Ejercicio Físico/fisiología , Población Rural/tendencias , Migrantes , Población Urbana/tendencias , Adulto , Índice de Masa Corporal , Estudios Transversales , Dieta/efectos adversos , Grasas de la Dieta/efectos adversos , Metabolismo Energético/fisiología , Femenino , Humanos , India/epidemiología , Masculino , Persona de Mediana Edad , Factores de Riesgo , Autoinforme
6.
Nat Rev Cancer ; 20(8): 455-469, 2020 08.
Artículo en Inglés | MEDLINE | ID: mdl-32546840

RESUMEN

Prostate cancer is a major cause of cancer morbidity and mortality. Intra-prostatic inflammation is a risk factor for prostate carcinogenesis, with diet, chemical injury and an altered microbiome being causally implicated. Intra-prostatic inflammatory cell recruitment and expansion can ultimately promote DNA double-strand breaks and androgen receptor activation in prostate epithelial cells. The activation of the senescence-associated secretory phenotype fuels further 'inflammatory storms', with free radicals leading to further DNA damage. This drives the overexpression of DNA repair and tumour suppressor genes, rendering these genes susceptible to mutagenic insults, with carcinogenesis accelerated by germline DNA repair gene defects. We provide updates on recent advances in elucidating prostate carcinogenesis and explore novel therapeutic and prevention strategies harnessing these discoveries.


Asunto(s)
Carcinogénesis/inmunología , Inflamación/inmunología , Próstata/inmunología , Neoplasias de la Próstata/inmunología , Receptores Androgénicos/inmunología , Carcinogénesis/genética , Transformación Celular Neoplásica/genética , Transformación Celular Neoplásica/inmunología , Enfermedad Crónica , Roturas del ADN de Doble Cadena , Daño del ADN/genética , Daño del ADN/inmunología , Reparación del ADN/genética , Reparación del ADN/inmunología , Dieta/efectos adversos , Grasas de la Dieta/efectos adversos , Grasas de la Dieta/inmunología , Humanos , Inflamación/etiología , Inflamación/genética , Masculino , Microbiota/inmunología , Obesidad/complicaciones , Obesidad/inmunología , Comunicación Paracrina/inmunología , Neoplasias de la Próstata/etiología , Neoplasias de la Próstata/genética , Receptores Androgénicos/genética , Microambiente Tumoral/genética , Microambiente Tumoral/inmunología
7.
J Nutr ; 150(8): 2101-2111, 2020 08 01.
Artículo en Inglés | MEDLINE | ID: mdl-32470979

RESUMEN

BACKGROUND: Dietary polyphenols including anthocyanins target multiple organs. OBJECTIVE: We aimed to assess the involvement of glucagon-like peptide 1 (GLP-1), leptin, insulin and fibroblast growth factor 21 (FGF21) in mediating metabolic beneficial effects of purified anthocyanin cyanidin-3-glucoside (Cy3G). METHODS: Intestinal proglucagon gene (Gcg; encoding GLP-1) and liver Fgf21 expression were assessed in 6-wk-old male C57BL-6J mice fed a low-fat-diet (LFD; 10% of energy from fat), alone or with 1.6 mg Cy3G/L in drinking water for 3 wk [experiment (Exp.) 1; n = 5/group]. Similar mice were fed the LFD or a high-fat diet (HFD; 60% energy from fat) with or without Cy3G for 20 wk. Half of the mice administered Cy3G also received 4 broad-spectrum antibiotics (ABs) in drinking water between weeks 11 and 14, for a total of 6 groups (n = 8/group). Metabolic tolerance tests were conducted between weeks 2 and 16. Relevant hormone gene expression and plasma hormone concentrations were assessed mainly at the end of 20 wk (Exp. 2). RESULTS: In Exp. 1, Cy3G administration increased ileal but not colonic Gcg level by 2-fold (P < 0.05). In Exp. 2, Cy3G attenuated HFD-induced body-weight gain (20.3% at week 16), and improved glucose tolerance (26.5% at week 15) but not insulin tolerance. Although Cy3G had no effect on glucose tolerance in LFD mice, LFD/Cy3G/AB mice showed better glucose tolerance than LFD/Cy3G mice (23%). In contrast, HFD/Cy3G/AB mice showed worse glucose tolerance compared with HFD/Cy3G mice (15%). Beneficial effects of Cy3G in HFD mice were not associated with changes in plasma leptin, insulin or GLP-1 concentrations. However, Cy3G increased hepatic Fgf21 expression in mice in Exp. 1 by 4-fold and attenuated Fgf21 overexpression in HFD mice (Exp. 2, 22%), associated with increased expression of genes that encode FGFR1 and ß-klotho (>3-fold, P < 0.05). CONCLUSIONS: Dietary Cy3G may reduce body weight and exert metabolic homeostatic effects in mice via changes in hepatic FGF21.


Asunto(s)
Antocianinas/farmacología , Dieta Alta en Grasa/efectos adversos , Grasas de la Dieta/administración & dosificación , Factores de Crecimiento de Fibroblastos/metabolismo , Intolerancia a la Glucosa , Glucósidos/farmacología , Aumento de Peso/efectos de los fármacos , Animales , Grasas de la Dieta/efectos adversos , Factores de Crecimiento de Fibroblastos/genética , Regulación de la Expresión Génica/efectos de los fármacos , Péptido 1 Similar al Glucagón/metabolismo , Incretinas/genética , Incretinas/metabolismo , Leptina/metabolismo , Hígado , Masculino , Ratones , Distribución Aleatoria , Pérdida de Peso/efectos de los fármacos
9.
Sci Rep ; 10(1): 7072, 2020 04 27.
Artículo en Inglés | MEDLINE | ID: mdl-32341369

RESUMEN

Balloon catheter endothelial denudation in New Zealand white rabbits fed high cholesterol diet is a validated atherosclerosis model. Well-characterized in terms of atherosclerosis induction and progression, the metabolic changes associated with the atherosclerosis progression remain indeterminate. Non-targeted metabolomics permits to develop such elucidation and allows to evaluate the metabolic consequences of colchicine treatment, an anti-inflammatory drug that could revert these changes. 16 rabbits underwent 18 weeks of atherosclerosis induction by diet and aortic denudation. Thereafter animals were randomly assigned to colchicine treatment or placebo for 18 weeks while on diet. Plasma samples were obtained before randomization and at 36 weeks. Multiplatform (GC/MS, CE/MS, RP-HPLC/MS) metabolomics was applied. Plasma fingerprints were pre-processed, and the resulting matrixes analyzed to unveil differentially expressed features. Different chemical annotation strategies were accomplished for those significant features. We found metabolites associated with either atherosclerosis progression, or colchicine treatment, or both. Atherosclerosis was profoundly associated with an increase in circulating bile acids. Most of the changes associated with sterol metabolism could not be reverted by colchicine treatment. However, the variations in lysine, tryptophan and cysteine metabolism among others, have shown new potential mechanisms of action of the drug, also related to atherosclerosis progression, but not previously described.


Asunto(s)
Aterosclerosis , Colchicina/farmacología , Animales , Aterosclerosis/sangre , Aterosclerosis/inducido químicamente , Aterosclerosis/tratamiento farmacológico , Grasas de la Dieta/efectos adversos , Grasas de la Dieta/farmacología , Modelos Animales de Enfermedad , Progresión de la Enfermedad , Humanos , Metabolómica , Conejos , Distribución Aleatoria
10.
Diabetes ; 69(6): 1292-1305, 2020 06.
Artículo en Inglés | MEDLINE | ID: mdl-32234722

RESUMEN

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have favorable cardiovascular outcomes in patients with diabetes. However, whether SGLT2i can improve obesity-related cardiac dysfunction is unknown. Sestrin2 is a novel stress-inducible protein that regulates AMPK-mammalian target of rapamycin (mTOR) and suppresses oxidative damage. The aim of this study was to determine whether empagliflozin (EMPA) improves obesity-related cardiac dysfunction via regulating Sestrin2-mediated pathways in diet-induced obesity. C57BL/6J mice and Sestrin2 knockout mice were fed a high-fat diet (HFD) for 12 weeks and then treated with or without EMPA (10 mg/kg) for 8 weeks. Treating HFD-fed C57BL/6J mice with EMPA reduced body weight and whole-body fat and improved metabolic disorders. Furthermore, EMPA improved myocardial hypertrophy/fibrosis and cardiac function and reduced cardiac fat accumulation and mitochondrial injury. Additionally, EMPA significantly augmented Sestrin2 levels and increased AMPK and endothelial nitric oxide synthase phosphorylation, but inhibited Akt and mTOR phosphorylation. These beneficial effects were partially attenuated in HFD-fed Sestrin2 knockout mice. Intriguingly, EMPA treatment enhanced the Nrf2/HO-1-mediated oxidative stress response, suggesting antioxidant and anti-inflammatory activity. Thus, EMPA improved obesity-related cardiac dysfunction via regulating Sestrin2-mediated AMPK-mTOR signaling and maintaining redox homeostasis. These findings provide a novel mechanism for the cardiovascular protection of SGLT2i in obesity.


Asunto(s)
Adenilato Quinasa/metabolismo , Compuestos de Bencidrilo/uso terapéutico , Glucósidos/uso terapéutico , Cardiopatías/tratamiento farmacológico , Obesidad/inducido químicamente , Peroxidasas/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Adenilato Quinasa/genética , Animales , Dieta Alta en Grasa/efectos adversos , Grasas de la Dieta/efectos adversos , Regulación de la Expresión Génica/efectos de los fármacos , Cardiopatías/etiología , Homeostasis , Ratones , Oxidación-Reducción , Peroxidasas/genética , Transducción de Señal , Serina-Treonina Quinasas TOR/genética
11.
Nat Commun ; 11(1): 1775, 2020 04 14.
Artículo en Inglés | MEDLINE | ID: mdl-32286299

RESUMEN

The increased incidence of inflammatory bowel disease (IBD) has become a global phenomenon that could be related to adoption of a Western life-style. Westernization of dietary habits is partly characterized by enrichment with the ω-6 polyunsaturated fatty acid (PUFA) arachidonic acid (AA), which entails risk for developing IBD. Glutathione peroxidase 4 (GPX4) protects against lipid peroxidation (LPO) and cell death termed ferroptosis. We report that small intestinal epithelial cells (IECs) in Crohn's disease (CD) exhibit impaired GPX4 activity and signs of LPO. PUFAs and specifically AA trigger a cytokine response of IECs which is restricted by GPX4. While GPX4 does not control AA metabolism, cytokine production is governed by similar mechanisms as ferroptosis. A PUFA-enriched Western diet triggers focal granuloma-like neutrophilic enteritis in mice that lack one allele of Gpx4 in IECs. Our study identifies dietary PUFAs as a trigger of GPX4-restricted mucosal inflammation phenocopying aspects of human CD.


Asunto(s)
Enfermedad de Crohn/metabolismo , Grasas de la Dieta/efectos adversos , Enteritis/metabolismo , Ácidos Grasos Insaturados/metabolismo , Inflamación/metabolismo , Fosfolípido Hidroperóxido Glutatión Peroxidasa/metabolismo , Adulto , Animales , Muerte Celular/genética , Muerte Celular/fisiología , Enfermedad de Crohn/genética , Enteritis/etiología , Enteritis/genética , Ácidos Grasos Insaturados/genética , Femenino , Glutatión Peroxidasa/metabolismo , Humanos , Inflamación/genética , Peroxidación de Lípido/genética , Peroxidación de Lípido/fisiología , Masculino , Ratones , Ratones Endogámicos C57BL , Persona de Mediana Edad , Fosfolípido Hidroperóxido Glutatión Peroxidasa/genética
12.
Toxicol Appl Pharmacol ; 396: 114997, 2020 06 01.
Artículo en Inglés | MEDLINE | ID: mdl-32259528

RESUMEN

High-fat high-fructose diet (HFF) in obesity can induce dyslipidemia and lipid accumulation both in kidney and liver which related to insulin resistance and lipotoxicity-induced cellular damage. We investigated whether dapagliflozin with or without atorvastatin could improve lipid accumulation-induced kidney and liver injury in HFF-induced insulin resistant rats. Male Wistar rats were fed with HFF for 16 weeks and then received drug treatments for 4 weeks; vehicle, dapagliflozin, atorvastatin and dapagliflozin plus atorvastatin treatment groups. HFF rats demonstrated insulin resistance, dyslipidemia, liver injury and renal dysfunction associated with impaired renal lipid metabolism and lipid accumulation. Dapagliflozin and combination treatment could improve HFF-induced insulin resistance, lipogenesis and lipotoxicity-related renal oxidative stress, inflammation, fibrosis and apoptosis leading to kidney dysfunction recovery. Liver injury-associated inflammation was also improved by these two regimens. Notably, the reduced lipid accumulation in liver and kidney that linked to an improvement of lipid oxidation was prominent in the combination treatment. Therefore, dapagliflozin combined with atorvastatin treatment exert the beneficial effects on lipid metabolism and lipotoxicity in liver and kidney injury via the attenuation of oxidative stress, fibrosis and apoptosis in insulin resistant model.


Asunto(s)
Lesión Renal Aguda/tratamiento farmacológico , Atorvastatina/uso terapéutico , Compuestos de Bencidrilo/uso terapéutico , Carbohidratos de la Dieta/efectos adversos , Grasas de la Dieta/efectos adversos , Hígado Graso/tratamiento farmacológico , Fructosa/efectos adversos , Glucósidos/uso terapéutico , Inhibidores de Hidroximetilglutaril-CoA Reductasas/uso terapéutico , Resistencia a la Insulina , Animales , Atorvastatina/administración & dosificación , Compuestos de Bencidrilo/administración & dosificación , Western Blotting , Carbohidratos de la Dieta/farmacología , Quimioterapia Combinada , Fructosa/farmacología , Glucósidos/administración & dosificación , Inhibidores de Hidroximetilglutaril-CoA Reductasas/administración & dosificación , Masculino , Ratas , Ratas Wistar
13.
Nutr. hosp ; 37(2): 313-320, mar.-abr. 2020. tab
Artículo en Inglés | IBECS | ID: ibc-190596

RESUMEN

INTRODUCTION: dietary fat has been reported as one of the significant risk factors in the development of cardiovascular diseases (CVD). OBJECTIVE: this study aimed at assessing the possible association between fat intake and CVD. METHODS: the present case-control study was conducted in the center of coronary angiography. Three-hundred and ninety nine patients who referred for elective coronary angiography with clinical suspicion of coronary artery disease were enrolled. Dietary data were collected from each patient using an interview-based food frequency questionnaire. RESULTS: the findings of the present study revealed no significant differences between cases and controls regarding the intake of all types of fat either before or after energy adjustment. For both cases and controls the percentage of fat intake from total energy and the intakes of polyunsaturated and monounsaturated fats, cholesterol, omega-6 and omega-3 were within the recommended amounts. The intake of all fat types (except trans-fat) was not associated with the risk of developing CVD. Trans-fat intake in the second and third quartile increased the risk of CVD by OR 1.86 (95 % CI: 1.03-3.34) and 2.01 (95 % CI: 1.12-3.60), respectively. CONCLUSIONS: while trans-fats may be significantly associated with the development of CVD in the first two quartiles, no association has been detected with other fat types


INTRODUCCIÓN: se ha establecido que la grasa en la dieta es uno de los factores de riesgo significativos en el desarrollo de enfermedades cardiovasculares (ECV). OBJETIVO: este estudio tuvo como objetivo evaluar la posible asociación entre la ingesta de grasa y la ECV. MÉTODOS: el presente estudio de casos y controles se realizó en el centro de la angiografía coronaria. Se inscribieron 399 pacientes que fueron remitidos para una angiografía coronaria electiva con sospecha clínica de enfermedad coronaria. Los datos dietéticos se obtuvieron de cada paciente mediante un cuestionario de frecuencia de alimentos basado en entrevistas. RESULTADOS: los hallazgos del presente estudio no revelaron diferencias significativas entre los casos y los controles con respecto a la ingesta de todos los tipos de grasa, ya sea antes o después del ajuste de energía. Para ambos casos y controles, el porcentaje de ingesta de grasas de la energía total y las ingestas de grasas poliinsaturadas y monoinsaturadas, colesterol, omega-6 y omega-3 se encuentran dentro de las cantidades recomendadas. La ingesta de todos los tipos de grasa (excepto las grasas trans) no se asoció con el riesgo de desarrollar ECV. La ingesta de grasas trans en el segundo y tercer cuartil aumentó el riesgo de ECV en OR 1,86 (IC 95 %: 1,03-3,34) y 2,01 (IC 95 %: 1,12-3,60), respectivamente. CONCLUSIONES: si bien las grasas trans pueden estar asociadas significativamente con el desarrollo de ECV en los dos primeros cuartiles, no se ha detectado asociación con otros tipos de grasa


Asunto(s)
Humanos , Masculino , Femenino , Persona de Mediana Edad , Dieta Alta en Grasa/efectos adversos , Enfermedad Coronaria/complicaciones , Grasas de la Dieta/efectos adversos , Enfermedad Coronaria/diagnóstico , Grasas de la Dieta/administración & dosificación , Enfermedad Coronaria/prevención & control , Factores de Riesgo , Dieta con Restricción de Grasas/métodos , Encuestas Nutricionales
14.
Cancer Res ; 80(12): 2564-2574, 2020 06 15.
Artículo en Inglés | MEDLINE | ID: mdl-32213543

RESUMEN

Obesity is associated with increased risk of many types of cancer and can be induced by various high-fat diets (HFD) from different fat sources. It remains unknown whether fatty acid composition in different HFD influences obesity-associated tumor development. Here we report that consumption of either a cocoa butter or fish oil HFD induced similar obesity in mouse models. While obesity induced by the cocoa butter HFD was associated with accelerated mammary tumor growth, consumption of the fish oil HFD uncoupled obesity from increased mammary tumor growth and exhibited a decrease in protumor macrophages. Compared with fatty acid (FA) components in both HFDs, n-3 FA rich in the fish oil HFD induced significant production of reactive oxygen species (ROS) and macrophage death. Moreover, A-FABP expression in the protumor macrophages facilitated intracellular transportation of n-3 FA and oxidation of mitochondrial FA. A-FABP deficiency diminished n-3 FA-mediated ROS production and macrophage death in vitro and in vivo. Together, our results demonstrate a novel mechanism by which n-3 FA induce ROS-mediated protumor macrophage death in an A-FABP-dependent manner. SIGNIFICANCE: This study provides mechanistic insight into dietary supplementation with fish oil for breast cancer prevention and advances a new concept that not all HFDs leading to obesity are tumorigenic. GRAPHICAL ABSTRACT: http://cancerres.aacrjournals.org/content/canres/80/12/2564/F1.large.jpg.


Asunto(s)
Dieta Alta en Grasa/métodos , Grasas de la Dieta/efectos adversos , Proteínas de Unión a Ácidos Grasos/metabolismo , Aceites de Pescado/administración & dosificación , Macrófagos/inmunología , Neoplasias Mamarias Experimentales/inmunología , Obesidad/complicaciones , Animales , Carcinogénesis/inmunología , Carcinogénesis/metabolismo , Línea Celular Tumoral/trasplante , Dieta Alta en Grasa/efectos adversos , Proteínas de Unión a Ácidos Grasos/genética , Femenino , Humanos , Macrófagos/citología , Macrófagos/metabolismo , Glándulas Mamarias Animales/citología , Glándulas Mamarias Animales/inmunología , Glándulas Mamarias Animales/patología , Neoplasias Mamarias Experimentales/genética , Neoplasias Mamarias Experimentales/metabolismo , Neoplasias Mamarias Experimentales/prevención & control , Ratones , Ratones Noqueados , Mitocondrias/metabolismo , Obesidad/inmunología , Obesidad/metabolismo , Cultivo Primario de Células , Especies Reactivas de Oxígeno/metabolismo
15.
Sci Rep ; 10(1): 3850, 2020 03 02.
Artículo en Inglés | MEDLINE | ID: mdl-32123215

RESUMEN

Hepatic fibrosis is a major consequence of chronic liver disease such as non-alcoholic steatohepatitis which is undergoing a dramatic evolution given the obesity progression worldwide, and has no treatment to date. Hepatic stellate cells (HSCs) play a key role in the fibrosis process, because in chronic liver damage, they transdifferentiate from a "quiescent" to an "activated" phenotype responsible for most the collagen deposition in liver tissue. Here, using a diet-induced liver fibrosis murine model (choline-deficient amino acid-defined, high fat diet), we characterized a specific population of HSCs organized as clusters presenting simultaneously hypertrophy of retinoid droplets, quiescent and activated HSC markers. We showed that hypertrophied HSCs co-localized with fibrosis areas in space and time. Importantly, we reported the existence of this phenotype and its association with collagen deposition in three other mouse fibrosis models, including CCl4-induced fibrosis model. Moreover, we have also shown its relevance in human liver fibrosis associated with different etiologies (obesity, non-alcoholic steatohepatitis, viral hepatitis C and alcoholism). In particular, we have demonstrated a significant positive correlation between the stage of liver fibrosis and HSC hypertrophy in a cohort of obese patients with hepatic fibrosis. These results lead us to conclude that hypertrophied HSCs are closely associated with hepatic fibrosis in a metabolic disease context and may represent a new marker of metabolic liver disease progression.


Asunto(s)
Intoxicación por Tetracloruro de Carbono , Grasas de la Dieta/efectos adversos , Células Estrelladas Hepáticas , Cirrosis Hepática , Animales , Intoxicación por Tetracloruro de Carbono/metabolismo , Intoxicación por Tetracloruro de Carbono/patología , Grasas de la Dieta/farmacología , Células Estrelladas Hepáticas/metabolismo , Células Estrelladas Hepáticas/patología , Humanos , Cirrosis Hepática/inducido químicamente , Cirrosis Hepática/metabolismo , Cirrosis Hepática/patología , Masculino , Ratones
16.
Diabetes ; 69(6): 1164-1177, 2020 06.
Artículo en Inglés | MEDLINE | ID: mdl-32184272

RESUMEN

Branched chain amino acids (BCAAs) are associated with the progression of obesity-related metabolic disorders, including type 2 diabetes and nonalcoholic fatty liver disease. However, whether BCAAs disrupt the homeostasis of hepatic glucose and lipid metabolism remains unknown. In this study, we observed that BCAAs supplementation significantly reduced high-fat (HF) diet-induced hepatic lipid accumulation while increasing the plasma lipid levels and promoting muscular and renal lipid accumulation. Further studies demonstrated that BCAAs supplementation significantly increased hepatic gluconeogenesis and suppressed hepatic lipogenesis in HF diet-induced obese (DIO) mice. These phenotypes resulted from severe attenuation of Akt2 signaling via mTORC1- and mTORC2-dependent pathways. BCAAs/branched-chain α-keto acids (BCKAs) chronically suppressed Akt2 activation through mTORC1 and mTORC2 signaling and promoted Akt2 ubiquitin-proteasome-dependent degradation through the mTORC2 pathway. Moreover, the E3 ligase Mul1 played an essential role in BCAAs/BCKAs-mTORC2-induced Akt2 ubiquitin-dependent degradation. We also demonstrated that BCAAs inhibited hepatic lipogenesis by blocking Akt2/SREBP1/INSIG2a signaling and increased hepatic glycogenesis by regulating Akt2/Foxo1 signaling. Collectively, these data demonstrate that in DIO mice, BCAAs supplementation resulted in serious hepatic metabolic disorder and severe liver insulin resistance: insulin failed to not only suppress gluconeogenesis but also activate lipogenesis. Intervening BCAA metabolism is a potential therapeutic target for severe insulin-resistant disease.


Asunto(s)
Aminoácidos de Cadena Ramificada/farmacología , Dieta Alta en Grasa/efectos adversos , Trastornos del Metabolismo de los Lípidos/inducido químicamente , Hígado/efectos de los fármacos , Obesidad/complicaciones , Proteínas Proto-Oncogénicas c-akt/metabolismo , Aminoácidos de Cadena Ramificada/administración & dosificación , Animales , Células Cultivadas , Grasas de la Dieta/administración & dosificación , Grasas de la Dieta/efectos adversos , Proteína Forkhead Box O1/genética , Proteína Forkhead Box O1/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Hepatocitos/metabolismo , Humanos , Riñón/metabolismo , Metabolismo de los Lípidos/efectos de los fármacos , Hígado/metabolismo , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Ratones , Proteínas Mitocondriales/genética , Proteínas Mitocondriales/metabolismo , Músculo Esquelético/metabolismo , Proteínas Proto-Oncogénicas c-akt/genética , Distribución Aleatoria , Ubiquitina-Proteína Ligasas/genética , Ubiquitina-Proteína Ligasas/metabolismo , Ubiquitinación
17.
Int J Mol Med ; 45(4): 1237-1249, 2020 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-32124969

RESUMEN

The present study aimed to investigate the relationship between the protective effects of exendin­4 (EX­4) on lipotoxicity­induced oxidative stress and meta­inflammation in ß­cells and the toll­like receptor 4 (TLR4)/NF­κB signaling pathway. Lipotoxicity, hydrogen peroxide (H2O2)­induced oxidative stress in ß cells, obese Sprague Dawley rats and TLR4 truncation rats were utilized in the present study. The expression levels were detected by western blotting; cell apoptosis was detected by TUNEL assay; and the intracellular reactive oxygen species (ROS) levels were analyzed using a ROS assay kit. The findings of the present study showed that EX­4 inhibited the expression of TLR4, NF­κB p65 subunit and p47phox in a concentration­dependent manner, and decreased the intracellular level of ROS. Additionally, silencing of TLR4 expression enhanced the protective effects of EX­4, while overexpression of TLR4 attenuated these protective influences. Simultaneously, it was demonstrated that TLR4 was involved in the process of EX­4 intervention to inhibit H2O2­induced oxidative stress in islet ß­cells. Moreover, it was found that EX­4 also inhibited TLR4­ or NF­κB agonist­induced oxidative stress. These results were also confirmed in an animal model of obese rats, in which EX­4 was able to improve the function of ß­cells, attenuate oxidative stress, and inhibit the expression levels of TLR4 and NF­κB p65 subunit in the pancreas of the diet­induced obese rats. Furthermore, truncation of the TLR4 gene in SD rats delayed the aforementioned damage. In summary, EX­4 may inhibit lipotoxicity­induced oxidative stress in ß­cells by inhibiting the activation of the TLR4/NF­κB signaling pathway.


Asunto(s)
Exenatida/farmacología , Células Secretoras de Insulina/metabolismo , Obesidad/metabolismo , Estrés Oxidativo/efectos de los fármacos , Transducción de Señal/efectos de los fármacos , Receptor Toll-Like 4/metabolismo , Factor de Transcripción ReIA/metabolismo , Animales , Línea Celular , Grasas de la Dieta/efectos adversos , Grasas de la Dieta/farmacología , Células Secretoras de Insulina/patología , Masculino , Ratones , Obesidad/inducido químicamente , Obesidad/tratamiento farmacológico , Obesidad/patología , Ratas , Ratas Sprague-Dawley , Especies Reactivas de Oxígeno/metabolismo
18.
PLoS One ; 15(2): e0228860, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32032383

RESUMEN

Several diseases are associated with excess of adipose tissue, and obesity is considered an independent risk factor for the development of cardiac remodeling and heart failure. Dietary aspects have been studied to elucidate the mechanisms involved in these processes. Thus, the purpose was the development and characterization of an obesity experimental model from hypercaloric diets, which resulted in cardiac remodeling and predisposition to heart failure. Thirty- day-old male Wistar rats (n = 52) were randomized into four groups: control (C), high sucrose (HS), high-fat (HF) and high-fat and sucrose (HFHS) for 20 weeks. General characteristics, comorbidities, weights of the heart, left (LV) and right ventricles, atrium, and relationships with the tibia length were evaluated. The LV myocyte cross sectional area and fraction of interstitial collagen were assayed. Cardiac function was determined by hemodynamic analysis and the contractility by cardiomyocyte contractile function. Heart failure was analyzed by pulmonary congestion, right ventricular hypertrophy, and hemodynamic parameters. HF and HFHS models led to obesity by increase in adiposity index (C = 8.3 ± 0.2% vs. HF = 10.9 ± 0.5%, HFHS = 10.2 ± 0.3%). There was no change in the morphological parameters and heart failure signals. HF and HFHS caused a reduction in times to 50% relaxation without cardiomyocyte contractile damage. The HS model presented cardiomyocyte contractile dysfunction visualized by lower shortening (C: 8.34 ± 0.32% vs. HS: 6.91 ± 0.28), as well as the Ca2+ transient amplitude was also increased when compared to HFHS. In conclusion, the experimental diets based on high amounts of sugar, lard or a combination of both did not promote cardiac remodeling with predisposition to heart failure under conditions of obesity or excess sucrose. Nevertheless, excess sucrose causes cardiomyocyte contractility dysfunction associated with alterations in the myocyte sensitivity to intracellular Ca2+.


Asunto(s)
Dieta de Carga de Carbohidratos/efectos adversos , Sacarosa en la Dieta/administración & dosificación , Sacarosa en la Dieta/efectos adversos , Insuficiencia Cardíaca/etiología , Animales , Señalización del Calcio , Colágeno/metabolismo , Dieta Alta en Grasa/efectos adversos , Grasas de la Dieta/administración & dosificación , Grasas de la Dieta/efectos adversos , Modelos Animales de Enfermedad , Ingestión de Energía , Insuficiencia Cardíaca/patología , Insuficiencia Cardíaca/fisiopatología , Masculino , Modelos Cardiovasculares , Contracción Miocárdica , Miocardio/metabolismo , Miocardio/patología , Miocitos Cardíacos/fisiología , Obesidad/complicaciones , Obesidad/patología , Obesidad/fisiopatología , Ratas , Ratas Wistar , Remodelación Ventricular/fisiología
19.
Sci Rep ; 10(1): 3407, 2020 02 25.
Artículo en Inglés | MEDLINE | ID: mdl-32099024

RESUMEN

Sodium is an essential component of the human body, with known influences on obesity. This paper reports the effect of cube natural sea salt (CNS) on the reduction of obesity in high fat diet-induced obese C57BL/6 mice and 3T3-L1 adipocytes, by ameliorating the obesity parameters and obesity-related gene mechanisms. The suppression of high fat diet-induced obesity and differentiated 3T3-L1 adipocytes by sea salt depends on the manufacturing process and mineral content. The manufacturing method using only new sea water (Cube natural sea salt) decreases the magnesium (Mg) and sulfur (S) content in the salt with different crystallization and morphologies, compared to the general manufacturing method (Generally manufactured sea salt, GS). Mg in salt is known to considerably affect obesity; an appropriate concentration of magnesium chloride (MgCl2) reduces lipid accumulation significantly and regulates the lipogenesis and liver enzyme activity. Our results indicate that sea salt contains an appropriate level of Mg as compared to table salt (purified salt, NaCl), and is important for regulating obesity, as observed in the in vivo and in vitro anti-obesity effects of CNS. The Mg content and mineral ratio of sea salt are important factors that ameliorate the lipid metabolism and liver enzyme activity in high fat diet induced obesity, and contents of Mg in sea salt can be altered by modifying the manufacturing process.


Asunto(s)
Grasas de la Dieta/efectos adversos , Magnesio/farmacología , Obesidad , Cloruro de Sodio Dietético/farmacología , Células 3T3-L1 , Animales , Grasas de la Dieta/farmacología , Masculino , Ratones , Obesidad/inducido químicamente , Obesidad/tratamiento farmacológico , Obesidad/metabolismo , Obesidad/patología
20.
Sci Rep ; 10(1): 3417, 2020 02 25.
Artículo en Inglés | MEDLINE | ID: mdl-32099031

RESUMEN

Insulin resistance increases patients' risk of developing type 2 diabetes (T2D), non-alcoholic steatohepatitis (NASH) and a host of other comorbidities including cardiovascular disease and cancer. At the molecular level, insulin exerts its function through the insulin receptor (IR), a transmembrane receptor tyrosine kinase. Data from human genetic studies have shown that Grb14 functions as a negative modulator of IR activity, and the germline Grb14-knockout (KO) mice have improved insulin signaling in liver and skeletal muscle. Here, we show that Grb14 knockdown in liver, white adipose tissues, and heart with an AAV-shRNA (Grb14-shRNA) improves glucose homeostasis in diet-induced obese (DIO) mice. A previous report has shown that germline deletion of Grb14 in mice results in cardiac hypertrophy and impaired systolic function, which could severely limit the therapeutic potential of targeting Grb14. In this report, we demonstrate that there are no significant changes in cardiac function as measured by echocardiography in the Grb14-knockdown mice fed a high-fat diet for a period of four months. While additional studies are needed to further confirm the efficacy and to de-risk potential negative cardiac effects in preclinical models, our data support the therapeutic strategy of inhibiting Grb14 to treat diabetes and related conditions.


Asunto(s)
Proteínas Adaptadoras Transductoras de Señales/metabolismo , Glucosa/metabolismo , Homeostasis , Insulina/metabolismo , Transducción de Señal , Proteínas Adaptadoras Transductoras de Señales/genética , Animales , Cardiomegalia/genética , Cardiomegalia/metabolismo , Grasas de la Dieta/efectos adversos , Grasas de la Dieta/farmacología , Técnicas de Silenciamiento del Gen , Insulina/genética , Ratones , Ratones Noqueados , Obesidad/inducido químicamente , Obesidad/genética , Obesidad/metabolismo
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