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1.
PLoS One ; 15(2): e0228860, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32032383

RESUMO

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+.


Assuntos
Dieta da Carga de Carboidratos/efeitos adversos , Sacarose na Dieta/administração & dosagem , Sacarose na Dieta/efeitos adversos , Insuficiência Cardíaca/etiologia , Animais , Sinalização do Cálcio , Colágeno/metabolismo , Dieta Hiperlipídica/efeitos adversos , Gorduras na Dieta/administração & dosagem , Gorduras na Dieta/efeitos adversos , Modelos Animais de Doenças , Ingestão de Energia , Insuficiência Cardíaca/patologia , Insuficiência Cardíaca/fisiopatologia , Masculino , Modelos Cardiovasculares , Contração Miocárdica , Miocárdio/metabolismo , Miocárdio/patologia , Miócitos Cardíacos/fisiologia , Obesidade/complicações , Obesidade/patologia , Obesidade/fisiopatologia , Ratos , Ratos Wistar , Remodelação Ventricular/fisiologia
2.
Invest Ophthalmol Vis Sci ; 61(2): 20, 2020 02 07.
Artigo em Inglês | MEDLINE | ID: mdl-32058563

RESUMO

Purpose: To evaluate the association between dietary fat intake and the presence of AMD. Methods: Cross-sectional, observational study with cohorts prospectively recruited from the United States and Portugal. AMD was diagnosed based on color fundus photographs with the AREDS classification. A validated food frequency questionnaire was used to calculate the percent energy intake of trans fat, saturated fat, monounsaturated fatty acid (MUFA), and polyunsaturated fatty acid (PUFA). Odds ratio (OR) and 95% confidence intervals for quintile of amount of FA were calculated. Multiple logistic regression was used to estimate the OR. Results: We included 483 participants, 386 patients with AMD and 97 controls. Higher intake of trans fat was associated with a 2.3-fold higher odds of presence of AMD (P for trend = 0.0156), whereas a higher intake of PUFA (OR, 0.25; P for trend = 0.006) and MUFA (OR, 0.24; P for trend < 0.0001) presented an inverse association. Subgroup analysis showed that higher quintile of trans fat was associated with increased odds of having intermediate AMD (OR, 2.26; P for trend = 0.02); and higher quintile of PUFA and MUFA were inversely associated with intermediate AMD (OR, 0.2 [P for trend = 0.0013]; OR, 0.17 [P for trend < 0.0001]) and advanced AMD (OR, 0.13 [P for trend = 0.02]; OR, 0.26 [P for trend = 0.004]). Additionally, a statistically significant effect modification by country was noted with inverse association between MUFA and AMD being significant (OR, 0.04; P for trend < 0.0001) for the Portugal population only. Conclusions: Our study shows that higher dietary intake of trans fat is associated with the presence of AMD, and a higher intake of PUFA and MUFA is inversely associated with AMD.


Assuntos
Ácidos Graxos Monoinsaturados/efeitos adversos , Ácidos Graxos Insaturados/efeitos adversos , Degeneração Macular/etiologia , Idoso , Estudos Transversais , Dieta/efeitos adversos , Gorduras na Dieta/administração & dosagem , Gorduras na Dieta/efeitos adversos , Gorduras Insaturadas na Dieta/administração & dosagem , Gorduras Insaturadas na Dieta/efeitos adversos , Ingestão de Energia , Ácidos Graxos Monoinsaturados/administração & dosagem , Ácidos Graxos Insaturados/administração & dosagem , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Portugal , Estudos Prospectivos , Estados Unidos
3.
Oxid Med Cell Longev ; 2020: 8172714, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31998444

RESUMO

High-fat diet (HFD) often increases oxidative stress and enhances inflammatory status in the body. Toll-like receptor 4 (TLR4) is widely expressed in the pancreatic tissues and plays an important role in pancreatitis. This study is aimed at investigating the effect of HFD on acute pancreatitis (AP) and the role of TLR4-mediated necroptosis and inflammation in this disease. Weight-matched rats were allocated for an 8-week feeding on the standard chow diet (SCD) or HFD, and then, the AP model was induced by infusion of 5% sodium taurocholate into the biliopancreatic duct. Rats were sacrificed at an indicated time point after modeling. Additionally, inhibition of TLR4 signaling by TAK-242 in HFD rats with AP was conducted in vivo. The results showed that the levels of serum free fatty acid (FFA) in HFD rats were higher than those in SCD rats. Moreover, HFD rats were more vulnerable to AP injury than SCD rats, as indicated by more serious pathological damage and much higher pancreatic malondialdehyde (MDA) and lipid peroxidation (LPO) levels as well as lower pancreatic superoxide dismutase (SOD) activities and reduced glutathione (GSH) contents and more intense infiltration of MPO-positive neutrophils and CD68-positive macrophages. In addition, HFD markedly increased the expressions of TLR4 and necroptosis marker (RIP3) and aggravated the activation of NF-κB p65 and the expression of TNF-α in the pancreas of AP rats at indicated time points. However, TLR4 inhibition significantly attenuated the structural and functional damage of the pancreas induced by AP in HFD rats, as indicated by improvement of the above indexes. Taken together, these findings suggest that HFD exacerbated the extent and severity of AP via oxidative stress, inflammatory response, and necroptosis. Inhibition of TLR4 signaling by TAK-242 alleviated oxidative stress and decreased inflammatory reaction and necroptosis, exerting a protective effect during AP in HFD rats.


Assuntos
Gorduras na Dieta/efeitos adversos , Necroptose/efeitos dos fármacos , Pancreatite/metabolismo , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismo , Animais , Gorduras na Dieta/farmacologia , Inflamação/metabolismo , Inflamação/patologia , Masculino , Pancreatite/patologia , Ratos , Ratos Sprague-Dawley , Sulfonamidas/farmacologia , Receptor 4 Toll-Like/antagonistas & inibidores
4.
Artigo em Inglês | MEDLINE | ID: mdl-31461687

RESUMO

The present study was performed to determine the effect of high fat diet in lipid accumulation, oxidative stress and autophagy, and to explore the underlying molecular mechanism of high fat diet induced hepatic oxidative damage in Chinese softshell turtle. To this end, the control group were fed a normal fat diet (NFD, 6.38% lipid) and the experimental group were bred high fat diet (HFD, 13.89% lipid) for eight weeks. Lipid accumulation, oxidative stress and autophagy, as well as the mRNA expression of genes related to the antioxidant system were determined in the liver. Results showed that high fat diet not only exacerbated lipid accumulation in the liver and serum through increasing contents of triglyceride, total cholesterol and low-density lipoprotein and decreasing content of high-density lipoprotein, but also induced liver injury through increasing activities of alanine aminotransferase and aspartate aminotransferase in the serum. In addition, the experimental subject induced oxidative injury for the increase of reactive oxygen species, malondialdehyde and protein carbonyl contents and the reduction of glutathione contents, anti-superoxide anion capacity and catalase, total superoxide dismutase, glutathione peroxidase, glutathione-S transferase activities. Meanwhile, antioxidant-related signaling molecule expression were also decreased, which might attribute to regulate antioxidant-related signaling molecule. On top of that, it indicated promote the occurrence of liver autophagy via up-regulating expressions of AMP activated protein kinase, UNC-51-like kinase 1, Microtubule-associated proteins 1A/1B light chain 3 and down-regulating gene expression of mammalian target of rapamycin. In conclusion, high fat diet could enhance lipid accumulation in the liver and serum, lead to liver injury and oxidative damage, impair liver antioxidant capacity, regulate antioxidant-related signaling molecule expression and activate hepatic autophagy.


Assuntos
Morte Celular Autofágica/efeitos dos fármacos , Gorduras na Dieta/efeitos adversos , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Tartarugas/metabolismo , Animais , Gorduras na Dieta/farmacologia , Fígado/patologia
5.
Mol Cell Biochem ; 465(1-2): 125-139, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31838625

RESUMO

Our previous studies have confirmed that proline/serine-rich coiled-coil 1 (PSRC1) overexpression can regulate blood lipid levels and inhibit atherosclerosis (AS) development. In the current study, the gene and transcript expression profiles in the livers of ApoE-/- mice overexpressing PSRC1 were investigated. HiSeq X Ten RNA sequencing (RNA-seq) analysis was used to examine the differentially expressed genes (DEGs) and differentially expressed transcripts in the livers of PSRC1-overexpressing ApoE-/- and control mice. Then, Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on these DEGs and on long noncoding RNA (lncRNA) predicted target genes. A total of 1892 significant DEGs were identified: 1431 were upregulated (e.g., Cyp2a4, Obp2a, and Sertad4), and 461 were downregulated (e.g., Moxd1, Egr1, and Elovl3). In addition, 8184 significant differentially expressed transcripts were identified, 4908 of which were upregulated and 3276 of which were downregulated. Furthermore, 1106 significant differentially expressed lncRNAs were detected, 713 of which were upregulated and 393 of which were downregulated. Quantitative reverse transcription PCR (qRT-PCR) verified changes in 10 randomly selected DEGs. GO analyses showed that the DEGs and predicted lncRNA target genes were mostly enriched for actin binding and lipid metabolism. KEGG biological pathway analyses showed that the DEGs in the livers of PSRC1-overexpressing ApoE-/- mice were enriched in the mitogen-activated protein kinase (MAPK) pathway. These findings reveal that PSRC1 may affect liver actin polymerization and cholesterol metabolism-related genes or pathways. These mRNAs and lncRNAs may represent new biomarkers and targets for the diagnosis and therapy of lipid metabolism disturbance and AS.


Assuntos
Aterosclerose , Gorduras na Dieta/efeitos adversos , Regulação da Expressão Gênica/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Fosfoproteínas/biossíntese , Animais , Aterosclerose/induzido quimicamente , Aterosclerose/genética , Aterosclerose/metabolismo , Aterosclerose/patologia , Gorduras na Dieta/farmacologia , Perfilação da Expressão Gênica , Camundongos , Camundongos Knockout para ApoE , Fosfoproteínas/genética
6.
Curr Pharm Biotechnol ; 21(2): 158-168, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31612827

RESUMO

BACKGROUND: Lopinavir/Ritonavir (LR) is a protease inhibitor used human immunodeficiency virus infection management. There have been issues regarding the effects of fat on LR efficacy and the possibility of neurological deficits following prolonged use, there is however a dearth of research examining this. AIMS: The effects of LR administered with normal or High-Fat Diet (HFD) on neurobehaviour, neurochemistry and oxidative stress in healthy mice were examined. METHODS: Mice were randomly-assigned into eight groups of ten (n=10) animals each. The groups were normal control [Standard Diet, (SD)], HFD control, 3 groups of LR incorporated into SD (100/25, 200/50 and 400/100 mg/kg of feed), and 3 groups of LR with HFD (100/25, 200/50 and 400/100 mg/kg of feed). Mice were fed daily for six weeks, following which open field, elevated-plus maze (EPM), radial-arm maze and Y-maze behaviours were scored. Twenty-four hours after tests, mice were euthanised and brains were homogenised for estimation of oxidative stress, L-glutamate level and acetylcholinesterase activity. RESULTS: LR was associated with a reduction in HFD-induced weight gain, suppression of open-field behaviours with SD, and counteraction of HFD-induced changes in working-memory, open-field and anxiety-related behaviours. Also, LR causes increased lipid peroxidation and superoxide dismutase activity; and a decrease in brain glutamate, irrespective of dietary composition. Increased fat catabolism leading to increased oxidative stress could possibly account for the weight changes, while a decrease in brain glutamate could account for the changes in open-field behaviours in mice fed SD. CONCLUSION: LR alters neurobehaviour, oxidative stress and brain glutamate in mice; however, only its effects on neurobehaviour are affected by diet.


Assuntos
Comportamento Animal/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Gorduras na Dieta/efeitos adversos , Inibidores da Protease de HIV/toxicidade , Lopinavir/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Ritonavir/toxicidade , Animais , Encéfalo/metabolismo , Dieta Hiperlipídica , Gorduras na Dieta/administração & dosagem , Ácido Glutâmico/metabolismo , Humanos , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos
7.
Curr Gastroenterol Rep ; 21(11): 62, 2019 Dec 02.
Artigo em Inglês | MEDLINE | ID: mdl-31792624

RESUMO

PURPOSE OF REVIEW: To review recent data on the role and interactions of fiber and fat as dietary risk factors associated with colorectal cancer (CRC) risk in humans. RECENT FINDINGS: Fiber intake shows convincing and linear dose-response negative correlation with CRC risk. Dietary fiber stimulates butyrogenic activity of the gut microbiota, providing high amounts of butyrate that shows extensive anti-neoplastic effects. A high-fat diet promotes CRC risk through stimulated bile acid metabolism, facilitating bile acid conversion by the gut microbiota to tumor-promoting deoxycholic acid. Comprehensive interactions of these microbial metabolites are likely to underlie mechanisms driving diet-dependent CRC risk in different populations, but require further experimental investigation. Dietary fiber and fat shape the composition and metabolic function of the gut microbiota, resulting in altered amounts of butyrate and deoxycholic acid in the colon. Fiber supplementation and restriction of fat intake represent promising strategies to reduce CRC risk in healthy individuals.


Assuntos
Neoplasias Colorretais/etiologia , Dieta Hiperlipídica/efeitos adversos , Gorduras na Dieta/administração & dosagem , Fibras na Dieta/administração & dosagem , Ácidos e Sais Biliares/metabolismo , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/microbiologia , Neoplasias Colorretais/prevenção & controle , Gorduras na Dieta/efeitos adversos , Gorduras na Dieta/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Microbioma Gastrointestinal/fisiologia , Humanos , Fatores de Risco
8.
Cell Mol Biol (Noisy-le-grand) ; 65(7): 5-9, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31880534

RESUMO

The association between dietary fat intake and bladder cancer had been inconsistent in the previous epidemiological studies. The aim of this study was to investigate the difference between fat intake and bladder cancer risk. Databases of PubMed, Embase, and Web of Science were systematically searched for suitable studies from inception to June 2018. A meta-analysis was performed to analyze the efficacy of dietary fat intake on bladder cancer risk. A Forest plot was prepared to indicate the relationship. Ten citations were used in this study. The Funnel plot suggested highest category of dietary fat intake could increase the risk of bladder cancer (summarized relative risk (RR)= 1.279, 95% confidence interval (CI)= 1.036-1.577, I2= 53.2%, P for heterogeneity = 0.019). A positive association was found among European populations (summarized RR= 1.359, 95%CI= 1.027-1.798), but not in North American populations. The association was not significant in the subgroup analysis by fat type on bladder cancer risk. Egger test (P= 0.239) and Funnel plot showed there was no significant publication bias in the included publications. In conclusions, compared with the lowest category of dietary fat intake, the highest category could significantly increase the bladder cancer risk, especially among European populations. As some limitations existed in our analysis, large scale studies with detailed amount of dietary fat intake are needed to verify our results.


Assuntos
Gorduras na Dieta/efeitos adversos , Neoplasias da Bexiga Urinária/epidemiologia , Idoso , Humanos , Pessoa de Meia-Idade , Fatores de Risco
9.
Int J Mol Sci ; 20(23)2019 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-31771102

RESUMO

Prolonged caloric intake above energy needs disturbs the body's ability to store and manage the excess of energy intake, leading to the onset of chronic degenerative diseases. This study aimed to compare the effect of three foods, which contain demonstrated bioactive compounds in the treatment of obesity and as an adjuvant in obesity energy restriction treatments. In a mice obesity model induced through a high-fat diet; fish oil, soluble fibre, and soy were incorporated to evaluate its capacity to modulate metabolic factors in adipose tissue during a continued fat intake or weight reduction through a normocaloric diet. As a result, fish oil improved mitochondrial related, adipose tissue hormone expression, and oxidation products when high-fat diets are consumed; while soluble fibre improved glucose and inflammation pathways during high-fat diet intake. In weight reduction treatments few differential features, as a treatment adjuvant, were observed for fish oil and soy; while soluble fibre was able to improve the weight reduction effects induced by a normocaloric diet. As a conclusion, soluble fibre supplementation compared to an energy reduction program, was the only treatment able to induce a significant additional effect in the improvement of weight loss and adipose tissue metabolism.


Assuntos
Tecido Adiposo , Dieta Redutora , Mitocôndrias , Obesidade , Perda de Peso , Tecido Adiposo/metabolismo , Tecido Adiposo/patologia , Animais , Gorduras na Dieta/efeitos adversos , Gorduras na Dieta/farmacologia , Modelos Animais de Doenças , Ingestão de Energia/efeitos dos fármacos , Óleos de Peixe/farmacologia , Masculino , Camundongos , Mitocôndrias/metabolismo , Mitocôndrias/patologia , Obesidade/induzido quimicamente , Obesidade/dietoterapia , Obesidade/metabolismo , Obesidade/patologia , Soja
10.
Biomed Res Int ; 2019: 7157865, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31781638

RESUMO

Background: Vascular remodeling is the most critical pathogenesis of atherosclerosis. Adipokine chemerin was known for its relationship with obesity as well as metabolism. Most recently, chemerin was found to play a crucial role in the pathologic process of cardiovascular diseases including coronary heart disease. In this study, we surveyed the role of chemerin in progression of atherosclerosis in ApoE-/- mice. Objective: To investigate the relationship between chemerin and progression of atherosclerosis in ApoE-/- mice and its mechanism. Methods: 8-week-old ApoE-/- mice were fed with high-fat diet to induce the atherosclerosis model. Adenoviruses were transfected for knockdown or overexpression of chemerin gene into aorta. Serums and aortic tissues of ApoE-/- mice were obtained after feeding high-fat diet for 16 weeks. HE staining and oil red staining were performed to evaluate aortic plaque. ELISA was performed to explore serum levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and transforming growth factor-ß1 (TGF-ß1). Real-time PCR and western blotting were carried out to investigate the mRNA and protein levels of chemerin, nuclear factor-κB p65 (NF-κBp65), proliferating cell nuclear antigen (PCNA), phosphorylated p38 mitogen-activated protein kinase (p-p38-MAPK), phosphorylated c-Jun N-terminal kinase (p-JNK), and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK 1/2). Result: Aortic plaque formation was significantly induced by high-fat diet in ApoE-/- mice. Simultaneously, elevated serum levels of TNF-α and IL-1ß and elevated mRNA and protein levels of chemerin, NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 were found in ApoE-/- mice. After aortic chemerin gene was inhibited by adenovirus, aortic atherosclerosis induced by high-fat diet was significantly meliorated, serum levels of TNF-α and IL-1ß decreased, mRNA and protein levels of NF-κBp65, PCNA, p-p38-MAPK, p-JNK, and p-ERK 1/2 decreased simultaneously. Conclusion: Our study revealed that chemerin stimulated the progression of atherosclerosis in ApoE-/- mice.


Assuntos
Adipocinas/metabolismo , Aorta/metabolismo , Aterosclerose/metabolismo , Quimiocinas/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Sistema de Sinalização das MAP Quinases , Placa Aterosclerótica/metabolismo , Adipocinas/genética , Animais , Aorta/patologia , Aterosclerose/induzido quimicamente , Aterosclerose/genética , Aterosclerose/patologia , Quimiocinas/genética , Gorduras na Dieta/efeitos adversos , Gorduras na Dieta/farmacologia , Peptídeos e Proteínas de Sinalização Intercelular/genética , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Camundongos , Camundongos Knockout para ApoE , Placa Aterosclerótica/induzido quimicamente , Placa Aterosclerótica/genética , Placa Aterosclerótica/patologia , Fator de Crescimento Transformador beta1/genética , Fator de Crescimento Transformador beta1/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Remodelação Vascular
11.
Vopr Pitan ; 88(4): 18-24, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31722137

RESUMO

Among various food proteins, soybean proteins have the greatest traditions of application for the dietary correction and prevention of lipid metabolism disorders and related complications. Aim. In an in vivo experiment using male Wistar rats, the lipid-lowering properties of soy protein and its enzymatic hydrolysate were tested to evaluate their possible use as ingredients of specialized foods. Material and methods. Animals were randomly divided into 3 groups: control group G1 and 2 experimental groups G2 and G3. The total duration of the experiment was 70 days. The animals of the control group G1 were fed with high-lipid semi-synthetic diet. Animals of the experimental groups G2 and G3 received the same high-fat semi-synthetic diet, but with a 50% replacement of casein with soy protein isolate (SPI) and enzymatic hydrolyzate of SPI (EHSPI), respectively. The blood glucose was measured once per 2 weeks. At the end of the experiment on the 71st day the level of glycated hemoglobin was determined in the blood; the levels of triglycerides, cholesterol, high density lipoproteins (HDL), low density lipoproteins (LDL) and the concentration of malon dialdehyde were determined in the serum. Results and discussion. Starting from the 6th week of the experiment and prior to its completion, the average food intake of animals from the G3 group was significantly (р<0.05) lower compared to animals of the G1 control group. The food intake of animals of group G2 was significantly (р<0.05) reduced compared with this indicator for animals of group G1, starting from the week 8 of the experiment and prior to its completion. The monitoring of the body weight gain did not reveal significant differences between all groups of animals, despite differences in the food intake. Replacing casein in the diet by 50% with SPI had a pronounced antioxidant and cholesterol-lowering effect. The total cholesterol content (1.65±0.05 mmol/l) decreased significantly (р<0.05) due to a decrease in LDL (0.90±0.03 mmol/l), and malon dialdehyde level lowered (3.7±0.5 µmol/l, р<0.05) in the serum of group G2 rats compared with animals of the control group G1 (2.01±0.13 and 1.12±0.09 mmol/l; 5.1±0.4 µmol/l, respectively). Replacing casein by 50% with EHSPI in the diet of G3 rats was unfavorable, significantly (р<0.05) increasing the level of total cholesterol (2.76±0.16 mmol/l) and cholesterol in LDL (1.66±0.12 mmol/l) in blood of these animals compared with animals of both comparison groups G1 and G2. Conclusion. A preclinical comparative study of the cholesterol-lowering and antioxidant properties of the SPI substantiates the prospect of its following clinical trials with the aim of including into the composition of specialized foods for prevention and diet therapy of the disorders of endogenous cholesterol homeostasis.


Assuntos
Gorduras na Dieta/efeitos adversos , Síndrome Metabólica , Obesidade , Hidrolisados de Proteína/farmacologia , Proteínas de Soja/farmacologia , Animais , Gorduras na Dieta/farmacologia , Masculino , Síndrome Metabólica/induzido quimicamente , Síndrome Metabólica/dietoterapia , Síndrome Metabólica/metabolismo , Síndrome Metabólica/patologia , Obesidade/induzido quimicamente , Obesidade/dietoterapia , Obesidade/metabolismo , Obesidade/patologia , Ratos , Ratos Wistar
12.
Nutrients ; 11(11)2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31731681

RESUMO

Obesity has become a major public health concern worldwide due to its high social and economic burden, caused by its related comorbidities, impacting physical and mental health. Dietary fat is an important source of energy along with its rewarding and reinforcing properties. The nutritional recommendations for dietary fat vary from one country to another; however, the dietary reference intake (DRI) recommends not consuming more than 35% of total calories as fat. Food rich in fat is hyperpalatable, and is liable to be consumed in excess amounts. Food addiction as a concept has gained traction in recent years, as some aspects of addiction have been demonstrated for certain varieties of food. Fat addiction can be a diagnosable condition, which has similarities with the construct of addictive disorders, and is distinct from eating disorders or normal eating behaviors. Psychological vulnerabilities like attentional biases have been identified in individuals described to be having such addiction. Animal models have provided an opportunity to explore this concept in an experimental setting. This discussion sheds light on fat addiction, and explores its physiological and psychological implications. The discussion attempts to collate the emerging literature on addiction to fat rich diets as a prominent subset of food addiction. It aims at addressing the clinical relevance at the community level, the psychological correlates of such fat addiction, and the current physiological research directions.


Assuntos
Dieta/psicologia , Gorduras na Dieta/efeitos adversos , Comportamento Alimentar/psicologia , Dependência de Alimentos/psicologia , Obesidade/psicologia , Dieta/efeitos adversos , Dependência de Alimentos/etiologia , Humanos , Obesidade/etiologia , Recomendações Nutricionais
13.
Nutrients ; 11(11)2019 Nov 12.
Artigo em Inglês | MEDLINE | ID: mdl-31726791

RESUMO

In the 1940s, the diet-heart hypothesis proposed that high dietary saturated fat and cholesterol intake promoted coronary heart disease in "at-risk" individuals. This hypothesis prompted federal recommendations for a low-fat diet for "high risk" patients and as a preventive health measure for everyone except infants. The low carbohydrate diet, first used to treat type 1 diabetes, became a popular obesity therapy with the Atkins diet in the 1970s. Its predicted effectiveness was based largely on the hypothesis that insulin is the causa prima of weight gain and regain via hyperphagia and hypometabolism during and after weight reduction, and therefore reduced carbohydrate intake would promote and sustain weight loss. Based on literature reviews, there are insufficient randomized controlled inpatient studies examining the physiological significance of the mechanisms proposed to support one over the other. Outpatient studies can be confounded by poor diet compliance such that the quality and quantity of the energy intake cannot be ascertained. Many studies also fail to separate macronutrient quantity from quality. Overall, there is no conclusive evidence that the degree of weight loss or the duration of reduced weight maintenance are significantly affected by dietary macronutrient quantity beyond effects attributable to caloric intake. Further work is needed.


Assuntos
Dieta com Restrição de Carboidratos , Dieta com Restrição de Gorduras , Dieta Saudável , Carboidratos da Dieta/administração & dosagem , Gorduras na Dieta/administração & dosagem , Ingestão de Energia , Valor Nutritivo , Obesidade/dietoterapia , Dieta com Restrição de Carboidratos/efeitos adversos , Dieta com Restrição de Gorduras/efeitos adversos , Dieta Saudável/efeitos adversos , Carboidratos da Dieta/efeitos adversos , Carboidratos da Dieta/metabolismo , Gorduras na Dieta/efeitos adversos , Gorduras na Dieta/metabolismo , Medicina Baseada em Evidências , Humanos , Obesidade/epidemiologia , Obesidade/fisiopatologia , Fatores de Risco , Perda de Peso
14.
Prog Cardiovasc Dis ; 62(5): 436-443, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31707063

RESUMO

In recent years, health professionals and laypersons have disseminated misinformation regarding the consumption of coconut oil. Those encouraging the supplementation of coconut oil argue that it provides health benefits and protective cardiovascular effects. Our article examines the effects of coconut oil intake on the cardiometabolic profile by exploring various lipid indices, as well as potential non-lipid effects, such as weight loss. The majority of randomized controlled trials show that coconut oil intake or its supplementation increases low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDLC), and total cholesterol when compared with other vegetable oils. Lauric acid, a medium-chain fatty acid and the main constituent of coconut oil, increases LDL-C and HDL-C concentrations, since it plays a main role as a substrate for apolipoprotein (apo)A1 and apoB synthesis, which are the key molecules in HDL-C and LDL-C particles, respectively.Despite some findings demonstrating an increase in HDL-C, definitive long-term clinical trials are imperative to ascertain whether this effect is clinically relevant. In addition, coconut oil intake has failed as a weight loss strategy and should not be considered as a supplementation strategy to increase satiety and/or thermogenesis.If one desires to include coconut oil in the diet, then we suggest that it should be limited and encompassed within the current recommendations of SFA intake, which are up to 10% of total caloric intake.


Assuntos
Óleo de Coco/administração & dosagem , Dieta Saudável , Gorduras na Dieta/administração & dosagem , Valor Nutritivo , Animais , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/prevenção & controle , Óleo de Coco/efeitos adversos , Gorduras na Dieta/efeitos adversos , Gorduras na Dieta/sangue , Ingestão de Energia , Humanos , Obesidade/dietoterapia , Obesidade/epidemiologia , Obesidade/fisiopatologia , Ensaios Clínicos Controlados Aleatórios como Assunto , Recomendações Nutricionais , Fatores de Risco , Perda de Peso
15.
Anticancer Res ; 39(11): 6197-6208, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31704848

RESUMO

AIM: This cross-sectional study aimed to evaluate the associations between low and high-fat dairy food (DF) intake and breast density (BD). MATERIALS AND METHODS: A total of 775 premenopausal and 771 postmenopausal women recruited during screening mammography completed a food frequency questionnaire. Adjusted linear regression models were used to assess the associations. RESULTS: As frequency quartiles of high-fat DF consumption increased, the adjusted mean of absolute BD increased from 31.5 to 36.1 cm2 for all women (ptrend=0.0034) and from 42.4 to 50.1 cm2 for premenopausal women (ptrend=0.0047). Conversely, as frequency quartiles of low-fat DF consumption increased, the adjusted mean of absolute BD decreased from 34.7 to 29.6 cm2 for all women (ptrend=0.001) and from 49.7 to 40.7 cm2 for premenopausal women (ptrend=0.0012). CONCLUSION: A higher intake of high-fat and low-fat DF is respectively associated with higher and lower BD, particularly in premenopausal women.


Assuntos
Densidade da Mama , Neoplasias da Mama/etiologia , Laticínios/efeitos adversos , Gorduras na Dieta/efeitos adversos , Neoplasias da Mama/patologia , Estudos Transversais , Feminino , Humanos , Prognóstico , Fatores de Risco , Inquéritos e Questionários
16.
Lipids Health Dis ; 18(1): 182, 2019 Oct 23.
Artigo em Inglês | MEDLINE | ID: mdl-31647036

RESUMO

BACKGROUND: This study investigated the effects of ingesting meals with the same calorie intake but distinct nutritional contents after exercise on postprandial lipemia the next day. METHODS: Eight healthy male participants completed two 2-day trials in a random order. On day 1, the participants underwent five 12 min bouts of cycling exercise with a bout of higher intensity exercise (4 min) after each and then a bout of lower intensity cycling (2 min). The total exercise time was 90 min. After the exercise, the participants ingested three high-fat or low-fat meals. On Day 2, the participants were asked to rest in the laboratory and ingest a high-fat meal. Their postprandial reaction after a high-fat meal was observed. RESULTS: Postprandial triglyceride concentrations in the high-fat diet trial and low-fat diet trial exhibited nonsignificant differences. Total TG AUC were no significantly different on HF trial and LF trial (HF: 6.63 ± 3.2; LF: 7.20 ± 3.4 mmol/L*4 h. p = 0.586). However, the postprandial fat oxidation rate total AUC (HF: 0.58 ± 0.1; LF: 0.39 ± 0.2 g/min*4 h. p = 0.045), plasma glucose, and insulin concentration of the high-fat trial were significantly higher than those of the low-fat trial. CONCLUSIONS: This study revealed that meals with distinct nutritional contents after a 90-min exercise increased the postprandial fat oxidation rate but did not influence the postprandial lipemia after a high-fat meal the next day.


Assuntos
Gorduras na Dieta/efeitos adversos , Músculos/metabolismo , Adulto , Glicemia/metabolismo , Índice de Massa Corporal , Metabolismo Energético/fisiologia , Exercício Físico/fisiologia , Ácidos Graxos não Esterificados/sangue , Humanos , Masculino , Oxirredução , Período Pós-Prandial/fisiologia , Inquéritos e Questionários , Triglicerídeos/sangue , Adulto Jovem
17.
Nutrients ; 11(10)2019 Oct 21.
Artigo em Inglês | MEDLINE | ID: mdl-31640155

RESUMO

Though the association between sleep duration and obesity has been generally acknowledged, there is little information about the mechanisms behind this association. The purpose of this study was to examine the effect of the fat intake and stress variables on the association between sleep duration and abdominal obesity. Data for 13,686 subjects aged ≥ 20 years from the 2013-2017 Korea National Health and Nutrition Examination Survey were used, and hierarchical and stratified logistic regression analyses were employed. In the hierarchical logistic regression analyses, fat intake and stress did not change the significance or the size of the sleep effects upon abdominal obesity. These results suggest that sleep duration does not affect abdominal obesity through fat intake or stress variables. In addition, fat intake and stress are not mediators of the sleep duration variable. However, subjects with different levels of fat intake and stress showed different associations between sleep duration and abdominal obesity. Subjects who were in the lowest or highest group of fat intake as well as self-reported stress level showed a weaker relationship between sleep duration and abdominal obesity, compared with the other groups. In conclusion, fat intake and stress modify the effects of sleep duration on abdominal obesity according to the stratified regression results.


Assuntos
Gorduras na Dieta/efeitos adversos , Obesidade Abdominal/epidemiologia , Sono/fisiologia , Estresse Psicológico/complicações , Adulto , Idoso , Consumo de Bebidas Alcoólicas , Gorduras na Dieta/administração & dosagem , Ingestão de Energia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Inquéritos Nutricionais , Obesidade Abdominal/fisiopatologia , Obesidade Abdominal/psicologia , República da Coreia/epidemiologia , Autorrelato , Fatores de Tempo
18.
World J Gastroenterol ; 25(37): 5676-5686, 2019 Oct 07.
Artigo em Inglês | MEDLINE | ID: mdl-31602167

RESUMO

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a frequently reported condition in patients with inflammatory bowel disease (IBD). Both intestinal inflammation and metabolic factors are believed to contribute to the pathogenesis of IBD-associated NAFLD. AIM: To evaluate the prevalence of steatosis and liver fibrosis (LF) in a cohort of IBD patients and the identification of metabolic- and IBD-related risk factors for NAFLD and LF. METHODS: IBD patients were consecutively enrolled from December 2016 to January 2018. Demographic, anthropometric and biochemical data were collected so as eating habits. Abdominal ultrasound and transient elastography were performed to evaluate the presence of NAFLD and LF respectively. RESULTS: A total of 178 consecutive patients were enrolled and included in the analysis (95 Ulcerative colitis, 83 Crohn's disease). NAFLD was detected by imaging in 72 (40.4%) patients. Comparison between patients with and without NAFLD showed no significant differences in terms of IBD severity, disease duration, location/extension, use of IBD-related medications (i.e., steroids, anti-TNFs, and immunomodulators) and surgery. NAFLD was significantly associated with the presence of metabolic syndrome [MetS; odds ratio (OR): 4.13, P = 0.001] and obesity defined by body mass index (OR: 9.21, P = 0.0002). IBD patients with NAFLD showed higher caloric intake and lipid consumption than those without NAFLD, regardless disease activity. At the multivariate analysis, male sex, advanced age and high lipid consumption were independent risk factors for the development of NAFLD. An increased liver stiffness was detected in 21 patients (16%) and the presence of MetS was the only relevant factor associated to LF (OR: 3.40, P = 0.01). CONCLUSION: In this study, we demonstrate that risk factors for NAFLD and LF in the IBD population do not differ from those in the general population.


Assuntos
Colite Ulcerativa/complicações , Doença de Crohn/complicações , Cirrose Hepática/epidemiologia , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Adulto , Fatores Etários , Idoso , Gorduras na Dieta/efeitos adversos , Progressão da Doença , Feminino , Seguimentos , Humanos , Cirrose Hepática/etiologia , Cirrose Hepática/patologia , Masculino , Pessoa de Meia-Idade , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/patologia , Prevalência , Fatores de Risco , Fatores Sexuais
19.
Andrologia ; 51(10): e13418, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31475727

RESUMO

Obesity is known to be associated with impaired testicular function potentially resulting in androgen deficiency and subfertility. While the underlying cause of obesity-related male hypogonadism is multi-factorial, here, we investigated the impact of dietary fat on testicular endocrine function. Ingestion of a high-fat "fast food" mixed meal, a common practice for obese men, produced a 25% fall in serum testosterone within an hour of eating, with levels remaining suppressed below fasting baseline for up to 4 hr. These changes in serum testosterone were not associated with any significant changes in serum gonadotrophins. The nadir in serum testosterone preceded the post-prandial increase in serum IL-6/IL-17 by several hours, suggesting that inflammation was unlikely the cause. Furthermore, intravenous administration of fat (Intralipid) had no impact on testosterone levels, while an identical oral dose of fat did suppress testosterone. These results suggest that fat does not directly impair Leydig cell function, but rather the passage of fat through the intestinal tract elicits a response that indirectly elicits a post-prandial fall in testosterone.


Assuntos
Hipogonadismo/sangue , Obesidade/complicações , Período Pós-Prandial/fisiologia , Reprodução/fisiologia , Testosterona/sangue , Adolescente , Adulto , Estudos Cross-Over , Gorduras na Dieta/efeitos adversos , Emulsões/administração & dosagem , Emulsões/efeitos adversos , Fast Foods/efeitos adversos , Humanos , Hipogonadismo/etiologia , Hipogonadismo/fisiopatologia , Infusões Intravenosas , Células Intersticiais do Testículo/metabolismo , Masculino , Pessoa de Meia-Idade , Obesidade/fisiopatologia , Fosfolipídeos/administração & dosagem , Fosfolipídeos/efeitos adversos , Óleo de Soja/administração & dosagem , Óleo de Soja/efeitos adversos , Testosterona/metabolismo , Adulto Jovem
20.
Nutrients ; 11(10)2019 Sep 23.
Artigo em Inglês | MEDLINE | ID: mdl-31547555

RESUMO

Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, amyotrophic lateral sclerosis, and Alzheimer's disease. In addition, it has attracted attention as a target for the prevention and treatment of these chronic diseases. As metabolic endotoxemia was first reported in mice that were fed a high-fat diet, research regarding its relationship with diets has been actively conducted in humans and animals. In this review, we summarize the relationship between fat intake and induction of metabolic endotoxemia, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS. We also summarize the recent findings about dietary factors that attenuate metabolic endotoxemia, focusing on the regulation of gut microbiota. We hope that in the future, control of metabolic endotoxemia using dietary factors will help maintain human health.


Assuntos
Gorduras na Dieta/efeitos adversos , Disbiose/microbiologia , Endotoxemia/microbiologia , Microbioma Gastrointestinal/fisiologia , Lipopolissacarídeos/sangue , Animais , Dieta Hiperlipídica/efeitos adversos , Disbiose/sangue , Disbiose/etiologia , Endotoxemia/sangue , Endotoxemia/etiologia , Humanos , Camundongos
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