RESUMO
The objective of this study was to assess whether acute green tea (GT) supplementation attenuates inflammatory and oxidative stress biomarkers induced by high-fat, high-saturated (HFHS) meals in obese women, and to assess its ability to modulate circulating microRNA (miRNA) expression. This was a randomized, double-blind, crossover study. The study included obese women over 18 years old who had no comorbidities. In the first moment, patients were instructed to take 2 capsules of placebo or GT (738 mg) at 10:00 p.m. and to fast overnight. The next morning, a blood sample was collected, and an HFHS meal was offered to the patients. Another blood sample was collected 5 hours after the meal. In the second moment, patients who received placebo in the first moment now received the GT and vice-versa. Serum inflammatory and oxidative stress biomarkers were measured, and circulating levels of miRNA were evaluated. Fifteen women with mean age of 35.5±9.9 years were included in the final analysis. There was no difference regarding inflammatory and oxidative stress biomarkers. However, patients who consumed GT had lower circulating expression of 62 miRNAs compared with patients who did not consume GT. Predictive analysis of target genes showed 1,757 targets regulated by the 62 miRNAs. Notably, 5 miRNAs (miR-1297, miR-192-5p, miR-373-3p, miR-595 and miR-1266-5p) regulate genes associated with TGF-beta, CARM1, RSK, and BMP pathways. Our study showed that GT inhibited the expression of miRNAs induced by HFHS meal intake. These results shed light on the mechanisms involved in the beneficial effects of GT ingestion.
Assuntos
MicroRNA Circulante , MicroRNAs , Humanos , Feminino , Adulto , Pessoa de Meia-Idade , Adolescente , MicroRNA Circulante/genética , Estudos Cross-Over , Chá , MicroRNAs/metabolismo , Obesidade , BiomarcadoresRESUMO
BACKGROUND: It is known that consuming a high-fat meal (HFM) induces microvascular dysfunction (MD) in eutrophic women and aggravates it in those with obesity. Our purpose was to investigate if the MD observed after a single HFM intake is caused by endothelial damage or increased inflammatory state, both determined by blood biomarkers. METHODS: Nineteen women with obesity (BMI 30-34.9 kg/m2) and 18 eutrophic ones (BMI 20.0-24.9 kg/m2) were enrolled into two groups: Obese (OBG) and Control (CG), respectively. Blood samples were collected at five-time points: before (fasting state) and 30, 60, 120, and 180 min after HFM intake to determine levels of adipokines (adiponectin, leptin), non-esterified fatty acid (NEFA), inflammatory [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)] and endothelium damage [soluble E-selectin, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), plasminogen activator inhibitor-1 (PAI-1)] biomarkers. RESULTS: Levels of soluble E-selectin, leptin, and PAI-1 were higher in OBG at all-time points (P < 0.05) compared to CG. In the fasting state, OBG had higher levels of NEFA compared to CG (P < 0.05). In intra-group analysis, no significant change in the levels of circulating inflammatory and endothelial injury biomarkers was observed after HFM intake, independently of the group. CONCLUSION: Our findings suggest that women with obesity have an increased pro-inflammatory state and more significant endothelial injury compared to eutrophic ones. However, the consumption of a HFM was not sufficient to change circulating levels of inflammatory and endothelial injury biomarkers in either group. REGISTRATION NUMBER FOR CLINICAL TRIALS: NCT01692327.
Assuntos
Adiposidade , Leptina , Feminino , Humanos , Adipocinas , Adiponectina , Biomarcadores , Estudos Transversais , Selectina E/metabolismo , Endotélio Vascular , Ácidos Graxos não Esterificados , Molécula 1 de Adesão Intercelular/metabolismo , Molécula 1 de Adesão Intercelular/farmacologia , Interleucina-6 , Obesidade , Inibidor 1 de Ativador de Plasminogênio/metabolismo , Inibidor 1 de Ativador de Plasminogênio/farmacologia , Fator de Necrose Tumoral alfa , Molécula 1 de Adesão de Célula Vascular/metabolismo , Molécula 1 de Adesão de Célula Vascular/farmacologiaRESUMO
CONTEXT: The sirtuins (SIRT1 to SIRT7) constitute a family of highly conserved nicotinamide adenine dinucleotide-dependent proteins. When activated, sirtuins control essential cellular processes to maintain metabolic homeostasis, while lack of expression of sirtuins has been related to chronic disease. OBJECTIVE: The aim of this systematic review is to analyze the role of fat consumption as a modulator of human sirtuins. DATA SOURCES: This review was conducted according to PRISMA guidelines. Studies were identified by searches of the electronic databases PubMed/MEDLINE, Scopus, and Web of Science. STUDY SELECTION: Randomized clinical trials assessing the effect of fatty acid consumption on sirtuin mRNA expression, sirtuin protein expression, or sirtuin protein activity were eligible for inclusion. DATA EXTRACTION: Two authors screened and determined the quality of the studies; disagreements were resolved by the third author. All authors compared the compiled data. RESULTS: Seven clinical studies with 3 different types of interventions involving healthy and nonhealthy participants were selected. Only SIRT1 and SIRT3 were evaluated. Overall, the evidence from clinical studies to date is insufficient to understand how lipid consumption modulates sirtuins in humans. The best-characterized mechanism highlights oleic acid as a natural activator of SIRT1. CONCLUSION: These results draw attention to a new field of interest in nutrition science. The possible activation of sirtuins by dietary fat manipulation may represent an important nutritional strategy for management of chronic and metabolic disease. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration number CRD42018114456.
Assuntos
Ácidos Graxos/administração & dosagem , Sirtuína 1/genética , Sirtuína 3/genética , Adulto , Idoso , Gorduras na Dieta/administração & dosagem , Feminino , Regulação da Expressão Gênica , Humanos , Masculino , Pessoa de Meia-Idade , Ensaios Clínicos Controlados Aleatórios como Assunto , Sirtuína 1/metabolismo , Sirtuína 3/metabolismo , Adulto JovemRESUMO
High-fat diet increase two to three times the plasma lipopolysaccharide (LPS) levels and induce subclinical inflammation. Diet can modify gene expression due to epigenetic processes related to MicroRNAs (miRNAs). MicroRNAs (miRNAs) play important role in the post-transcriptional mechanisms involved in regulation of expression of genes related to the inflammatory response. Also, diet can indirectly induce post-transcriptional regulation of gene expression by miRNAs, which may affect the risk for the development of chronic diseases. OBJECTIVE: This study investigated the effect of high-fat high-saturated meal ingestion on plasma miRNA expression and LPS levels during the postprandial period in healthy women. METHODS: An interventional study was carried out in which a high-fat breakfast (1067.45 kcal), composed mainly of saturated fatty acids (56 g), and 500 mL of water, was offered. Blood samples were collected at baseline and 1, 3 and 5 h after meal intake. The studied population consisted of healthy women (n = 11), aged between 20 and 40 years, and body mass index (BMI) between 18.5 and 25 kg/m2. Plasma levels of lipid profile, cytokines, adhesion molecules, and LPS were measured at the 3 time points. A profile of 752 human plasma miRNA expression was analyzed by real-time PCR assay. These analyzes were performed for all blood collection time-points. RESULTS: Expression profile analysis revealed 33 differentially expressed plasma circulating miRNAs compared to that of the control group. MiR-145-5p and miR-200 were differentially modulated in all time-points post meal consumption. In addition, there was a significant increase in plasma LPS, triglycerides, myristic and palmitic saturated fatty acids levels at the 3 time-points in comparison with the control basal levels. We also observed increased levels of the plasma tumor necrosis factor alpha (TNF-α) cytokine and the vascular cell adhesion molecule 1 (VCAM-1) levels after 5 h post meal ingestion. CONCLUSION: Ingestion of high-fat high-saturated meal was able to induce metabolic endotoxemia and increase the expression of pro-inflammatory molecules such as TNF-alpha and VCAM-1, as well as modulating circulating miRNAs possibly controlling inflammatory and lipid metabolism proteins at the postprandial period.
Assuntos
MicroRNA Circulante/sangue , Dieta Hiperlipídica/efeitos adversos , Endotoxemia/sangue , Endotoxemia/etiologia , Adulto , Brasil , Dieta Hiperlipídica/métodos , Feminino , Humanos , Inflamação/sangue , Inflamação/etiologia , Lipopolissacarídeos/sangue , Adulto JovemRESUMO
ABSTRACT Objective We investigated the postprandial response of lipid markers to a high-fat meal (HFM) with two different beverages in apparently healthy normal-weight and overweight/obese women. Subjects and methods This crossover, randomized study enrolled 36 women, of whom 21 had normal weight (body mass index [BMI] 22 ± 1.8 kg/m2) and 15 had overweight/obesity (BMI 31 ± 3.7 kg/m2). In two different test days, the participants ingested a HFM (37% of energy as saturated fat) with 500 mL of water (HFM-W) or 500 mL of orange juice (HFM-OJ). Blood samples were collected at baseline (12-hour fasting), and at 2, 3, and 5 hours postprandial. The analysis included fasting and postprandial total cholesterol, HDL-c, LDL-c, triglycerides (TG), uric acid, and complement C3. Brazilian Clinical Trials Registry (ReBEC); Primary Identification Number: RBR-2h3wjn (www.ensaiosclinicos.gov.br). Results TG levels increased at 3 hours with HFM-OJ in normal-weight women (p = 0.01) and returned to normal levels at 5h. TG increased at 3 hours with HFM-W (p = 0.01) and HFM-OJ (p = 0.02), and remained high at 5 hours (p = 0.03) in overweight/obese women. Complement C3 remained unchanged, but showed different responses between meals (p = 0.01 for positive incremental area under the curve [piAUC] HFM-OJ vs. HFM-W, respectively). Conclusions In apparently healthy overweight/obese women compared with normal-weight ones, the concomitant intake of orange juice with a HFM prolonged postprandial lipemia but had no effect on postprandial complement C3 concentrations.