RESUMO
Acute mental stress (AMS) increases heart rate (HR) and blood pressure. Since obesity can impair the cardiovascular reactivity to AMS, a better understanding of the mechanisms involved in this response is needed. We aimed to evaluate the cardiovascular reactivity to AMS in young men with normal or excess body fat. We also assessed the association between cardiovascular reactivity to AMS and cardiovascular risk factors, including autonomic modulation, carotid artery distensibility, physical activity levels, and sleep efficiency. Sixty-six young men (26.1 ± 4.1 years old) underwent anthropometric and body fat assessment (dual-energy X-ray absorptiometry) and had right-carotid artery ultrasonography. Accelerometers assessed physical activity levels and sleep efficiency. AMS was induced through the Stroop color-word test while blood pressure, HR, and cardiac interval were measured. Analyses were performed in Normal and Excess fat groups divided by fat mass index (FMI). Continuous data was used for multiple linear regression analyses. An interaction between FMI and time for HR reactivity was observed. Cardiac interval variability analysis showed that only participants with normal fat displayed parasympathetic withdrawal during AMS (P < 0.05). Multiple linear regression analysis supported the role of adiposity and autonomic modulation in the HR reactivity to AMS and showed involvement of carotid distensibility and sleep efficiency (P < 0.05). Carotid distensibility was the only predictor for blood pressure reactivity (P < 0.05). Physical activity was not associated with AMS's cardiovascular reactivity. We conclude that increased adiposity is associated with reduced HR reactivity to AMS, which is possibly linked to an impaired parasympathetic withdrawal. Carotid distension and sleep efficiency seem to contribute to this response.
Assuntos
Adiposidade , Artérias Carótidas , Adulto , Frequência Cardíaca/fisiologia , Humanos , Masculino , Obesidade/diagnóstico por imagem , Sono , Adulto JovemRESUMO
BACKGROUND & AIMS: Diabetes mellitus (DM) and cardiovascular disease (CVD) are among the biggest causes of death and health expenses worldwide. A higher dietary acid load (DAL) is associated with chronic low-grade metabolic acidosis, and may increase the risk of insulin resistance (IR), DM, hypertension, and CVD mortality. However, the association between DAL and IR still lacks population-based studies to confirm laboratory findings. METHODS: This is a population-based observational study including a sample of 545 individuals aged 25-64 years from Florianópolis (Southern Brazil) who participated in the EpiFloripa cohort study. All diet variables were obtained through two 24-h Food Recalls adjusted to obtain an estimate of habitual food consumption. DAL was measured by Potential Renal Acid Load (PRAL) and Net Endogenous Acid production (NEAP). Fasting blood samples were obtained from all participants. The primary outcome was IR, which was estimated by HOMA-IR. Secondary outcomes included HOMA-ß, glycosylated hemoglobin, and fasting blood glucose and insulin. Multiple linear regression models adjusted for sociodemographics, lifestyle, and clinical variables were used for analysis, with exposure and outcome variables standardized as Z-scores to allow comparability of the results. RESULT: The mean PRAL and NEAP in the sample were 16.9 ± 4.8 and 66.1 ± 7.1 mEq/day, respectively. The average HOMA-IR score was 2.4 ± 1.6. In adjusted analyses, PRAL was positively associated with HOMA-IR, fasting insulin, and fasting blood glucose (p-value <0.05 in all cases), but not with HOMA-ß or glycated hemoglobin. NEAP also showed a direct-trend relationship with HOMA-IR and fasting insulin, but not with fasting blood glucose or the other outcomes. The strongest association was between PRAL and HOMA-IR (ß, 0.20; 95% CI, 0.06-0.35). CONCLUSIONS: A higher DAL was consistently associated with higher IR and insulin levels but not with other glycaemic parameters. Apparently, ß-pancreatic cells function is not affected by DAL in this population. This is the first study that describes the DAL in a population-based sample of adults in Latin America and in a middle-income country population. Further longitudinal and interventional studies are required to establish a better causal effect between DAL and IR.
Assuntos
Doenças Cardiovasculares , Diabetes Mellitus , Resistência à Insulina , Ácidos , Adulto , Glicemia/metabolismo , Estudos de Coortes , Dieta , Hemoglobinas Glicadas , Humanos , InsulinaRESUMO
BACKGROUND: The energy-adjusted Dietary Inflammatory Index (E-DII™) has been associated with a high body mass index and markers of chronic diseases. Also, pro-inflammatory diets with a high E-DII have been positively associated with metabolic disturbances such as glucose intolerance and type II diabetes mellitus. However, it is unclear whether E-DII scores are positively associated with body fat percentage and visceral fat per se. This cross-sectional study aimed to evaluate whether the E-DII is associated with body fat content and metabolic health indicators in lean and obese young men. METHODS: The present study was conducted on 59 participants, without comorbidities, not using tobacco, medication and nutritional supplements. Dietary data were obtained by 3-day food records to calculate E-DII scores based on 28 food parameters. Body composition was assessed by dual X-ray absorptiometry (DXA). Blood samples were taken to measure fasting glucose, insulin, triacylglycerols, total cholesterol, and low- and high-density lipoprotein cholesterol. An oral glucose tolerance test also was performed. Associations were determined by mixed-effects linear regression. RESULTS: E-DII scores ranged from -3.48 to +3.10. Energy intake was similar across E-DII tertiles. After adjusting for covariates, the highest E-DII tertile was associated with increased body fat, visceral adipose tissue and waist circumference. There was no association between E-DII scores and glycaemic parameters. CONCLUSIONS: In young participants, a dietary pattern with a higher E-DII (i.e., pro-inflammatory) score was associated with high body fat and markers of central adiposity assessed by DXA, regardless of body mass.
Assuntos
Diabetes Mellitus Tipo 2 , Gordura Intra-Abdominal , Adulto , Masculino , Humanos , Diabetes Mellitus Tipo 2/complicações , Estudos Transversais , Dieta , Índice de Massa Corporal , Obesidade/complicações , Tecido Adiposo , HDL-Colesterol , Biomarcadores , InflamaçãoRESUMO
Chronic stress is a risk factor for cardiovascular diseases (CVD) and anxiety disorders (AD). Obesity also increases the risk of CVD and AD. The modern lifestyle commonly includes high-fat diet (HFD) intake and daily exposure to stressful events. However, it is not completely understood whether chronic stress exacerbates HFD-induced behavioral and physiological changes. Thus, this study aimed to evaluate the effects of the exposure to chronic variable stress (CVS) on behavioral, cardiovascular, and endocrine parameters in rats fed an HFD. Male Wistar rats were divided into four groups: control-standard chow diet (control-SD), control-HFD, CVS-SD, and CVS-HFD. The control-HFD and CVS-HFD groups were fed with HFD for six weeks. The CVS-HFD and CVS-SD groups were exposed to a CVS protocol in the last ten days of the six weeks. The behavioral analysis revealed that CVS decreased the open-arm exploration time during the elevated plus-maze test (p < 0.05). HFD promoted metabolic disorders and increased angiotensin II and leptin blood levels (p < 0.05). CVS or HFD increased blood pressure and the sympathetic nervous system (SNS) modulation of the heart and vessels and decreased baroreflex activity (p < 0.05). Combining CVS and HFD exacerbated the cardiac SNS response and increased basal heart rate (HR) (p < 0.05). CVS or HFD did not affect vascular function and aorta nitrate (p > 0.05). Taken together, these data indicate a synergism between HFD and CVS on the HR and cardiac SNS responses, suggesting an increased cardiovascular risk. Besides, neuroendocrine and anxiogenic disturbers may contribute to the cardiovascular changes induced by HFD and CVS, respectively.
Assuntos
Sistema Cardiovascular , Dieta Hiperlipídica , Animais , Barorreflexo , Pressão Sanguínea , Dieta Hiperlipídica/efeitos adversos , Masculino , Ratos , Ratos WistarRESUMO
L-Leucine has been used to improve metabolic outcomes in glucose-intolerant rodent models. However, because studies have used different experimental models and conditions it is difficult to establish the best approach for new clinical trials evaluating the potential effects of L-leucine on glucose homeostasis. We performed a systematic review to report the effect of L-leucine supplementation on glucose homeostasis in rodents with glucose intolerance. The search engines MEDLINE and ScienceDirect were applied using MeSH terms. Thirty-four studies were included in this systematic review. Based on the current data, ingestion of 90-140 mg day-1 of isolated L-leucine in diet-induced obesity (DIO) models shows improvement in metabolic markers if offered during the development of the metabolic disorder in almost all the studies, but not after. Branched-chain amino acid supplementation was effective in streptozotocin-induced ß-cells death but not in DIO models. L-Leucine supplementation seems to have an optimal dose and timing for supplementation to improve glucose homeostasis in DIO.
Assuntos
Glicemia/efeitos dos fármacos , Suplementos Nutricionais , Intolerância à Glucose/dietoterapia , Homeostase/efeitos dos fármacos , Leucina/administração & dosagem , Animais , Diabetes Mellitus Tipo 2/prevenção & controle , Modelos Animais de Doenças , Humanos , Insulina/metabolismo , Leucina/farmacologia , Camundongos Obesos , Obesidade/dietoterapia , RoedoresRESUMO
Context: Omega-3 (n-3) polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid and eicosapentaenoic acid, demonstrate possible beneficial effects as adjuvants in cancer treatment. One mechanism seems to be related to alterations in the redox status of cancer cells. Such alterations are thought to act in synergy with conventional anticancer agents. Objective: This review examines published data on the effects of cotreatment with anticancer agents and n-3 PUFAS on oxidative stress parameters to determine whether any patterns of oxidative stress alterations can be identified. Data Sources: A systematic search of MEDLINE (via PubMed) was conducted to identify articles published in English, Spanish, or Portuguese until November 2017. Study Selection: The following inclusion criteria were applied: (1) individuals or animals with cancer or malignant cell lines supplemented with some source of n-3 PUFAs; (2) concomitant use of anticancer treatment; and (3) evaluation of oxidative stress-related variables. Data Extraction: A standardized outline was used to extract the following data: study type, supplement used, type of cells, tumor or patient characteristics, study design, anticancer treatment used, and oxidative stress-related outcomes. Results: After the literature search and screening of 1563 citations, 28 studies were included for data extraction and evaluation: 16 in vitro studies (2 of which also used in vivo studies), 8 animal studies, and 4 human studies (3 clinical trials and 1 case series). In most in vitro and animal studies, intervention groups receiving cotreatment with n-3 PUFAs showed enhanced lipid peroxidation and cytotoxicity compared with groups receiving anticancer treatment alone. Eleven of the 12 studies that investigated the effect of vitamin E on the sensitivity of cancer cells to the oxidative stress caused by n-3 PUFAs showed that vitamin E abolished the positive effects of cotreatment. Conclusions: Alterations in oxidative stress caused by cotreatment with anticancer agents and n-3 PUFAs can exert positive effects on the efficacy of conventional treatment. This seems to occur in most cells and tumors tested thus far, but not all. Identifying tumors that are sensitive to these oxidative effects may provide support for the rational use of n-3 PUFAs as an adjuvant treatment in specific types of cancer.
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Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Suplementos Nutricionais , Ácidos Graxos Ômega-3/farmacologia , Neoplasias/terapia , Estresse Oxidativo/efeitos dos fármacos , Animais , Ácidos Docosa-Hexaenoicos/farmacologia , Ácido Eicosapentaenoico/farmacologia , Humanos , Neoplasias/metabolismo , Processos Neoplásicos , Vitamina E/farmacologiaRESUMO
Obesity and chronic stress are considered independent risk factors for the development of cardiovascular diseases and changes in autonomic system activity. However, the cardiovascular consequences induced by the association between high-fat diet (HFD) and chronic stress are not fully understood. We hypothesized that the association between HFD and exposure to a chronic variable stress (CVS) protocol for four weeks might exacerbate the cardiovascular and metabolic disturbances in rats when compared to these factors singly. To test this hypothesis, male Wistar rats were divided into four groups: control-standard chow diet (SD; n = 8); control-HFD (n = 8); CVS-SD (n = 8); and CVS-HFD (n = 8). The CVS consisted of repeated exposure of the rats to different inescapable and unpredictable stressors (restraint tress; damp sawdust, cold, swim stress and light cycle inversion). We evaluated cardiovascular function, autonomic activity, dietary intake, adiposity and metabolism. The HFD increased body weight, adiposity and blood glucose concentration (â¼15%) in both control and CVS rats. The CVS-HFD rats showed decreased insulin sensitivity (25%) compared to CVS-SD rats. The control-HFD and CVS-HFD rats presented increased intrinsic heart rate (HR) values (â¼8%). CVS increased cardiac sympathetic activity (â¼65%) in both SD- and HFD-fed rats. The HFD increased basal HR (â¼10%). Blood pressure and baroreflex analyzes showed no differences among the experimental groups. In conclusion, the present data indicate absence of interaction on autonomic imbalance evoked by either CVS or HFD. Additionally, HFD increased HR and evoked metabolic disruptions which are independent of stress exposure.
Assuntos
Fenômenos Fisiológicos Cardiovasculares , Dieta Hiperlipídica/efeitos adversos , Estresse Psicológico/metabolismo , Estresse Psicológico/fisiopatologia , Adiposidade , Animais , Sistema Nervoso Autônomo/fisiopatologia , Glicemia/análise , Peso Corporal , Doença Crônica , Temperatura Baixa , Frequência Cardíaca , Hemodinâmica , Resistência à Insulina , Masculino , Metabolismo , Tamanho do Órgão , Ratos , Ratos WistarRESUMO
Sepsis is associated with high mortality. Both critically ill humans and animal models of sepsis exhibit changes in their glucose homeostasis, that is, hypoglycaemia, with the progression of infection. However, the relationship between basal glycaemia, glucose tolerance and insulin sensitivity is not well understood. Thus, we aimed to evaluate this glucose homeostasis triad at the late stage of sepsis (24 h after surgery) in male Swiss mice subjected to lethal and sublethal sepsis by the caecal ligation and puncture (CLP) model. The percentage of survival 24 h after CLP procedure in the Lethal and Sublethal groups was around 66% and 100% respectively. Both Lethal and Sublethal groups became hypoglycaemic in fasting and fed states 24 h after surgery. The pronounced fed hypoglycaemia in the Lethal group was not due to worsening anorexic behaviour or hepatic inability to deliver glucose in relation to the Sublethal group. Reduction in insulin sensitivity in CLP mice occurred in a lethality-dependent manner and was not associated with glucose intolerance. Analysis of oral and intraperitoneal glucose tolerance tests, as well as the gastrointestinal motility data, indicated that CLP mice had reduced intestinal glucose absorption. Altogether, we suggest cessation of appetite and intestinal glucose malabsorption are key contributors to the hypoglycaemic state observed during experimental severe sepsis.
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Glicemia/biossíntese , Ceco/metabolismo , Homeostase/fisiologia , Sepse/mortalidade , Animais , Ceco/cirurgia , Modelos Animais de Doenças , Hipoglicemiantes , Resistência à Insulina , Ligadura/métodos , Fígado/metabolismo , Masculino , Camundongos , Punções/métodosRESUMO
Background. Continuous fructose consumption may cause elevation of circulating triacylglycerol. However, how much of this alteration is reverted after the removal of fructose intake is not known. We explored this question and compared the efficacy of this approach with fish oil supplementation. Methods. Male Wistar rats were divided into the following groups: control (C), fructose (F) (water intake with 10% or 30% fructose for 9 weeks), fish oil (FO), and fructose/fish oil (FFO). Fish oil was supplemented only for the last 33 days of fructose ingestion. Half of the F group remained for additional 8 weeks without fructose ingestion (FR). Results. Fructose ingestion reduced food intake to compensate for the increased energy obtained through water ingestion, independent of fructose concentration. Fish oil supplementation exerted no impact on these parameters, but the removal of fructose from water recovered both ingestion behaviors. Plasma triacylglycerol augmented significantly during the second and third weeks (both fructose groups). Fish oil supplementation did not attenuate the elevation in triacylglycerol caused by fructose intake, but the interruption of sugar consumption normalized this parameter. Conclusion. Elevation in triacylglyceridemia may be recovered by removing fructose from diet, suggesting that it is never too late to repair improper dietary habits.
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Suplementos Nutricionais , Óleos de Peixe/administração & dosagem , Frutose/administração & dosagem , Glucose/metabolismo , Metabolismo dos Lipídeos , Animais , Dieta , Ingestão de Alimentos , Comportamento Alimentar , Óleos de Peixe/metabolismo , Frutose/metabolismo , Homeostase , Masculino , Ratos , Ratos WistarRESUMO
OBJECTIVE: Polyunsaturated fatty acids n-3 (PUFA n-3) have shown effects in reducing tumor growth, in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) abundantly present in fish oil (FO). When these fatty acids are provided in the diet, they alter the functions of the cells, particularly in tumor and immune cells. However, the effects of α-linolenic fatty acid (ALA), which is the precursor of EPA and DHA, are controversial. Thus, our objective was to test the effect of this parental fatty acid. METHODS: Non-tumor-bearing and tumor-bearing Wistar rats (70 days) were supplemented with 1 g/kg body weight of FO or Oro Inca® (OI) oil (rich in ALA). Immune cells function, proliferation, cytokine production, and subpopulation profile were evaluated. RESULTS: We have shown that innate immune cells enhanced phagocytosis capacity, and increased processing and elimination of antigens. Moreover, there was a decrease in production of pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6)) by macrophages. Lymphocytes showed decreased proliferation capacity, increased cluster of differentiation 8 (CD8+) subpopulation, and increased TNF-α production. CONCLUSIONS: Oil rich in ALA caused similar immune modulation in cancer when compared with FO.