Josefina Bressan

Effects of food form on appetite and energy intake in lean and obese young adults

Objective:To investigate the independent effect of food form on appetite and energy intake in lean and obese adults using high carbohydrate, fat or protein food stimuli.Design:Crossover dietary challenge with matched beverage and solid food forms: high carbohydrate (watermelon and watermelon juice); high protein (cheese and milk); high fat (coconut meat and coconut milk).Subjects:A total of 120 lean (18–23 kg/m2; N=60) and obese (30–35 kg/m2; N=60) adults (18–50 years old) with stable body weight. Forty different participants (N=20 lean and 20 obese) were tested with each of the food systems.Measurements:Appetitive sensations, food palatability and dietary intake.Results:Regardless of the predominant energy source, the beverage food form elicited a weaker compensatory dietary response than the matched solid food form. Thus, total daily energy intake was significantly higher by 12.4, 19 and 15% on days the beverage forms of the high-carbohydrate, -fat and -protein foods were ingested, respectively. This was due more to a weak effect on satiety than satiation. The obese participants had higher energy intake at the lunch, including the beverage high-protein load, but overall differences between lean and obese participants were small and not systematic.Conclusion:Food rheology exerts an independent effect on energy intake. Dietary compensation for beverages is weaker than for solid food forms of comparable nutrient content. Thus, they pose a greater risk for promoting positive energy balance.

Metabolic responses to high glycemic index and low glycemic index meals: a controlled crossover clinical trial

BackgroundThe consumption of low glycemic index (LGI) foods before exercise results in slower and more stable glycemic increases. Besides maintaining an adequate supply of energy during exercise, this response may favor an increase in fat oxidation in the postprandial period before the exercise compared to high glycemic index (HGI) foods. The majority of the studies that evaluated the effect of foods differing in glycemic index on substrate oxidation during the postprandial period before the exercise are acute studies in which a single meal is consumed right before the exercise. The purpose of this study was to investigate the effect of consuming two daily HGI or LGI meals for five consecutive days on substrate oxidation before the exercise and in the concentrations of glucose, insulin and free fatty acids before and during a high intensity exercise.MethodsFifteen male cyclists, aged 24.4 ± 3.8 years, with body mass index of 21.9 ± 1.4 kg.m-2 and a VO2 max of 70.0 ± 5.3 mL.kg-1.min-1, participated in this crossover study. All test meals were consumed in the laboratory. On days 1 and 5, substrate oxidation (30 minutes before and 90 minutes after breakfast (HGI or LGI)) and diet-induced thermogenesis (90 minutes postprandial) were assessed before the exercise. The levels of glucose, insulin, and free fatty acids were determined during 2 h after breakfast on these same days. Ninety minutes after breakfast, subjects completed a 30 min cycloergometric exercise at 85 to 95% of their maximum heart rate, during which lactate concentrations were assessed.ResultsThe consumption of HGI meals resulted in higher areas under the glycemic and insulinemic curves in the postprandial period. However, glycemia did not differ by study treatment during exercise. There were no differences in free fatty acids in the postprandial period or in lactate levels during exercise. LGI meals resulted in lower fat oxidation and higher carbohydrate oxidation than the HGI meal in the postprandial period.ConclusionsThe results do not support a differential glycemia according to glycemic index during exercise. The ingestion of LGI foods did not lead to higher fat oxidation relative to the ingestion of HGI foods.Trial registrationACTRN: ACTRN12609000522213

Potential mechanisms for the emerging link between obesity and increased intestinal permeability

Recently, increased attention has been paid to the link between gut microbial composition and obesity. Gut microbiota is a source of endotoxins whose increase in plasma is related to obesity and insulin resistance through increased intestinal permeability in animal models; however, this relationship still needs to be confirmed in humans. That intestinal permeability is subject to change and that it might be the interface between gut microbiota and endotoxins in the core of metabolic dysfunctions reinforce the need to understand the mechanisms involved in these aspects to direct more efficient therapeutic approaches. Therefore, in this review, we focus on the emerging link between obesity and increased intestinal permeability, including the possible factors that contribute to increased intestinal permeability in obese subjects. We address the concept of intestinal permeability, how it is measured, and the intestinal segments that may be affected. We then describe 3 factors that may have an influence on intestinal permeability in obesity: microbial dysbiosis, dietary pattern (high-fructose and high-fat diet), and nutritional deficiencies. Gaps in the current knowledge of the role of Toll-like receptors ligands to induce insulin resistance, the routes for lipopolysaccharide circulation, and the impact of altered intestinal microbiota in obesity, as well as the limitations of current permeability tests and other potential useful markers, are discussed. More studies are needed to reveal how changes occur in the microbiota. The factors such as changes in the dietary pattern and the improvement of nutritional deficiencies appear to influence intestinal permeability, and impact metabolism must be examined. Also, additional studies are necessary to better understand how probiotic supplements, prebiotics, and micronutrients can improve stress-induced gastrointestinal barrier dysfunction and the influence these factors have on host defense. Hence, the topics presented in this review may be beneficial in directing future studies that assess gut barrier function in obesity.

Noncoding RNAs, cytokines, and inflammation-related diseases

Chronic inflammation is involved in the onset and development of many diseases, including obesity, atherosclerosis, type 2 diabetes, osteoarthritis, autoimmune and degenerative diseases, asthma, periodontitis, and cirrhosis. The inflammation process is mediated by chemokines, cytokines, and different inflammatory cells. Although the molecules and mechanisms that regulate this primary defense mechanism are not fully understood, recent findings offer a putative role of noncoding RNAs, especially microRNAs (miRNAs), in the progression and management of the inflammatory response. These noncoding RNAs are crucial for the stability and maintenance of gene expression patterns that characterize some cell types, tissues, and biologic responses. Several miRNAs, such as miR‐126, miR‐132, miR‐146, miR‐155, and miR‐221, have emerged as important transcriptional regulators of some inflammation‐related mediators. Additionally, little is known about the involvement of long noncoding RNAs, long intergenic noncoding RNAs, and circular RNAs in inflammation‐mediated processes and the homeostatic imbalance associated with metabolic disorders. These noncoding RNAs are emerging as biomarkers with diagnosis value, in prognosis protocols, or in the personalized treatment of inflammation‐related alterations. In this context, this review summarizes findings in the field, highlighting those noncoding RNAs that regulate inflammation, with emphasis on recognized mediators such as TNF‐α, IL‐1, IL‐6, IL‐18, intercellular adhesion molecule 1, VCAM‐1, and plasminogen activator inhibitor 1. The down‐regulation or antagonism of the noncoding RNAs and the administration of exogenous miRNAs could be, in the near future, a promising therapeutic strategy in the treatment of inflammation‐related diseases.—Marques‐Rocha, J. L., Samblas, M., Milagro, F. I., Bressan, J., Martínez, J. A., Marti, A. Noncoding RNAs, cytokines, and inflammation‐related diseases. FASEB J. 29, 3595‐3611 (2015). www.fasebj.org

Estresse oxidativo: conceito, implicações e fatores modulatórios

There is evidence that oxidative stress, defined as a persistent imbalance between the production of highly oxidative compounds and antioxidant defenses, leads to tissue damage. Oxygen metabolism generates free radicals and/or non-radical reactive oxygen species. The mitochondria, through the electron transport chain, are the main generator of these species. The antioxidant defense system has the function of inhibiting and/or reducing the damage caused by the deleterious free radicals and/or non-radical reactive oxygen species. This system is divided into enzymatic (superoxide dismutase, catalase and glutathione peroxidase), and nonenzymatic. The nonenzymatic system consists of a variety of antioxidant substances, which may be endogenous or dietary. This study proposed to review the main mechanisms of reactive oxygen species generation and the role of the most relevant agents of the antioxidant defense system on the biomarkers of oxidative stress. The main exogenous factors that modulate oxidative stress will also be discussed.O estresse oxidativo decorre de um desequilibrio entre a geracao de compostos oxidantes e a atuacao dos sistemas de defesa antioxidante. A geracao de radicais livres e/ou especies reativas nao radicais e resultante do metabolismo de oxigenio. A mitocondria, por meio da cadeia transportadora de eletrons, e a principal fonte geradora. O sistema de defesa antioxidante tem a funcao de inibir e/ou reduzir os danos causados pela acao deleteria dos radicais livres e/ou especies reativas nao radicais. Esse sistema, usualmente, e dividido em enzimatico (superoxido dismutase, catalase e glutationa peroxidase) e nao-enzimatico. No ultimo caso, e constituido por grande variedade de substâncias antioxidantes, que podem ter origem endogena ou dietetica. Objetivou-se revisar os principais mecanismos de geracao de radicais livres, bem como a acao dos agentes mais relevantes do sistema de defesa antioxidante, ressaltando suas implicacoes sobre os marcadores do estresse oxidativo. Tambem serao abordados os principais fatores exogenos moduladores do estresse oxidativo.

Saturated fatty acids trigger TLR4-mediated inflammatory response.

Toll-like receptors (TLR) mediate infection-induced inflammation and sterile inflammation by endogenous molecules. Among the TLR family, TLR4 is the best understood. However, while its downstream signaling pathways have been well defined, not all ligands of TLR4 are currently known. Current evidence suggests that saturated fatty acids (SFA) act as non-microbial TLR4 agonists, and trigger its inflammatory response. Thus, our present review provides a new perspective on the potential mechanism by which SFAs could modulate TLR4-induced inflammatory responses: (1) SFAs can be recognized by CD14-TLR4-MD2 complex and trigger inflammatory pathways, similar to lipopolysaccharide (LPS). (2) SFAs lead to modification of gut microbiota with an overproduction of LPS after a high-fat intake, enhancing this natural TLR4 ligand. (3) In addition, this metabolic endotoxemia leads to an oxidative stress thereby producing atherogenic lipids - oxLDL and oxidized phospholipids - which trigger CD36-TLR4-TLR6 inflammatory response. (4) Also, the high SFA consumption increases the lipemia and the mmLDL and oxLDL formation through oxidative modifications of LDL. The mmLDL, unlike oxLDL, is involved in activation of the CD14-TLR4-MD2 inflammatory pathway. Those molecules can induce TLR4 inflammatory response by MyD88-dependent and/or MyD88-independent pathways that, in turn, promotes the expression of proinflammatory transcript factors such as factor nuclear kappa B (NF-κB), which plays a crucial role in the induction of inflammatory mediators (cytokines, chemokines, or costimulatory molecules) implicated in the development and progression of many chronic diseases.

Role of bariatric-metabolic surgery in the treatment of obese type 2 diabetes with body mass index <35 kg/m2: a literature review.

Bariatric surgery has been used to treat type 2 diabetes mellitus (T2DM); however, its efficacy is still debatable. This literature review analyzed articles that evaluated the effects of bariatric surgery in treatment of T2DM in obese patients with a body mass index (BMI) of <35 kg/m(2). A paired t test was applied for the analysis of pre- and postintervention mean BMI, fasting plasma glucose (FPG), and glycosylated hemoglobin (A1c) values. A significant (P<0.001) reduction in BMI (from 29.95±0.51 kg/m(2) to 24.83±0.44 kg/m(2)), FPG (from 207.86±8.51 mg/dL to 113.54±4.93 mg/dL), and A1c (from 8.89±0.15% to 6.35±0.18%) was observed in 29 articles (n=675). T2DM resolution (A1c <7% without antidiabetes medication) was achieved in 84.0% (n=567) of the subjects. T2DM remission, control, and improvement were observed in 55.41%, 28.59%, and 14.37%, respectively. Only 1.63% (n=11) of the subjects presented similar or worse glycemic control after the surgery. T2DM remission (A1c <6% without antidiabetes medication) was higher after mini-gastric bypass (72.22%) and laparoscopic/Roux-en-Y gastric bypass (70.43%). According to the Foregut and Hindgut Hypotheses, T2DM results from the imbalance between the incretins and diabetogenic signals. The procedures that remove the proximal intestine and do ileal transposition contribute to the increase of glucagon-like peptide-1 levels and improvement of insulin sensitivity. These findings provide preliminary evidence of the benefits of bariatric-metabolic surgery on glycemic control of T2DM obese subjects with a BMI of <35 kg/m(2). However, more clinical trials are needed to investigate the metabolic effects of bariatric surgery in T2DM remission on pre-obese and obese class I patients.

Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors

BACKGROUND & AIMS Altered intestinal permeability has been shown to be associated with metabolic alterations in animal models of obesity, but not in humans. The aim of this study was to assess intestinal permeability in obese women and verify if there is any association with anthropometric measurements, body composition or biochemical variables. METHODS Twenty lean and twenty obese females participated in the study. Anthropometric measurements, body composition and blood pressure were assessed and biochemical analyses were performed. Administration of lactulose and mannitol followed by their quantification in urine was used to assess the intestinal permeability of volunteers. RESULTS The obese group showed lower HDL (p < 0.05), higher fasting glucose, insulin, HOMA index and lactulose excretion than the lean group (p < 0.05), suggesting increased paracellular permeability. Lactulose excretion showed positive correlation (p < 0.05) with waist and abdominal circumference. Blood insulin and the HOMA index also increased with the increase in mannitol and lactulose excretion and in the L/M ratio (p < 0.05). L/M ratio presented a negative correlation with HDL concentration (p < 0.05). CONCLUSIONS We demonstrated that intestinal permeability parameters in obese women are positively correlated with anthropometric measurements and metabolic variables. Therapeutic interventions focused on intestine health and the modulation of intestinal permeability should be explored in the context of obesity.

Dietary total antioxidant capacity is inversely related to central adiposity as well as to metabolic and oxidative stress markers in healthy young adults

BackgroundDietary total antioxidant capacity (TAC) has been assumed as a useful tool to assess the relationship between the cumulative antioxidant food capacity and several chronic disorders. The aim of this cross-sectional study was to investigate the potential relationships of dietary TAC with adiposity, metabolic and oxidative stress markers in healthy young adults.MethodsThis study enrolled 266 healthy subjects (105 men/ 161 women; 22 ± 3 years-old; 22.0 ± 2.7 kg/m2). Dietary intake, anthropometry, blood pressure, lifestyle features, and biochemical data were assessed with validated procedures.ResultsIn linear regression analyses, dietary TAC values were inversely associated with glycemia, total cholesterol:HDL-c ratio, triglycerides and oxidized-LDL concentrations, and positively associated with HDL-c concentrations, independently of gender, age, smoking status, physical activity, vitamin use supplement, waist circumference, energy intake, fatty acid intake. In addition, plasma TAC was negatively correlated with ox-LDL concentrations (r= -0.20, P = 0.003), independently of the assessed confounding variables. Finally, dietary TAC values were inversely related to waist circumference values (r= -0.17, P = 0.005) as well as to lower mild central obesity occurrence (waist circumference ≥ 80/ 94 cm for women/ men, respectively).ConclusionDietary TAC values are inversely associated with glucose and lipid biomarkers as well as with central adiposity measurements in healthy young adults, indicating dietary TAC as a useful tool to assess the health benefits of cumulative antioxidant capacity from food intake. In addition, the independent and inverse relationships of ox-LDL concentrations with dietary and plasma TAC respectively suggest a putative role of antioxidant rich-diet in the link between redox state and atherogenesis at early stage.

Vitamin C and fibre consumption from fruits and vegetables improves oxidative stress markers in healthy young adults.

The aim of the present cross-sectional study was to assess the potential relationships between fruit and vegetable (FV) consumption and some oxidative stress markers in young adults, with particular emphasis on fibre and vitamin C intake. The study enrolled 246 healthy subjects (eighty-eight men and 158 women), with a mean age of 22 (sd 3) years and a mean BMI of 21·9 (sd 2·8) kg/m2. Dietary intake, anthropometry, blood pressure, lifestyle features and blood biochemical data were assessed with validated procedures. Those subjects in the highest tertile (T) of FV consumption ( ≥ 705 g/d) had statistically lower oxidised LDL (ox-LDL) concentrations as well as higher plasma total antioxidant capacity (TAC) and glutathione peroxidase (GPx) activity (P for trend <0·05), after adjusting for sex, age, energy intake, physical activity, smoking, BMI, vitamin supplement use and other confounding factors. Moreover, plasma ox-LDL concentrations showed a decreasing trend and TAC an increasing trend across tertiles of fibre (T3: ≥14 g/d) and vitamin C (T3: ≥150 mg/d) from FV intake, while GPx activity was positively associated with vitamin C intake (P for trend < 0·05). In conclusion, greater FV consumption was independently associated with reduced ox-LDL as well as increased TAC and GPx activity in healthy young adults, with dietary fibre and vitamin C from FV clearly being implicated in this beneficial relationship.