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Curcumin, a natural polyphenolic component from Curcuma longa roots, is the main bioactive component of turmeric spice and has gained increasing interest due to its proposed anti-cancer, anti-obesity, anti-inflammatory, antioxidant, and lipid-lowering effects, in addition to its thermogenic capacity. While intake from dietary sources such as curry may be sufficient to affect the intestinal microbiome and thus may act indirectly, intact curcumin in the body may be too low (<1 microM) and not sufficient to affect signaling and gene expression, as observed in vitro with cultured cells (10–20 microM). Several strategies can be envisioned to increase curcumin levels in the body, such as decreasing its metabolism or increasing absorption through the formation of nanoparticles. However, since high curcumin levels could also lead to undesired regulatory effects on cellular signaling and gene expression, such studies may need to be carefully monitored. Here, we review the bioavailability of curcumin and to what extent increasing curcumin levels using nanoformulations may increase the bioavailability and bioactivity of curcumin and its metabolites. This enhancement could potentially amplify the disease-preventing effects of curcumin, often by leveraging its robust antioxidant properties. [ABSTRACT FROM AUTHOR]

Obesity is the result of the long‐term energy imbalance between the excess calories consumed and the few calories expended. Reducing the intake of energy dense foods (fats, sugars), and strategies such as fasting and caloric restriction can promote body weight loss. Not only energy in terms of calories, but also the specific composition of the diet can affect the way the food is absorbed and how its energy is stored, used or dissipated. Recent research has shown that bioactive components of food, such as polyphenols and vitamins, can influence obesity and its pathologic complications such as insulin resistance, inflammation and metabolic syndrome. Individual micronutrients can influence lipid turnover but for long‐term effects on weight stability, dietary patterns containing several micronutrients may be required. At the molecular level, these molecules modulate signaling and the expression of genes that are involved in the regulation of energy intake, lipid metabolism, adipogenesis into white, beige and brown adipose tissue, thermogenesis, lipotoxicity, adipo/cytokine synthesis, and inflammation. Higher concentrations of these molecules can be reached in the intestine, where they can modulate the composition and action of the microbiome. In this review, the molecular mechanisms by which bioactive compounds and vitamins modulate energy metabolism, inflammation and obesity are discussed. [ABSTRACT FROM AUTHOR]

Dietary restriction (DR) reduces adiposity and improves metabolism in patients with one or more symptoms of metabolic syndrome. Nonetheless, it remains elusive whether the benefits of DR in humans are mediated by calorie or nutrient restriction. This study was conducted to determine whether isocaloric dietary protein restriction is sufficient to confer the beneficial effects of dietary restriction in patients with metabolic syndrome. We performed a prospective, randomized controlled dietary intervention under constant nutritional and medical supervision. Twenty-one individuals diagnosed with metabolic syndrome were randomly assigned for caloric restriction (CR; n = 11, diet of 5941 ± 686 KJ per day) or isocaloric dietary protein restriction (PR; n = 10, diet of 8409 ± 2360 KJ per day) and followed for 27 days. Like CR, PR promoted weight loss due to a reduction in adiposity, which was associated with reductions in blood glucose, lipid levels, and blood pressure. More strikingly, both CR and PR improved insulin sensitivity by 62.3% and 93.2%, respectively, after treatment. Fecal microbiome diversity was not affected by the interventions. Adipose tissue bulk RNA-Seq data revealed minor changes elicited by the interventions. After PR, terms related to leukocyte proliferation were enriched among the upregulated genes. Protein restriction is sufficient to confer almost the same clinical outcomes as calorie restriction without the need for a reduction in calorie intake. The isocaloric characteristic of the PR intervention makes this approach a more attractive and less drastic dietary strategy in clinical settings and has more significant potential to be used as adjuvant therapy for people with metabolic syndrome. [ABSTRACT FROM AUTHOR]

Introduction: Background: reduced cognitive performance has been observed in patients with severe obesity. Bariatric surgery and subsequent adipose tissue loss seem to affect cognitive functioning positively; however, improvement predictors are not well established. Aim: to evaluate the cognitive performance and the nutritional status of patients with severe obesity 6-month after bariatric surgery. Methods: we assessed the neuropsychological performance of 22 patients with obesity (body mass index: ~ 42.9 kg/m²). The nutritional evaluation consisted of the routine tests performed in the baseline and postoperative periods. Lastly, we calculated the correlation between neuropsychological assessment results and blood biomarkers. Results: the patients did not present cognitive impairment in the preoperative assessment, but performed below the standard range. The patients underwent significant weight loss after 6 months from surgery (~ 22 kg), with a change in obesity class III to I. Also, the patients presented a significant improvement in attention, mental flexibility, inhibitory control, and processing speed. Additionally, we observed a significant improvement in serum folic acid (108 %), gamma-glutamyl transferase (-41 %), uric acid (-32 %), ferritin (-28 %), triglycerides (-19 %), and high-density lipoprotein (9 %). Lastly, we found a moderate positive correlation between processing speed and body weight (r = 0.46), gamma-glutamyl transferase (r = 0.54), and total protein and mental flexibility (r = 0.75). Conclusion: bariatric surgery promoted significant weight loss and improved attention, mental flexibility, processing speed, and several nutritional biomarkers. Nevertheless, the surgery had limited effects on other cognitive functions such as short- and long-term memory and language. [ABSTRACT FROM AUTHOR]

Short bowel syndrome is a severe malabsorption disorder, and prolonged parenteral nutrition is essential for survival in some cases. Among the undesirable effects of long-term parenteral nutrition is an increase in proinflammatory cytokines. The aim of the present study was to measure the serum levels of interleukin-6, interleukin-10, tumor necrosis factor alpha, and transforming growth factor beta, in patients with short bowel syndrome on cyclic parenteral nutrition and patients who had previously received but no longer require parenteral nutrition. The study was cross-sectional and observational. Three groups were studied as follows: Parenteral nutrition group, 9 patients with short bowel syndrome that receive cyclic parenteral nutrition; Oral nutrition group, 10 patients with the same syndrome who had been weaned off parenteral nutrition for at least 1 year prior to the study; Control group, 13 healthy adults, matched for age and sex to parenteral and oral groups. The following data were collected: age, tobacco use, drug therapies, dietary intake, body weight, height, blood collection. All interleukins were significantly higher in the parenteral group compared with the control group as follows: interleukin-6: 22 ± 19 vs 1.5 ± 1.4 pg/mL, P = .0002; transforming growth factor β : 854 ± 204 vs 607 ± 280 pg/mL, P = .04; interleukin-10: 8 ± 37 vs 0.6 ± 4, P = .03; tumor necrosis factor α : 20 ± 8 vs 8 ± 4 pg/mL, P < .0001. We concluded that parenteral nutrition in short bowel syndrome patients, regardless of its duration, increases serum proinflammatory cytokines. [ABSTRACT FROM AUTHOR]