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Habitual intake of dietary advanced glycation end products is not associated with generalized microvascular function-the Maastricht Study.
Linkens, AMA, Houben, AJHM, Kroon, AA, Schram, MT, Berendschot, TTJM, Webers, CAB, van Greevenbroek, M, Henry, RMA, de Galan, B, Stehouwer, CDA, et al
The American journal of clinical nutrition. 2022;(2):444-455
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Abstract
BACKGROUND Endogenously formed advanced glycation end products (AGEs) may be important drivers of microvascular dysfunction and the microvascular complications of diabetes. AGEs are also formed in food products, especially during preparation methods involving dry heat. OBJECTIVES We aimed to assess cross-sectional associations between dietary AGE intake and generalized microvascular function in a population-based cohort. METHODS In 3144 participants of the Maastricht Study (mean ± SD age: 60 ± 8 y, 51% men) the dietary AGEs Nε-(carboxymethyl)lysine (CML), Nε-(1-carboxyethyl)lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) were estimated using the combination of our ultra-performance LC-tandem MS dietary AGE database and an FFQ. Microvascular function was determined in the retina as flicker light-induced arteriolar and venular dilation and as central retinal arteriolar and venular equivalents, in plasma as a z score of endothelial dysfunction biomarkers (soluble vascular adhesion molecule 1 and soluble intracellular adhesion molecule 1, soluble E-selectin, and von Willebrand factor), in skin as the heat-induced skin hyperemic response, and in urine as 24-h albuminuria. Associations were evaluated using multiple linear regression adjusting for demographic, cardiovascular, lifestyle, and dietary factors. RESULTS Overall, intakes of CML, CEL, and MG-H1 were not associated with the microvascular outcomes. Although higher intake of CEL was associated with higher flicker light-induced venular dilation (β percentage change over baseline: 0.14; 95% CI: 0.02, 0.26) and lower plasma biomarker z score (β: -0.04 SD; 95% CI: -0.08, -0.00 SD), the effect sizes were small and their biological relevance can be questioned. CONCLUSIONS We did not show any strong association between habitual intake of dietary AGEs and generalized microvascular function. The contribution of dietary AGEs to generalized microvascular function should be further assessed in randomized controlled trials using specifically designed dietary interventions.
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The impact of dietary macronutrient intake on cognitive function and the brain.
Muth, AK, Park, SQ
Clinical nutrition (Edinburgh, Scotland). 2021;(6):3999-4010
Abstract
Macronutrients - carbohydrates, fats, and proteins - supply the nutrients required for optimal functioning. Inadequate intake compromises both physical and brain health. We synthesized research on macronutrients from whole meals on cognitive function in healthy adults and identified underlying mechanisms. Intake of simple carbohydrates ('sugars') is consistently associated with decreased global cognition whereas consumption of complex carbohydrates correlates with successful brain aging and improved memory both in the short- and long-term. Saturated fatty acid intake correlates with decreased memory and learning scores whereas omega-3 intake correlates positively with memory scores. Protein intake boosts executive function and working memory when task-demands are high. Individual differences affecting the macronutrient-cognition relationship are age, physical activity, and glucose metabolism. Neural correlates reflect findings on cognitive functions: cortical thickness and cerebral amyloid burden correlate with sugar intake, inflammatory status and cerebral glucose metabolism correlate with fatty acid intake. Key mechanisms by which dietary macronutrients affect the brain and cognition include glucose and insulin metabolism, neurotransmitter actions, and cerebral oxidation and inflammation. In conclusion, macronutrient intake affects cognitive function both acutely and in the long-term, involving peripheral and central mechanisms. A healthy diet supports brain integrity and functionality, whereas inadequate nutrition compromises it. Studying diet can be key to nutritional recommendations, thereby improving the landscape of mental health and healthy brain aging.
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A Link between Chronic Kidney Disease and Gut Microbiota in Immunological and Nutritional Aspects.
Mertowska, P, Mertowski, S, Wojnicka, J, Korona-Głowniak, I, Grywalska, E, Błażewicz, A, Załuska, W
Nutrients. 2021;(10)
Abstract
Chronic kidney disease (CKD) is generally progressive and irreversible, structural or functional renal impairment for 3 or more months affecting multiple metabolic pathways. Recently, the composition, dynamics, and stability of a patient's microbiota has been noted to play a significant role during disease onset or progression. Increasing urea concentration during CKD can lead to an acceleration of the process of kidney injury leading to alterations in the intestinal microbiota that can increase the production of gut-derived toxins and alter the intestinal epithelial barrier. A detailed analysis of the relationship between the role of intestinal microbiota and the development of inflammation within the symbiotic and dysbiotic intestinal microbiota showed significant changes in kidney dysfunction. Several recent studies have determined that dietary factors can significantly influence the activation of immune cells and their mediators. Moreover, dietary changes can profoundly affect the balance of gut microbiota. The aim of this review is to present the importance and factors influencing the differentiation of the human microbiota in the progression of kidney diseases, such as CKD, IgA nephropathy, idiopatic nephropathy, and diabetic kidney disease, with particular emphasis on the role of the immune system. Moreover, the effects of nutrients, bioactive compounds on the immune system in development of chronic kidney disease were reviewed.
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Impact of Genetic Polymorphism on Response to Therapy in Non-Alcoholic Fatty Liver Disease.
Martínez-Montoro, JI, Cornejo-Pareja, I, Gómez-Pérez, AM, Tinahones, FJ
Nutrients. 2021;(11)
Abstract
In the last decades, the global prevalence of non-alcoholic fatty liver disease (NAFLD) has reached pandemic proportions with derived major health and socioeconomic consequences; this tendency is expected to be further aggravated in the coming years. Obesity, insulin resistance/type 2 diabetes mellitus, sedentary lifestyle, increased caloric intake and genetic predisposition constitute the main risk factors associated with the development and progression of the disease. Importantly, the interaction between the inherited genetic background and some unhealthy dietary patterns has been postulated to have an essential role in the pathogenesis of NAFLD. Weight loss through lifestyle modifications is considered the cornerstone of the treatment for NAFLD and the inter-individual variability in the response to some dietary approaches may be conditioned by the presence of different single nucleotide polymorphisms. In this review, we summarize the current evidence on the influence of the association between genetic susceptibility and dietary habits in NAFLD pathophysiology, as well as the role of gene polymorphism in the response to lifestyle interventions and the potential interaction between nutritional genomics and other emerging therapies for NAFLD, such as bariatric surgery and several pharmacologic agents.
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Nutrient-Induced Cellular Mechanisms of Gut Hormone Secretion.
Lu, VB, Gribble, FM, Reimann, F
Nutrients. 2021;(3)
Abstract
The gastrointestinal tract can assess the nutrient composition of ingested food. The nutrient-sensing mechanisms in specialised epithelial cells lining the gastrointestinal tract, the enteroendocrine cells, trigger the release of gut hormones that provide important local and central feedback signals to regulate nutrient utilisation and feeding behaviour. The evidence for nutrient-stimulated secretion of two of the most studied gut hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), along with the known cellular mechanisms in enteroendocrine cells recruited by nutrients, will be the focus of this review. The mechanisms involved range from electrogenic transporters, ion channel modulation and nutrient-activated G-protein coupled receptors that converge on the release machinery controlling hormone secretion. Elucidation of these mechanisms will provide much needed insight into postprandial physiology and identify tractable dietary approaches to potentially manage nutrition and satiety by altering the secreted gut hormone profile.
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Calcium Absorption from Food Products: Food Matrix Effects.
Shkembi, B, Huppertz, T
Nutrients. 2021;(1)
Abstract
This article reviews physicochemical aspects of calcium absorption from foods. Notable differences are observed between different food products in relation to calcium absorption, which range from <10% to >50% of calcium in the foods. These differences can be related to the interactions of calcium with other food components in the food matrix, which are affected by various factors, including fermentation, and how these are affected by the conditions encountered in the gastrointestinal tract. Calcium absorption in the intestine requires calcium to be in an ionized form. The low pH in the stomach is critical for solubilization and ionization of calcium salts present in foods, although calcium oxalate complexes remain insoluble and thus poorly absorbable. In addition, the rate of gastric transit can strongly affect fractional absorption of calcium and a phased release of calcium into the intestine, resulting in higher absorption levels. Dairy products are the main natural sources of dietary calcium in many diets worldwide, which is attributable to their ability to provide high levels of absorbable calcium in a single serving. For calcium from other food products, lower levels of absorbable calcium can limit contributions to bodily calcium requirements.
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The Complex Interplay between Immunonutrition, Mast Cells, and Histamine Signaling in COVID-19.
Kakavas, S, Karayiannis, D, Mastora, Z
Nutrients. 2021;(10)
Abstract
There is an ongoing need for new therapeutic modalities against SARS-CoV-2 infection. Mast cell histamine has been implicated in the pathophysiology of COVID-19 as a regulator of proinflammatory, fibrotic, and thrombogenic processes. Consequently, mast cell histamine and its receptors represent promising pharmacological targets. At the same time, nutritional modulation of immune system function has been proposed and is being investigated for the prevention of COVID-19 or as an adjunctive strategy combined with conventional therapy. Several studies indicate that several immunonutrients can regulate mast cell activity to reduce the de novo synthesis and/or release of histamine and other mediators that are considered to mediate, at least in part, the complex pathophysiology present in COVID-19. This review summarizes the effects on mast cell histamine of common immunonutrients that have been investigated for use in COVID-19.
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Dietary Selenium Regulates microRNAs in Metabolic Disease: Recent Progress.
Huang, X, Dong, YL, Li, T, Xiong, W, Zhang, X, Wang, PJ, Huang, JQ
Nutrients. 2021;(5)
Abstract
Selenium (Se) is an essential element for the maintenance of a healthy physiological state. However, due to environmental and dietary factors and the narrow safety range of Se, diseases caused by Se deficiency or excess have gained considerable traction in recent years. In particular, links have been identified between low Se status, cognitive decline, immune disorders, and increased mortality, whereas excess Se increases metabolic risk. Considerable evidence has suggested microRNAs (miRNAs) regulate interactions between the environment (including the diet) and genes, and play important roles in several diseases, including cancer. MiRNAs target messenger RNAs to induce changes in proteins including selenoprotein expression, ultimately generating disease. While a plethora of data exists on the epigenetic regulation of other dietary factors, nutrient Se epigenetics and especially miRNA regulated mechanisms remain unclear. Thus, this review mainly focuses on Se metabolism, pathogenic mechanisms, and miRNAs as key regulatory factors in Se-related diseases. Finally, we attempt to clarify the regulatory mechanisms underpinning Se, miRNAs, selenoproteins, and Se-related diseases.
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Nutrient Intake and Gut Microbial Genera Changes after a 4-Week Placebo Controlled Galacto-Oligosaccharides Intervention in Young Females.
Johnstone, N, Dart, S, Knytl, P, Nauta, A, Hart, K, Cohen Kadosh, K
Nutrients. 2021;(12)
Abstract
Recent interest in the gut-brain-axis has highlighted the potential of prebiotics to impact wellbeing, and to affect behavioral change in humans. In this clinical trial, we examined the impact of four-weeks daily supplementation of galacto-oligosaccharides (GOS) on self-reported nutrient intake and relationships on gut microbiota in a four-week two-armed parallel double-blind placebo controlled GOS supplement trial in young adult females. Food diaries and stool samples were collected prior to and following 28 days of supplement consumption. It was found that four weeks of GOS supplementation influenced macronutrient intake, as evident by reduced carbohydrate and sugars and increased fats intake. Further analysis showed that the reduction in carbohydrates was predicted by increasing abundances of Bifidobacterium in the GOS group in comparison to the placebo group. This suggests that Bifidobacterium increase via GOS supplementation may help improve the gut microbiota composition by altering the desire for specific types of carbohydrates and boosting Bifidobacterium availability when fiber intake is below recommended levels, without compromising appetite for fiber from food.
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Food and Nutrition in the Pathogenesis of Liver Damage.
Mega, A, Marzi, L, Kob, M, Piccin, A, Floreani, A
Nutrients. 2021;(4)
Abstract
The liver is an important organ and plays a key role in the regulation of metabolism and in the secretion, storage, and detoxification of endogenous and exogenous substances. The impact of food and nutrition on the pathophysiological mechanisms of liver injury represents a great controversy. Several environmental factors including food and micronutrients are involved in the pathogenesis of liver damage. Conversely, some xenobiotics and micronutrients have been recognized to have a protective effect in several liver diseases. This paper offers an overview of the current knowledge on the role of xenobiotics and micronutrients in liver damage.