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Dietary Patterns, Food Intake, Nutrients and Physical Activity with Anti-inflammatory Properties

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Sports Nutrition".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 14387

Special Issue Editor


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Guest Editor
1. Department of Nutrition, Food Sciences and Physiology / Centre for Nutrition Research, University of Navarra, 31008 Pamplona, Spain
2. CIBERobn Physiopathology of Obesity and Nutrition, Centre of Biomedical Research Network, ISCIII, Madrid, Spain
3. IDISNA, Navarra’s Health Research Institute, Pamplona, Spain
Interests: hypoxia;omega-3; MaR1; adipose tissue; muscle; altitude; inflammation, oxidative stress, obesity, metabolic syndrome
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Special Issue Information

Dear Colleagues,

Inflammation is a physiological process with an undoubtedly relevant role. Unfortunately, it also has a dark side. For example, this process in its pathological form (usually when it is chronified) is involved in Metabolic Syndrome, Type 2 diabetes, Cardiovascular diseases, Obesity, Cancer, and even Aging. To initiate this pernicious inflammation, three culprits have been mentioned in the scientific literature: oxidative stress, hypoxia, and stress of the endoplasmic reticulum. Each of these can trigger this process either by itself or in conjunction with the others. In this sense, we must bear in mind that the aforementioned medical conditions are responsible for the majority of deaths in developed countries and they are becoming increasingly important in developing countries. To protect living beings from this end, many factors have been thoroughly studied. For example, a dietary pattern world-wide recognised to be anti-inflammatory would be the Mediterranean Diet. Furthermore, a diet which restricts intake but maintains good quality has been linked with lower oxidative stress. In addition, nutrients such as the famous Omega-3 seem to modulate several pathways exerting beneficial actions counteracting inflammation’s deleterious effects. Interestingly, physical activity has been linked to both sides of the inflammation issue, requiring further analysis of its mechanisms of action. We would welcome articles that shed some light in any or several of these areas, or other ones, preferentially in human beings, but animals and cell culture will also be accepted, as well as basic and applied research. Please, do not miss the opportunity of collaborating in an area of great interest.

Dr. Pedro Gonzalez-Muniesa
Guest Editor

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Keywords

  • Aging
  • Metabolic syndrome
  • Hypoxia
  • Oxidative stress

Published Papers (5 papers)

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Research

22 pages, 1602 KiB  
Article
Changes Induced by Aging and Long-Term Exercise and/or DHA Supplementation in Muscle of Obese Female Mice
by Alejandro Martínez-Gayo, Elisa Félix-Soriano, Neira Sáinz, Pedro González-Muniesa and María J. Moreno-Aliaga
Nutrients 2022, 14(20), 4240; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14204240 - 12 Oct 2022
Cited by 4 | Viewed by 2298
Abstract
Obesity and aging promote chronic low-grade systemic inflammation. The aim of the study was to analyze the effects of long-term physical exercise and/or omega-3 fatty acid Docosahexaenoic acid (DHA) supplementation on genes or proteins related to muscle metabolism, inflammation, muscle damage/regeneration and myokine [...] Read more.
Obesity and aging promote chronic low-grade systemic inflammation. The aim of the study was to analyze the effects of long-term physical exercise and/or omega-3 fatty acid Docosahexaenoic acid (DHA) supplementation on genes or proteins related to muscle metabolism, inflammation, muscle damage/regeneration and myokine expression in aged and obese mice. Two-month-old C57BL/6J female mice received a control or a high-fat diet for 4 months. Then, the diet-induced obese (DIO) mice were distributed into four groups: DIO, DIO + DHA, DIO + EX (treadmill training) and DIO + DHA + EX up to 18 months. Mice fed a control diet were sacrificed at 2, 6 and 18 months. Aging increased the mRNA expression of Tnf-α and decreased the expression of genes related to glucose uptake (Glut1, Glut4), muscle atrophy (Murf1, Atrogin-1, Cas-9) and myokines (Metrnl, Il-6). In aged DIO mice, exercise restored several of these changes. It increased the expression of genes related to glucose uptake (Glut1, Glut4), fatty acid oxidation (Cpt1b, Acox), myokine expression (Fndc5, Il-6) and protein turnover, decreased Tnf-α expression and increased p-AKT/AKT ratio. No additional effects were observed when combining exercise and DHA. These data suggest the effectiveness of long-term training to prevent the deleterious effects of aging and obesity on muscle dysfunction. Full article
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13 pages, 324 KiB  
Article
Associations between Family-Based Stress and Dietary Inflammatory Potential among Families with Preschool-Aged Children
by Valerie Hruska, Nitin Shivappa, James R. Hébert, Alison M. Duncan, Jess Haines and David W. L. Ma
Nutrients 2021, 13(5), 1464; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051464 - 26 Apr 2021
Cited by 4 | Viewed by 3250
Abstract
Chronic stress is known to influence dietary choices, and stressed families often report poorer diet quality; however, little is known about how family-based stress is linked with dietary patterns that promote inflammation. This study investigated associations between family-based stress and the inflammatory potential [...] Read more.
Chronic stress is known to influence dietary choices, and stressed families often report poorer diet quality; however, little is known about how family-based stress is linked with dietary patterns that promote inflammation. This study investigated associations between family-based stress and the inflammatory potential of the diet among preschool-aged children and their parents. Parents (n = 212 mothers, n = 146 fathers) and children (n = 130 girls, n = 123 boys; aged 18 months to 5 years) from 241 families participating in the Guelph Family Health Study were included in the analyses. Parents reported levels of parenting distress, depressive symptoms, household chaos, and family functioning. The inflammatory potential of parents’ and children’s diets was quantified using the Dietary Inflammatory Index (DII®), adjusted for total energy intake (i.e., the E-DIITM). E-DII scores were regressed onto family stress using generalized estimating equations to account for shared variance among family clusters. Compared to those in homes with low chaos, parents in chaotic homes had significantly more proinflammatory dietary profiles (β = 0.973; 95% CI: 0.321, 1.624, p = 0.003). Similarly, compared to those in well-functioning families, parents in dysfunctional families had significantly more proinflammatory dietary profiles (β = 0.967; 95% CI: 0.173, 1.761, p = 0.02). No significant associations were found between parents’ E-DII scores and parenting distress or depressive symptoms, nor were any associations found for children’s E-DII scores. Results were not found to differ between males and females. Parents in chaotic or dysfunctional family environments may be at increased risk of chronic disease due to proinflammatory dietary profiles. Children’s dietary inflammatory profiles were not directly associated with family stress; however, indirect connections through family food-related behaviours may exist. Future research should prioritize elucidating these mechanisms. Full article
12 pages, 1207 KiB  
Article
High-Protein, Low-Glycaemic Meal Replacement Decreases Fasting Insulin and Inflammation Markers—A 12-Month Subanalysis of the ACOORH Trial
by Kerstin Kempf, Martin Röhling, Winfried Banzer, Klaus Michael Braumann, Martin Halle, David McCarthy, Hans Georg Predel, Isabelle Schenkenberger, Susanne Tan, Hermann Toplak, Aloys Berg, Stephan Martin and on behalf of ACOORH Study Group
Nutrients 2021, 13(5), 1433; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051433 - 23 Apr 2021
Cited by 10 | Viewed by 2898
Abstract
Lifestyle interventions, including meal replacement, are effective in the prevention and treatment of type-2-diabetes and obesity. Since insulin is the key weight regulator, we hypothesised that the addition of meal replacement to a lifestyle intervention reduces insulin levels more effectively than lifestyle intervention [...] Read more.
Lifestyle interventions, including meal replacement, are effective in the prevention and treatment of type-2-diabetes and obesity. Since insulin is the key weight regulator, we hypothesised that the addition of meal replacement to a lifestyle intervention reduces insulin levels more effectively than lifestyle intervention alone. In the international multicentre randomised controlled ACOORH (Almased Concept against Overweight and Obesity and Related Health Risk) trial, overweight or obese persons who meet the criteria for metabolic syndrome (n = 463) were randomised into two groups. Both groups received nutritional advice focusing on carbohydrate restriction and the use of telemonitoring devices. The intervention group substituted all three main meals per day in week 1, two meals per day in weeks 2–4, and one meal per day in weeks 5–26 with a protein-rich, low-glycaemic meal replacement. Data were collected at baseline and after 1, 3, 6 and 12 months. All datasets providing insulin data (n = 446) were included in this predefined subanalysis. Significantly higher reductions in insulin (−3.3 ± 8.7 µU/mL vs. −1.6 ± 9.8 µU/mL), weight (−6.1 ± 5.2 kg vs. −3.2 ± 4.6 kg), and inflammation markers were observed in the intervention group. Insulin reduction correlated with weight reduction and the highest amount of weight loss (−7.6 ± 4.9 kg) was observed in those participants with an insulin decrease > 2 µU/mL. These results underline the potential for meal replacement-based lifestyle interventions in diabetes prevention, and measurement of insulin levels may serve as an indicator for adherence to carbohydrate restriction. Full article
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16 pages, 921 KiB  
Article
Macronutrient Quality and All-Cause Mortality in the SUN Cohort
by Susana Santiago, Itziar Zazpe, Cesar I. Fernandez-Lazaro, Víctor de la O, Maira Bes-Rastrollo and Miguel Ángel Martínez-González
Nutrients 2021, 13(3), 972; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13030972 - 17 Mar 2021
Cited by 10 | Viewed by 2896
Abstract
No previous study has assessed the relationship between overall macronutrient quality and all-cause mortality. We aimed to prospectively examine the association between a multidimensional macronutrient quality index (MQI) and all-cause mortality in the SUN (Seguimiento Universidad de Navarra) (University of Navarra Follow-Up) study, [...] Read more.
No previous study has assessed the relationship between overall macronutrient quality and all-cause mortality. We aimed to prospectively examine the association between a multidimensional macronutrient quality index (MQI) and all-cause mortality in the SUN (Seguimiento Universidad de Navarra) (University of Navarra Follow-Up) study, a Mediterranean cohort of middle-aged adults. Dietary intake information was obtained from a validated 136-item semi-quantitative food-frequency questionnaire. We calculated the MQI (categorized in quartiles) based on three quality indexes: the carbohydrate quality index (CQI), the fat quality index (FQI), and the healthy plate protein source quality index (HPPQI). Among 19,083 participants (mean age 38.4, 59.9% female), 440 deaths from all causes were observed during a median follow-up of 12.2 years (IQR, 8.3–14.9). No significant association was found between the MQI and mortality risk with multivariable-adjusted hazard ratio (HR) for the highest vs. the lowest quartile of 0.79 (95% CI, 0.59–1.06; Ptrend = 0.199). The CQI was the only component of the MQI associated with mortality showing a significant inverse relationship, with HR between extreme quartiles of 0.64 (95% CI, 0.45–0.90; Ptrend = 0.021). In this Mediterranean cohort, a new and multidimensional MQI defined a priori was not associated with all-cause mortality. Among its three sub-indexes, only the CQI showed a significant inverse relationship with the risk of all-cause mortality. Full article
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15 pages, 1852 KiB  
Article
The Mechanisms of the Anti-Inflammatory and Anti-Apoptotic Effects of Omega-3 Polyunsaturated Fatty Acids during Methotrexate-Induced Intestinal Damage in Cell Line and in a Rat Model
by Tal Koppelmann, Yulia Pollak, Yoav Ben-Shahar, Gregory Gorelik and Igor Sukhotnik
Nutrients 2021, 13(3), 888; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13030888 - 10 Mar 2021
Cited by 12 | Viewed by 2097
Abstract
Background: The aim of this study was to examine the anti-inflammatory and anti-apoptotic patterns of omega-3 polyunsaturated fatty acids (n-3 PUFAs) during methotrexate (MTX) induced intestinal damage in cell culture and in a rat model. Methods: Non-treated and treated with MTX HT 29 [...] Read more.
Background: The aim of this study was to examine the anti-inflammatory and anti-apoptotic patterns of omega-3 polyunsaturated fatty acids (n-3 PUFAs) during methotrexate (MTX) induced intestinal damage in cell culture and in a rat model. Methods: Non-treated and treated with MTX HT 29 and HCT116cells were exposed to increasing doses of n-3 PUFAs and cell viability was evaluated using PrestoBlue® assay. Male Sprague-Dawley rats were divided into 4 experimental groups: Control rats, CONTR+n-3 PUFA rats that were treated with oral n-3 PUFA, MTX rats were treated with MTX given IP, and MTX+n-3 PUFA rats were treated with oral n-3 PUFA before and following injection of MTX. Intestinal mucosal parameters and mucosal inflammation, enterocyte proliferation and apoptosis, TNF-α in mucosal tissue and plasma (ELISA), NF-κB, COX-2, TNF-α, Fas, FasL, Fadd, Bid, Bax and Bcl-2gene and protein levels were determined 72 h following MTX injection. Results: Exposure of HT 29 and HCT116cells to n-3 PUFA attenuated inhibiting effects of MTX on cell viability. MTX-n-3 PUFA rats demonstrated a lower intestinal injury score and enhanced intestinal repair. A significant decrease in enterocyte apoptosis in MTX+n-3 PUFA rats was accompanied by decreased TNF-α, FAS, FasL, FADD and BID mRNA levels. Decreased NF-κB, COX-2 and TNF-α levels in mucosa was accompanied by a decreased number of IELs and macrophages. Conclusions: n-3 PUFAs inhibit NF-κB/COX-2 induced production of pro-inflammatory cytokines and inhibit cell apoptosis mainly by extrinsic pathway in rats with MTX-induced intestinal damage. Full article
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