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Influence of Carbohydrates Intake on Inflammation

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

Deadline for manuscript submissions: closed (10 September 2021) | Viewed by 18724

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Special Issue Editor

Prof. Dr. David C. Nieman

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Guest Editor

1. Department of Biology, Appalachian State University, Boone, NC 28608, USA
2. Director of the Human Performance Laboratory, North Carolina Research Campus, Kannapolis, NC 28081, USA
Interests: sports nutrition; exercise; immunology; inflammation; obesity; metabolomics; proteomics; lipid mediators
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Special Issue Information

Dear Colleagues,

Dietary carbohydrates come in many forms, including monosaccharides (glucose, galactose, fructose, xylose), disaccharides (sucrose, lactose, maltose, trehalose), polyols (sorbitol, mannitol), oligosaccharides (maltodextrins, raffinose, stachyose, fructo-oligosaccharides), and polysaccharides (amylose, amylopectin, modified starches, glycogen, cellulose, hemicellulose, pectins, hydrocolloids). Epidemiological and randomized clinical trials indicate that systemic inflammation undergirds most of the common chronic diseases and can be linked in part to dietary patterns and the types of carbohydrates consumed. Healthy dietary patterns high in dietary fiber and low in processed sugars have been linked to decreased serum C-reaction protein (CRP) and other biomarkers of inflammation. Conversely, diets high in processed sugars and refined starches promote chronic low-grade inflammation. The physiological context, however, is important when evaluating the relationship between dietary carbohydrates and inflammation. For example, individuals running and cycling for prolonged distances experience reduced post-exercise inflammation when ingesting 20–60 grams of sugars each hour. By contrast, very low carbohydrate diets may reduce inflammation in overweight individuals with the metabolic syndrome because they have an inherent inability to process carbohydrates in a healthy manner. This Special Issue will include manuscripts that focus on the complex relationship between dietary carbohydrates and inflammation across all physiological and disease states.

Prof. Dr. David C. Nieman
Guest Editor

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Keywords

Inflammation
Carbohydrates
Cytokines
C-reactive protein
Exercise
Metabolic syndrome
Sugars
Dietary fiber
Oligosaccharides
Polysaccharides
Polyols

Published Papers (4 papers)

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Research

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19 pages, 1845 KiB

Open AccessArticle

Anti-Inflammatory Properties of Fructo-Oligosaccharides in a Calf Lung Infection Model and in Mannheimia haemolytica-Infected Airway Epithelial Cells

by Yang Cai, Myrthe S. Gilbert, Walter J. J. Gerrits, Gert Folkerts and Saskia Braber

Nutrients 2021, 13(10), 3514; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103514 - 06 Oct 2021

Cited by 5 | Viewed by 2091

Abstract

Emerging antimicrobial-resistant pathogens highlight the importance of developing novel interventions. Here, we investigated the anti-inflammatory properties of Fructo-oligosaccharides (FOS) in calf lung infections and in airway epithelial cells stimulated with pathogens, and/or bacterial components. During a natural exposure, 100 male calves were fed milk replacer with or without FOS for 8 weeks. Then, immune parameters and cytokine/chemokine levels in the bronchoalveolar lavage fluid (BALF) and blood were measured, and clinical scores were investigated. Calf primary bronchial epithelial cells (PBECs) and human airway epithelial cells (A549) were treated with Mannheimia haemolytica, lipopolysaccharides (LPS), and/or flagellin, with or without FOS pretreatment. Thereafter, the cytokine/chemokine levels and epithelial barrier function were examined. Relative to the control (naturally occurring lung infections), FOS-fed calves had greater macrophage numbers in BALF and lower interleukin (IL)-8, IL-6, and IL-1β concentrations in the BALF and blood. However, FOS did not affect the clinical scores. At slaughter, FOS-fed calves had a lower severity of lung lesions compared to the control. Ex vivo, FOS prevented M. haemolytica-induced epithelial barrier dysfunction. Moreover, FOS reduced M. haemolytica- and flagellin-induced (but not LPS-induced) IL-8, TNF-α, and IL-6 release in PBECs and A549 cells. Overall, FOS had anti-inflammatory properties during the natural incidence of lung infections but had no effects on clinical symptoms. Full article

(This article belongs to the Special Issue Influence of Carbohydrates Intake on Inflammation)

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15 pages, 675 KiB

Open AccessArticle

Identification of Inflammatory and Disease-Associated Plasma Proteins that Associate with Intake of Added Sugar and Sugar-Sweetened Beverages and Their Role in Type 2 Diabetes Risk

by Stina Ramne, Isabel Drake, Ulrika Ericson, Jan Nilsson, Marju Orho-Melander, Gunnar Engström and Emily Sonestedt

Nutrients 2020, 12(10), 3129; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12103129 - 14 Oct 2020

Cited by 12 | Viewed by 4633

Abstract

It has been suggested that high intake of added sugar and sugar-sweetened beverages (SSBs) increase the level of circulating inflammatory proteins and that chronic inflammation plays a role in type 2 diabetes (T2D) development. We aim to examine how added sugar and SSB intake associate with 136 measured plasma proteins and C-reactive protein (CRP) in the Malmö Diet and Cancer–Cardiovascular Cohort (n = 4382), and examine if the identified added sugar- and SSB-associated proteins associate with T2D incidence. A two-step iterative resampling approach was used to internally replicate proteins that associated with added sugar and SSB intake. Nine proteins were identified to associate with added sugar intake, of which only two associated with T2D incidence (p < 0.00045). Seven proteins were identified to associate with SSB intake, of which six associated strongly with T2D incidence (p < 6.9 × 10⁻⁸). No significant associations were observed between added sugar and SSB intake and CRP concentrations. In summary, our elucidation of the relationship between plasma proteome and added sugar and SSB intake, in relation to future T2D risk, demonstrated that SSB intake, rather than the total intake of added sugar, was related to a T2D-pathological proteomic signature. However, external replication is needed to verify the findings. Full article

(This article belongs to the Special Issue Influence of Carbohydrates Intake on Inflammation)

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14 pages, 2389 KiB

Open AccessArticle

Physiologic Effects of Exogenous Dextrose in Murine Klebsiella pneumoniae Sepsis Vary by Route of Provision

by Byron Chuan, Lanping Guo, Bryce Cooper, Sagar Rawal, Teresa Gallego-Martin, Yingze Zhang, Bryan J. McVerry, Christopher P. O’Donnell and Faraaz Ali Shah

Nutrients 2020, 12(10), 2901; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12102901 - 23 Sep 2020

Cited by 2 | Viewed by 2670

Abstract

Sepsis is characterized by a dysregulated immune response to infection. Nutrition is important in the care of septic patients, but the effects of specific nutrients on inflammation in sepsis are not well defined. Our prior work has shown benefits from early enteral dextrose infusion in a preclinical endotoxemia model of sepsis. In the current study, we extend our initial work to examine the effects of dextrose infusions, varying by route of administration, on inflammation and glycemic control in a more clinically relevant and translational model of Klebsiella pneumoniae (KP) bacteremia. Ten-week old C57BL6/J male mice (n = 31) underwent the implantation of indwelling vascular catheters, followed by inoculation with oropharyngeal KP. The mice were randomized 24 h after inoculation to (1) intravenous (IV) dextrose, (2) enteral dextrose, or (3) enteral saline (control) to study the effects on systemic inflammation, hemodynamics, and glycemic control. At 72 h, 77% of the control mice died, whereas IV dextrose induced 100% mortality, associated with increased inflammation, hyperglycemia, and hypotension. Enteral dextrose reduced mortality to 27%, promoted euglycemia, and reduced inflammation compared to IV dextrose. We conclude, in a bacteremic model of sepsis, that enteral (but not IV) dextrose administration is protective, suggesting that the route of nutrient support influences inflammation in sepsis. Full article

(This article belongs to the Special Issue Influence of Carbohydrates Intake on Inflammation)

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Review

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14 pages, 408 KiB

Open AccessReview

Glycemic Variability and CNS Inflammation: Reviewing the Connection

by Charles Watt, Elizabeth Sanchez-Rangel and Janice Jin Hwang

Nutrients 2020, 12(12), 3906; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12123906 - 21 Dec 2020

Cited by 30 | Viewed by 6445

Abstract

Glucose is the primary energy source for the brain, and exposure to both high and low levels of glucose has been associated with numerous adverse central nervous system (CNS) outcomes. While a large body of work has highlighted the impact of hyperglycemia on peripheral and central measures of oxidative stress, cognitive deficits, and vascular complications in Type 1 and Type 2 diabetes, there is growing evidence that glycemic variability significantly drives increased oxidative stress, leading to neuroinflammation and cognitive dysfunction. In this review, the latest data on the impact of glycemic variability on brain function and neuroinflammation will be presented. Because high levels of oxidative stress have been linked to dysfunction of the blood–brain barrier (BBB), special emphasis will be placed on studies investigating the impact of glycemic variability on endothelial and vascular inflammation. The latest clinical and preclinical/in vitro data will be reviewed, and clinical/therapeutic implications will be discussed. Full article

(This article belongs to the Special Issue Influence of Carbohydrates Intake on Inflammation)

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