Red Wine High-Molecular-Weight Polyphenolic Complex: An Emerging Modulator of Human Metabolic Disease Risk and Gut Microbiota

2021 ◽  
Vol 69 (37) ◽  
pp. 10907-10919
Author(s):  
Hao Suo ◽  
Mohammad Rezaul Islam Shishir ◽  
Jianbo Xiao ◽  
Mingfu Wang ◽  
Feng Chen ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Molecular Weight ◽  
Gut Microbiota ◽  
High Molecular Weight ◽  
Red Wine ◽  
Disease Risk ◽  
Metabolic Disease Risk

scholarly journals High Molecular Weight Barley β-Glucan Alters Gut Microbiota Toward Reduced Cardiovascular Disease Risk

2016 ◽  
Vol 7 ◽  
Author(s):  
Yanan Wang ◽  
Nancy P. Ames ◽  
Hein M. Tun ◽  
Susan M. Tosh ◽  
Peter J. Jones ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Molecular Weight ◽  
Gut Microbiota ◽  
High Molecular Weight ◽  
Disease Risk ◽  
Cardiovascular Disease Risk

Advanced glycation end products (AGEs) in metabolic disease: linking diet, inflammation and microbiota

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Giulia Gaudioso ◽  
Debora Collotta ◽  
Fausto Chiazza ◽  
Raffaella Mastrocola ◽  
Alessia Cento ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Gut Microbiota ◽  
Advanced Glycation End Products ◽  
Disease Risk ◽  
In Vivo Studies ◽  
Blood Levels ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
The Impact

AbstractIntroduction:High sugar consumption promotes endogenous formation of advanced glycation end-products (AGEs), a heterogeneous class of molecules originated from non-enzymatic glycation between reducing sugars and free amino groups of proteins, nucleic acids, or lipids. AGEs accumulation in tissues has been linked to aging and diabetes complications. AGEs might also play an independent role in inflammation and development of cardiovascular disease (CVD). Exogenous dietary AGEs, due to excess intake of modern heat-treated foods, might act synergistically with endogenous AGEs, thus contributing to increase inflammation and CVD. A large amount of ingested AGEs reaches the colon, where they might affect gut microbial metabolism, for example, by acting as substrate for colonic bacterial fermentation, driving alterations of microbiota composition and of intestinal permeability. However in vitro and in vivo studies (animal and human) on the impact of AGEs on the gut microbiota are discordant. This study on mice aims to link the modulation of gut microbiota by AGEs-enriched diet (AGE-D) with metabolic and inflammatory markers.Materials and methods:C57BL/6 mice were randomly allocated into the following dietary regimens: Control (n = 24) and AGE-D (n = 20) for 22 weeks. AGE-D was prepared replacing casein (200 g/kg diet) by an equal amount of modified casein where 10% of arginine was glycated with MG-H1 (methylglyoxal 5-hydro-5-methylimidazolone) for a total of 4 μmol of MG-H1 per g of diet. Faeces were collected using metabolic cages (18 h starving) at week 0, 11 and 22 for fecal DNA extraction and 16SrRNA analysis through Illumina MiSeq using V3-V4 targeted primers. After 22 weeks of dietary manipulation, mice were sacrificed, plasma and organ lipid profiles and serum metabolic and inflammatory profiles were determined.Results and discussion:AGE-D caused a significant reduction in the blood levels of two important components of the incretin system, GIP and GLP-1, when compared to control diet, suggestive of unbalance in the incretin-insulin axis. AGE-D exposure was associated with a significant increase in systemic concentrations of inflammatory cytokines, e.g. IL-1β and IL-17, and PAI-1, which has been suggested as both reliable marker and critical mediator of cellular senescence. We will present how AGEs impact on microbiome community structure and correlate changes in gut microbiota with GIP and GLP-1 levels.Conclusions:AGEs, characteristic of modern processed foods, appear to impact on the incretin-insulin axis, a key regulator of metabolic disease risk. Diets rich in AGEs may mediate these physiological effects at least in part, by reshaping intestinal microbiota structure.

Sex differences in lipid metabolism and metabolic disease risk

2012 ◽  
Vol 90 (2) ◽  
pp. 124-141 ◽  
Author(s):  
Michael G. Sugiyama ◽  
Luis B. Agellon
Keyword(s):  
Metabolic Disease ◽  
Sex Differences ◽  
Body Fat ◽  
Molecular Mechanisms ◽  
Sex Chromosome ◽  
Disease Risk ◽  
Treatment Strategies ◽  
Metabolic Complications ◽  
Metabolic Disease Risk ◽  
Organ Systems

The ability of nutrients to regulate specific metabolic pathways is often overshadowed by their role in basic sustenance. Consequently, the mechanisms whereby these nutrients protect against or promote a variety of acquired metabolic syndromes remains poorly understood. Premenopausal women are generally protected from the adverse effects of obesity despite having a greater proportion of body fat than men. Menopause is often associated with a transformation in body fat morphology and a gradual increase in the susceptibility to metabolic complications, eventually reaching the point where women and men are at equal risk. These phenomena are not explained solely by changes in food preference or nutrient intake suggesting an important role for the sex hormones in regulating the metabolic fate of nutrients and protecting against metabolic disease pathophysiology. Here, we discuss how differences in the acquisition, trafficking, and subceullular metabolism of fats and other lipid soluble nutrients in major organ systems can create overt sex-specific phenotypes, modulate metabolic disease risk, and contribute to the rise in obesity in the modern sedentary climate. Identifying the molecular mechanisms underpinning sex differences in fat metabolism requires the unravelling of the interactions among sex chromosome effects, the hormonal milieu, and diet composition. Understanding the mechanisms that give rise to sex differences in metabolism will help to rationalize treatment strategies for the management of sex-specific metabolic disease risk factors.

scholarly journals Lactational programming of glucose homeostasis: a window of opportunity

Reproduction ◽  
2018 ◽  
Vol 156 (2) ◽  
pp. R23-R42 ◽  
Author(s):  
Lindsay Ellsworth ◽  
Emma Harman ◽  
Vasantha Padmanabhan ◽  
Brigid Gregg
Keyword(s):  
Metabolic Disease ◽  
Glucose Homeostasis ◽  
Critical Period ◽  
Disease Risk ◽  
Milk Composition ◽  
Lactation Period ◽  
Cellular Functions ◽  
Environmental Endocrine Disruptors ◽  
Metabolic Disease Risk ◽  
Underlying Mechanisms

The window of lactation is a critical period during which nutritional and environmental exposures impact lifelong metabolic disease risk. Significant organ and tissue development, organ expansion and maturation of cellular functions occur during the lactation period, making this a vulnerable time during which transient insults can have lasting effects. This review will cover current literature on factors influencing lactational programming such as milk composition, maternal health status and environmental endocrine disruptors. The underlying mechanisms that have the potential to contribute to lactational programming of glucose homeostasis will also be addressed, as well as potential interventions to reduce offspring metabolic disease risk.

scholarly journals Cardio-metabolic disease risk factors among South Asian labour migrants to the Middle East: a scoping review and policy analysis

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Shiva Raj Mishra ◽  
Saruna Ghimire ◽  
Chandni Joshi ◽  
Bishal Gyawali ◽  
Archana Shrestha ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Disease ◽  
Middle East ◽  
Policy Analysis ◽  
South Asian ◽  
Scoping Review ◽  
Disease Risk ◽  
Metabolic Disease Risk

scholarly journals Weight Loss Efficacy of 4-Hour Versus 6-Hour Time Restricted Feeding in Adults with Obesity

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 584-584
Author(s):  
Sofia Cienfuegos ◽  
Kelsey Gabel ◽  
Faiza Kalam ◽  
Mark Ezpeleta ◽  
Vasiliki Pavlou ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Disease ◽  
Insulin Resistance ◽  
Blood Pressure ◽  
Weight Loss ◽  
Body Weight ◽  
Fat Mass ◽  
Disease Risk ◽  
Metabolic Disease Risk ◽  
Ad Libitum

Abstract Objectives This study was undertaken to compare the effects of 4-h TRF to that of 6-h TRF on body weight, body composition, and metabolic disease risk factors in adults with obesity. We hypothesized that 4-h TRF would produce the greatest decreases in body weight, fat mass, blood pressure, and insulin resistance, compared to 6-h TRF. Methods Adults with obesity (n = 49) were randomized to 1 of 3 interventions for 8 weeks: 4-h TRF (ad libitum eating between 3:00 to 7:00 pm, water fasting between 7:00 to 3:00 pm); 6-h TRF (ad libitum eating between 1:00 to 7:00 pm, water fasting between 7:00 to 1:00 pm); or control (ad libitum food intake with no timing restrictions). Results Body weight decreased similarly in the 4-h TRF group (–3.3 ± 0.5%) and 6-h TRF group (–2.6 ± 0.5%) relative to controls over 8 weeks (P < 0.001). Fat mass, blood pressure and insulin sensitivity also decreased in the 4-h TRF and 6-h TRF groups versus controls. LDL cholesterol, HDL cholesterol, triglycerides, fasting glucose, and HbA1c were not significantly different from controls after 8 weeks. Conclusions This is the first trial to examine the effects of 4-h vs. 6-h TRF on body weight and metabolic disease risk factors. We show here that 8 weeks of 4-h and 6-h TRF decreases body weight by ∼3–4% relative to controls. We also demonstrate that this fasting regimen produces significant reductions in blood pressure, fat mass, insulin and insulin resistance. These preliminary data offer promise for the use of 4-h and 6-h TRF as a weight loss techniques in adults with obesity, but larger, longer-term trials are needed to confirm these findings. Funding Sources Department of Kinesiology and Nutrition, University of Illinois Chicago

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