scholarly journals Understanding the role of gut microbiome in metabolic disease risk

2014 ◽  
Vol 77 (1-2) ◽  
pp. 236-244 ◽  
Author(s):  
Yolanda Sanz ◽  
Marta Olivares ◽  
Ángela Moya-Pérez ◽  
Carlo Agostoni
2006 ◽  
Vol 65 (1) ◽  
pp. 125-134 ◽  
Author(s):  
Louise M. Aston

There is growing evidence that the type of carbohydrate consumed is important in relation to metabolic disease risk, and there is currently particular interest in the role of low-glycaemic-index (GI) foods. Observational studies have associated low-GI diets with decreased risk of type 2 diabetes and CHD, and improvements in various metabolic risk factors have been seen in some intervention studies. However, findings have been mixed and inconsistent. There are a number of plausible mechanisms for the effects of these foods on disease risk, which arise from the differing metabolic responses to low- and high-GI foods, with low-GI foods resulting in reductions in hyperglycaemia, hyperinsulinaemia and late postprandial circulating NEFA levels. Low-GI foods may also increase satiety and delay the return of hunger compared with high-GI foods, which could translate into reduced energy intake at later time points. However, the impact of a low-GI diet on body weight is controversial, with many studies confounded by dietary manipulations that differ in aspects other than GI. There is currently much interest in GI from scientists, health professionals and the public, but more research is needed before clear conclusions can be drawn about relationships with metabolic disease risk.


2021 ◽  
Vol 69 (37) ◽  
pp. 10907-10919
Author(s):  
Hao Suo ◽  
Mohammad Rezaul Islam Shishir ◽  
Jianbo Xiao ◽  
Mingfu Wang ◽  
Feng Chen ◽  
...  

2012 ◽  
Vol 90 (2) ◽  
pp. 124-141 ◽  
Author(s):  
Michael G. Sugiyama ◽  
Luis B. Agellon

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.


Reproduction ◽  
2018 ◽  
Vol 156 (2) ◽  
pp. R23-R42 ◽  
Author(s):  
Lindsay Ellsworth ◽  
Emma Harman ◽  
Vasantha Padmanabhan ◽  
Brigid Gregg

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.


2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Shiva Raj Mishra ◽  
Saruna Ghimire ◽  
Chandni Joshi ◽  
Bishal Gyawali ◽  
Archana Shrestha ◽  
...  

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 584-584
Author(s):  
Sofia Cienfuegos ◽  
Kelsey Gabel ◽  
Faiza Kalam ◽  
Mark Ezpeleta ◽  
Vasiliki Pavlou ◽  
...  

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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