The traditional risk factors for obesity are inappropriate diet, lack of exercise and genetic factors. However, recent observations have involved gut microbiota profiles as having an additional influence. In this case, there exists the possibility to modulate this through diet. Research has shown that the gut microbiota of both obese humans and mouse models of obesity is altered towards less beneficial one compared to lean counterparts. This raises the possibility of modulating the gut microbiota as a novel strategy in tackling the epidemic of obesity and diabetes sweeping the developed world. In addition, a more direct effect of high-fat induced disruption of the intestinal microbiota has also been seen with a murine model. Elevated circulating levels of lipopolysaccharide (LPS) a major building block and antigen of Gram-negative bacteria, was shown to generate a low grade chronic inflammation, termed metabolic endotoxemia, which then onsets insulin resistance. High-fat diets were shown to disrupt the Gram-negative intestinal populations of these animals, liberating LPS. The effects of prebiotics on the microbiota or metabolic syndrome (combination of disorders that increase the risk of developing cardiovascular disease and diabetes) in overweight adults have not been investigated thus far. The investigators therefore propose to investigate the effect of galactooligosaccharide (GOS) on the faecal microbiota and metabolic syndrome risk factors in overweight adults in a double-blind, randomised, placebo controlled, cross-over trial.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
TRIPLE
Enrollment
48
5.5g daily intake
5.5g daily intake
School of Chemistry, Food Biosciences and Pharmacy, The University of Reading
Reading, Berkshire, United Kingdom
Faecal microbiota changes enumerated by Fluorescent In Situ Hybridisation and qualitatively assessed by Denaturing Gradient Gel Electrophoresis.
Time frame: 3 months
Lipid profile (total, LDL and HDL cholesterol, triglycerides and non-esterified fatty acids)
Time frame: 3 months
Inflammatory/thrombotic biomarkers (including C-reactive protein, TNF-a, IL6, IL-8, IL-10, sCD40L, sP-selectin, t-PA)
Time frame: 3 months
Insulin resistance derived from fasted measures of glucose and insulin ratio
Time frame: 3 months
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