Worldwide obesity is a public health concern that is defined by the World Health Organization as abnormal or excessive fat accumulation that may impair health. The main drivers of obesity pathogenesis seem to be a long-term of energy discrepancy between too many calories consumed and an increase of sedentary behavior. A growing body of evidence suggests that the set of microbes that live within the digestive tract, making up the gut microbiota (GM), play a metabolic role in energy regulation and substrate metabolism. Various factors can impact GM, one of these are dietary compounds that deeply affect the growth and metabolism of gut bacteria, since fermentation of nutrients is one core function of the intestinal microbes. Among fermentation products an array of small organic metabolites are short-chain fatty acids (SCFAs) acetate, propionate and butyrate. Among SCFAs, the C-4 fatty acid butyrate, the main fuel for the colonocytes, might have a potential in alleviating obesity and related metabolic complications. Butyrate could act as a regulator of body weight: a reasonable speculation is that butyrate acts on components of the energy balance, promoting energy expenditure and/or reducing energy intake. Preclinical studies have shown that butyrate supplementation prevent high-fat diet-induced obesity and it is able to treat obesity. With the sharp increase of obesity prevalence seen in the pediatric population, novel insights are necessary to counteract this epidemic disease, the outcome of the study is to see whether oral butyrate supplementation could exert similar effect in obese children.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
QUADRUPLE
Enrollment
54
University of Naples Federico II
Naples, Italy
BMI z-score change
BMI z-score change at least of ≥ 0.25
Time frame: after 6 months from the start of intervention
waist circumference
mean waist circumference change
Time frame: after 6 months from the start of intervention
HOMA index change
mean of HOMA index change
Time frame: after 6 months from the start of intervention
fasting glucose change
mean of fasting glucose change
Time frame: after 6 months from the start of intervention
fasting insulin change
mean of fasting insulin change
Time frame: after 6 months from the start of intervention
total cholesterol change
mean of total cholesterol change
Time frame: after 6 months from the start of intervention
Low density Lipoprotein cholesterol change
mean of Low density Lipoprotein cholesterol change
Time frame: after 6 months from the start of intervention
High density Lipoprotein cholesterol change
mean of high density Lipoprotein cholesterol change
Time frame: after 6 months from the start of intervention
plasma triglycerides change
mean of plasma triglycerides change
Time frame: after 6 months from the start of intervention
micro RNA 221- expression
mean of mir221- expression
Time frame: after 6 months from the start of intervention
serum ghrelin
mean of serum ghrelin
Time frame: after 6 months from the start of intervention
serum Interleukin-6
mean of Interleukin-6
Time frame: after 6 months from the start of intervention
composition of the intestinal microbiota (metagenomics characteristics)
evaluation of gut microbiota structure by shotgun analysis
Time frame: after 6 months from the start of intervention
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