Overweight and obesity have reached worldwide epidemic level. Both overweight and obesity are characterized by comorbidities such as cardio-metabolic risk factors (i.e., insulin resistance, type 2 diabetes, hypertension, dyslipidemia, low-grade inflammation) representing a major public health problem. Therefore, it is urgent to find a therapeutic solution to target all these metabolic disorders. Among the environmental factors able to influence the individual susceptibility to gain weight and to develop metabolic disorders associated with obesity, more and more evidence show that the trillions of bacteria housed in our gastro-intestinal tract (i.e, gut microbiota) influence host metabolism. The investigators recently discovered a putative interesting microbial candidate, namely Akkermansia muciniphila (Akk). More exactly, we found that the administration of Akkermansia muciniphila reduced body weight gain, fat mass gain, glycemia and inflammatory markers in diet-induced obese mice. Moreover, in overweight/obese patients with cardiovascular risk factors subjected to a calorie restriction diet (calorie restriction diet for 6 weeks and an additional 6 weeks of weight maintenance), a higher abundance of Akkermansia muciniphila was associated with a better cardio-metabolic status in these patients. The investigators also discovered that patients having more Akkermansia muciniphila in their gut before the calorie restriction exhibited a greater improvement in glucose homoeostasis, blood lipids and body composition after calorie restriction. These observations suggested that the administration of Akkermansia muciniphila in overweight or obese people could be a very interesting therapeutic solution. Currently, no human study has investigated the beneficial effects of Akkermansia muciniphila administration on obesity and metabolic disorders. The overall objective of this study is to evaluate the effects associated with the administration of live or heat-killed Akkermansia muciniphila on the metabolic disorders (insulin-resistance, type-2 diabetes, dyslipidemia, inflammation) related to overweight and obesity in humans.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
DOUBLE
Enrollment
54
Consumption of one dose-sachet per day. This dose-sachet contains a placebo (PBS/Glycerol)
Consumption of one dose-sachet per day. This dose-sachet contains Live Akkermansia muciniphila (one billion per dose-sachet)
Consumption of one dose-sachet per day. This dose-sachet contains Live Akkermansia muciniphila (ten billion per dose-sachet)
Consumption of one dose-sachet per day. This dose-sachet contains heat-killed Akkermansia muciniphila
Cliniques universitaires Saint-Luc
Brussels, Belgium
Tolerance
self reporting of gastrointestinal symptoms (nausea, bloating, flatulence, cramp, borborygmi and gastric reflux)
Time frame: 15 days
Tolerance
self reporting of gastrointestinal symptoms (nausea, bloating, flatulence, cramp, borborygmi and gastric reflux)
Time frame: 3 months
Concentration of urea (mg/dl)
measure of urea as marker of renal function
Time frame: 15 days
Concentration of urea (mg/dl)
measure of urea as marker of renal function
Time frame: 3 months
Glomerular filtration rate (mL/min/1.73m2)
measure of glomerular filtration rate as marker of renal function
Time frame: 15 days
Glomerular filtration rate (mL/min/1.73m2)
measure of glomerular filtration rate as marker of renal function
Time frame: 3 months
Concentration of creatinine (mg/dl)
measure of creatinine as marker of renal function
Time frame: 15 days
Concentration of creatinine (mg/dl)
measure of creatinine as marker of renal function
Time frame: 3 months
Concentration of liver transaminases
measure of alanine aminotransferase (U/L); aspartate aminotransferase (U/L); gamma glutamyl transpeptidase (U/L). Lactate dehydrogenase (UI/L) as markers of hepatic inflammation
Time frame: 15 days
Concentration of liver transaminases
measure of alanine aminotransferase (U/L); aspartate aminotransferase (U/L); gamma glutamyl transpeptidase (U/L). Lactate dehydrogenase (UI/L) as markers of hepatic inflammation
Time frame: 3 months
Concentration of white blood cells (10exp3/µl)
measured as a marker of inflammation
Time frame: 15 days
Concentration of white blood cells (10exp3/µl)
measured as a marker of inflammation
Time frame: 3 months
concentration of CRP (c-reactive protein) (mg/dl)
measured as a marker of inflammation
Time frame: 15 days
concentration of CRP (c-reactive protein) (mg/dl)
measured as a marker of inflammation
Time frame: 3 months
Insulin resistance
HOMA-Homeostasis Model Assessment calculated from fasted glycemia and insulinemia
Time frame: 3 months
Concentration of blood lipids
Analysis of circulating lipids : total, LDL and HDL cholesterol (mg/dl), triglycerides (md/dl)
Time frame: 3 months
Obesity
Body weight
Time frame: 3 months
Adiposity
Fat mass evaluated by bioimpedance measurements
Time frame: 3 months
Visceral adiposity
Waist and hip circumference
Time frame: 3 months
Measure of the concentration of Akkermansia in the feces (bacterial cells/g of feces)
Metagenomic analysis of the gut bacteria by using sequencing technology and by using quantitative polymerase chain reaction (qPCR).
Time frame: 3 months
Gut barrier function
Fecal calprotectin, fecal zonulin, plasma lipopolysaccharides (LPS) binding protein (LBP)
Time frame: 3 months
Metabolic endotoxemia
Plasma lipopolysaccharides (LPS) by the limulus amebocyte lysate kinetic chromogenic methodology
Time frame: 3 months
Gut microbial-related metabolites in urine
Metabolomic analysis of the bacterial metabolites present in the urine by combining nuclear magnetic resonance (1H-NMR) and mass spectrometry
Time frame: 3 months
Gut microbial-related metabolites in plasma
Metabolomic analysis of the bacterial metabolites present in the plasma by combining nuclear magnetic resonance (1H-NMR) and mass spectrometry
Time frame: 3 months
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