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Probiotics and prebiotics

Gut microbiota - therapeutic target for metabolic syndrome

The combination of both pre- and probiotics, also referred to as synbiotics, constitutes another nutritional tool for modulating the microbiota

Manipulating gut microbiota through the administration of prebiotics or probiotics may assist in weight loss and reduce plasma glucose and serum lipid levels, decreasing the incidence of cardiovascular diseases and type 2 diabetes mellitus, according to a paper, ‘Gut microbiota as a potential target of metabolic syndrome: the role of probiotics and prebiotics’, published in Cell and Bioscience by researchers from The First Affiliated Hospital of Xi’an Jiaotong University, Xi'an, Shaanxi, China.

The authors state that short-chain fatty acids (SCFAs), bile salt hydrolase (BSH), metabolic endotoxemia and the endocannabinoid (eCB) system are essential in regulating the initiation and progression of metabolic syndrome through the normalisation of adipogenesis and the regulation of insulin secretion, fat accumulation, energy homeostasis, and plasma cholesterol levels. Consequently, they hypothesise that the gut microbiota may serve as a potential therapeutic target for metabolic syndrome.

Probiotics (mainly bifidobacteria and lactobacilli) reside in the human colon, where they exert actions such as modulating colon micro-flora and immunogenic responses and producing certain materials; altogether, these functions improve the host’s health. Probiotics may help prevent infections, reduce cholesterol levels, promote vitamin and cytokine synthesis and inhibit cancer progression.

Diet-induced weight loss and bariatric surgery can promote significant changes in gut microbial composition and thus changed treatment strategies. Manipulation of the gut microbiota through the administration of prebiotics or probiotics can reduce intestinal low-grade inflammation and improve gut barrier integrity, thus ameliorating metabolic balance and promoting weight loss. Therefore, a comprehensive understanding of the gut microbiota manipulation and an assessment of risk factors in related disorders was necessary to generate therapeutic approaches to cure these diseases.

Gut microbiota can be modulated via the administration of prebiotics and the employment of specific non-digestible carbohydrates (NDO) devoted to modulation of the gut microbiota raised researchers’ attention. To date, the most studied prebiotics are the fructooligosaccharides (FOS) inulin and oligofructose [22, 23]. Nevertheless, many other OS, such as xylo-oligosaccharides (XOS), pectic oligosaccharides (POS), cyclodextrins, palatinose and OS from pullulan, are also important prebiotic candidates.

Probiotic manipulation of the microbiota may therefore be complementary to the application of prebiotic supplementation. The combination of both pre- and probiotics, also referred to as synbiotics, constitutes another nutritional tool for modulating the microbiota.

Most studies regarding the ‘anti-obesity’ effect of probiotics performed in rodents were achieved with members of the genus Lactobacillus. The results from several studies suggests that in addition to effects on body weight and fat mass, the administration of probiotics could counteract some metabolic diseases related to obesity. Additional studies indicate that the probiotic LG2055 lowered abdominal adiposity, body weight and other measures, suggesting its beneficial influence on metabolic disorders.

Gut microbiota regulate obesity-related biological systems, such as nutrient supply, fat accumulation and energy storage. In addition, gut ecology could be influenced by insulin-type fructans, which also activated immune cells. Accumulating studies have indicated that insulin-type fructans decreased fat accumulation and body weight in vivo, such as in obese individuals and further studies showed that oral administration of probiotics and/or prebiotics could decrease serum glucose levels. It has also reported that an oral administration of probiotics significantly reduced cholesterol levels by as much as 22–33% and controlled elevated cholesterol levels in mice fed a fat-enriched diet.


The gut microbiota is now considered to be involved in the regulation of multitudinous physiological pathways and to impact different host functions. Given the developing knowledge of how probiotics and prebiotics interact with the gut microbiota, there has been a growing interest in exploring the effect of probiotics and prebiotics on specific constituents of MS.

Four main mechanisms have been proposed in this review to explain the action of probiotics:

  • The first mechanism is raising bacteria-derived SCFAs, which activates GPR-43 on L cells and triggers the secretion of GLP-1 and GLP-2 - these hormones exhibit an enormous variety of metabolic and proliferative actions.
  • The second mechanism is increasing BSH activity - bacterial BSH enzymes in the gut influence host physiological processes, resulting in decreases in body weight gain and plasma cholesterol levels.
  • The third mechanism is leveraging the anti-inflammatory function of probiotics, which improves low-grade inflammation, steatosis, glucose intolerance and insulin sensitivity.
  • The fourth mechanism is down-regulation of eCB system responsiveness, which impacts the regulation of energy homeostasis and the normalization of adipogenesis.

“Accumulating evidence suggests that gut microbiota plays a significant role in the initiation and progression of MS. The gut microbiota was proven to modulate plasma glucose, appetite, serum lipids and pro-inflammation. In addition, prebiotics or probiotics, which are widely used to manipulate the microbiota, can reduce low-grade intestinal inflammation and improve gut barrier integrity to reduce plasma glucose and serum lipid levels, induce weight loss and decrease insulin resistance,” they conclude. “Based on these current achievements, the gut microbiota may be a potential therapeutic target for MS. However, clinical trials addressing the efficacy and efficiency of current or potential treatments on therapeutic applications in metabolic syndrome are needed.”

To access this paper, please click here

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