Probiotics for weight loss
Obesity is a complex chronic metabolic disease that impairs health and shortens lifespan. Therefore, it is necessary to develop effective strategies to prevent and treat obesity. Although several studies have demonstrated that gut dysbiosis is associated with obesity, whether altered gut microbiota is a risk factor or a consequence of obesity remains controversial. Recent randomized clinical trials (RCTs) evaluating whether probiotic modulation of gut microbiota benefit weight loss have had conflicting results, which can be attributed to heterogeneity in study design. The aim of this article is to comprehensively review the heterogeneity of interventions and body fat assessment methods in randomized controlled trials evaluating the effects of probiotics on body weight and body fat in overweight and obese individuals. Thirty-three randomized controlled trials were identified by the search strategy. As primary outcomes, the authors observed that about 30% of RCTs reported significant reductions in body weight and body mass index (BMI), and about 50% of RCTs reported significant reductions in waist circumference and total fat mass. The beneficial effects of probiotics were more consistent in the 12-week trial at doses of 1010 CFU/d in capsules, sachets or powders with no accompanying energy restriction. Evidence for the effects of probiotics on body adiposity may improve and be more consistent in future randomized controlled trials that include methodological features such as longer durations, higher doses, non-dairy vehicles, Asynchronous energy restriction and the use of more accurate measures of body fat deposition (e.g., body fat mass and waist circumference) rather than weight and BMI.
The relationship between Probiotics and obesity
Numerous studies have found quantitative and qualitative changes in the microbiota composition of obese individuals compared with lean individuals, including a decrease in microbial diversity. Furthermore, an increased ratio of Firmicutes to Bacteroidetes was frequently observed. A recent systematic review of 32 studies found that obese individuals had a higher ratio of Firmicutes/Bacteroidetes, Firmicutes, Fusobacteria, Proteobacteria, Mollicutes, Lactobacillus (reuteri ) were higher, whereas Akkermansia muciniphila, Faecalibacterium (prausnitzii), Bacteroidetes, Prucifera, Lactobacillus plantarum and Lactobacillus paracasei were less abundant.
Although studies have shown that gut microbiota dysbiosis is associated with obesity, whether changes in the gut microbiota precede obesity (causation) or reflect an obese phenotype (consequence) remains controversial. Therefore, the causal role of the gut microbiota in the pathogenesis of obesity remains controversial and remains a matter of debate.
Diet affects the composition of the gut microbiota. Numerous studies have shown that nutrients, such as fiber and fat, as well as specific foods and dietary patterns can modulate gut microbiota composition and function. For example, high-fat diets and Western dietary patterns (characterized by high intakes of processed foods, saturated fats, and sugars) are associated with unfavorable microbiota, while high fiber intake and adherence to healthy eating patterns, such as the Mediterranean diet, are associated with gut microbiota beneficial effects of the group.
Mechanisms linking Probiotics for weight loss
As mentioned above, the literature suggests an important relationship between gut microbiota and weight control. Candidate mechanisms explaining the potential role of gut microbiota dysbiosis in obesity include increased energy harvesting by gut microbiota, increased fat storage in adipose tissue, decreased secretion of anaerobic hormones, and low-grade inflammation due to increased gut permeability .
The gut flora contains glycosidases and lyases that degrade and ferment polysaccharides and food components that cannot be digested by the human body into absorbable monosaccharides and (short-chain fatty acids) such as propionate, butyrate and acetate to important. These short-chain fatty acids are used by the host as an energy source, increasing the energy obtained from the diet. Obesity is associated with bacteria that ferment carbohydrates in large quantities, increasing the synthesis of short-chain fatty acids, which provide an additional energy substrate for the host.
Gut microbiota plays an important role in regulating genes related to fat storage. Alterations in the gut microbiota suppress the expression of fasting-induced adipokine (FIAF), which, in addition to its inhibitory effect on lipoprotein lipase, is a potent regulator of fatty acid oxidation, leading to increased triglyceride deposition in adipose tissue.
Another potential mechanism involves adenosine monophosphate-activated protein kinase (AMPK), an enzyme that monitors energy status and regulates energy metabolism. In gut dysbiosis, AMPK is inhibited, leading to decreased fatty acid oxidation and increased triglyceride synthesis.
Studies have shown that gut microbiota-derived short-chain fatty acids play an important role in regulating energy expenditure. Several studies have shown that SCFAs are able to reduce gut motility and regulate satiety by affecting the production of satiety hormones such as glucagon-like peptide 1, peptide YY, and leptin.
Another potential mechanism linking obesity to gut microbiota dysbiosis is gut permeability, possibly due to increased LPS-carrying bacterial species in the gut and subsequent activation of toll-like receptors on immune cells. Thus, with increased gut permeability, pathogen-associated molecular patterns, such as lipopolysaccharides and peptidoglycans (pro-inflammatory molecules of the gut microbiota), are recognized by host receptors, promoting chronic inflammation.