Abstract
Obesity is becoming the most dangerous lifestyle disease of our time, and its effects are already being observed in both developed and developing countries. The aim of this study was to investigate the impact of gut microbiota on the prevalence of obesity and associated morbidities, taking into consideration underlying molecular mechanisms. In addition to exploring the relationship between obesity and fecal microorganisms with their metabolites, the study also focused on the factors that would be able to stimulate growth and remodeling of microbiota. Assessed articles were carefully classified according to a predetermined criterion and were critically appraised and used as a basis for conclusions. The considered articles and reviews acknowledge that intestinal microbiota forms a multifunctional system that might significantly affect human homeostasis. It has been proved that alterations in the gut microbiota are found in obese and metabolically diseased patients. The imbalance of microbiome composition, such as changes in Bacteroidetes/Firmicutes ratio and presence of different species of genus Lactobacillus, might promote obesity and comorbidities (type 2 diabetes mellitus, hypertension, dyslipidemia, depression, obstructive sleep apnea). However, there are also studies that contradict this theory. Therefore, further well-designed studies are needed to improve the knowledge about the influence of microbiota, its metabolites, and probiotics on obesity.
Highlights
There is a strong association of genetics with obesity, which means that the involvement of multiple genes and their complex interaction can result in the manifestation of the disease, which can be a monogenic (5% of the cases) or a polygenic obesity type [9]
The gut microbiome interacts with the formation of gut-associated lymphoid tissue (GALT) because the bacterial peptidoglycan can be recognized through pattern recognition receptors (PRR), nucleotide-binding oligomerization domain-containing protein 1 (NOD1), and Toll-like receptors (TLRs) that are present in the epithelial cells
Increased production of short chain fatty acids (SCFAs) by gut microbiota provides additional calories to the host, leading to weight gain. They can bind to the G proteincoupled receptor (GPCR) GPR41 and induce expression of the enteroendocrine hormone peptide YY (PYY) in gut epithelial L-cells, which inhibits gut motility and increases energy harvest from the diet in mice
Summary
Obesity is recognized as a global epidemic affecting both developed and poorresource countries [1], which lowers life expectancy [2] and has extensive consequences for countries’ health care systems [1]. The etiology of obesity is multifactorial and includes genetic, hormonal, socioeconomic, environmental, and cultural influences [3]. The primary causes of obesity can be classified as being related to genetic disorders in the form of monogenic diseases and genetic syndromes [6]. Monogenic obesity is a rare and severe early-onset obesity inherited in a Mendelian pattern with abnormal feeding behavior and endocrine abnormalities It is mainly caused by autosomal recessive mutations in genes of leptin, pro-opiomelanocortin (POMC), pro-hormone convertase 1, and melanocortin. There is a strong association of genetics with obesity, which means that the involvement of multiple genes and their complex interaction can result in the manifestation of the disease, which can be a monogenic (5% of the cases) or a polygenic obesity type [9]. Obesity treatment consists of bariatric surgery and medical treatment, of which undergoing a surgery provides a longer life expectancy [10]
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