[The role of gut microbiota in the pathogenesis of obesity].
Obesity is a disease that develops as a result of long-term positive energy balance. In recent years, the influence of gut microflora composition, as a potential factor affecting the energy balance and contributing to fat accumulation, has been studied. It seems that bacteria can affect host energy balance through several mechanisms, such as increased fermentation of undigested polysaccharides and obtaining extra energy from the portion of food, reduced expression of FIAF (fasting-induced adipocyte factor) in the enterocytes with inhibitory activity towards intestinal lipoprotein lipase, and the increased release of peptide YY that slows the intestinal motility. It is also believed that changes in the composition of gut microflora may be one of the factors that induce systemic microinflammation in the obese, an important link in the pathogenesis of obesity related complications, including dyslipidaemia, hypertension and type 2 diabetes. However, the results of previous studies are inconclusive. Many of them have been carried out in an animal model and were not confirmed in studies involving humans. These discrepancies may be due to different composition of the diet, distinct physiological gut microflora and the methodology used in these studies. The present article reviews the current literature on the potential role of gut microflora in the pathogenesis of obesity.
Zakład Patofizjologii, Katedra Patofizjologii Śląskiego Uniwersytetu Medycznego w Katowicach.
Agnieszka
A
Zak-Gołąb
Zakład Promocji Zdrowia i Leczenia Otyłości Katedry Patofizjologii Śląskiego Uniwersytetu Medycznego w Katowicach.
Magdalena
M
Olszanecka-Glinianowicz
Zakład Promocji Zdrowia i Leczenia Otyłości Katedry Patofizjologii Śląskiego Uniwersytetu Medycznego w Katowicach.
Piotr
P
Kocełak
Zakład Patofizjologii, Katedra Patofizjologii Śląskiego Uniwersytetu Medycznego w Katowicach.
Jerzy
J
Chudek
D000075803:Angiopoietin-Like Protein 4; D042682:Angiopoietins / Q000378:metabolism; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000382:microbiology*; D004032:Diet; D004195:Disease Models, Animal; D050171:Dyslipidemias / Q000382:microbiology*; D004734:Energy Metabolism; D020895:Enterocytes / Q000378:metabolism; D005769:Gastrointestinal Motility / Q000502:physiology; D041981:Gastrointestinal Tract / Q000382:microbiology*; D006801:Humans; D006973:Hypertension / Q000382:microbiology; D007422:Intestines / Q000382:microbiology*; D008049:Lipase / Q000378:metabolism; D064307:Microbiota / Q000502:physiology*; D009765:Obesity / Q000382:microbiology*; D019894:Peptide YY / Q000378:metabolism
C474772:ANGPTL4 protein, human; D000075803:Angiopoietin-Like Protein 4; D042682:Angiopoietins; D019894:Peptide YY; D008049:Lipase