Jun Ogawa, Ph.D.
Division of Applied Life Sciences, Graduate School of Agriculture, Kyoto University.
The human gut is inhabited by a large and diverse microbiota consisting of approximately 100 trillion cells of 500 to 1000 species. Reports show that the gut microbiota affects the physiology, metabolism, and immune response of the host, and a loss of balance can lead to diseases such as bowel disease, carcinogenesis, and obesity. Some researchers suggest that gut microbiota can be viewed as ‘a metabolic organ’ that provides hosts with nutrients such as vitamins and energy sources. Recent, increases in cases of metabolic syndrome has led researchers to focus their attention on the metabolism of fat metabolism by both the host and the gut microbiota.
Jun Ogawa and colleagues at Kyoto University addressed the question of “what kind molecular species of fat, especially bioactive polyunsaturated fatty acids (PUFA), are generated by our gut microbes and how do they affect our health”. The researchers analyzed PUFA metabolism in anaerobic bacteria, especially in lactic acid bacteria, that are gut microorganisms with industrial importance.
The following aspects of PUFA metabolism in lactic acid bacteria were analyzed: gut microbial PUFA saturation metabolism; distribution of gut microbial PUFA metabolites in the host; physiological activities of gut microbial PUFA metabolites; preparation of gut microbial PUFA metabolites; and probiotic and prebiotic applications.
The main findings were: Intestinal barrier recovering-function; Enhanced gut hormone secretion; hypolipidemic effects; anti-diabetic activity; anti-oxidative effects; anti-inflammatory and immune controlling effects; and anti Helicobacter pylori activity.
“The combination of fatty acid composition in dietary fat and the fatty acid-metabolizing activity in gut microbe would regulate the intestinal disorders and lipid metabolisms of the host,” says Ogawa.
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 Matsui, H. et al., Protective efficacy of a hydroxy fatty acid against gastric Helicobacter infections, Helicobacter, 22 (4), e12430 (2017).
 Yamada M. et al., A bacterial metabolite ameliorates periodontal pathogen-induced gingival epithelial barrier disruption via GPR40 signaling, Sci. Rep., 8, 9008 (2018).