Metabolic Disease: Obesity, Malnutrition, and Intestinal Microbiota

Abstract

Abstract Obesity is a worldwide epidemic that is accompanied by a dramatic increase in obesity-related disorders; it threatens both industrialized and developing countries. Recent studies have shown that the gut microbial community (microbiota) is an environmental factor of developmental origins of health and diseases (DOHaD) that regulates obesity by increasing energy harvest from the diet and regulating peripheral metabolism. Dysbiosis in neonates and infants is caused by a disrupted environment that influences the initial colonization of microbes in the gut; such disruptions include a C-section delivery, formula feeding, excessive use of antibiotics, or the introduction of inappropriate solid foods containing a high amount of saturated fat. Dysbiosis delays the development of mucosal host defense and immunity, leading to a high risk of obesity, metabolic disease, and immune-mediated disease later in life. Bifidobacteria and Bacteroides, which are found in human milk and are predominant mutualists in healthy microbiota, colonize the gut initially as “pioneer” bacteria; in this way, human milk and its oligosaccharides confer benefits, such as reducing the risks of obesity and metabolic syndrome, to the offspring. As the microbial exposure of neonates is provided mainly from the maternal microbiota, maternal obesity with dysbiosis has an impact on infant microbiota development that can lead to major shifts in the microbiota composition of the child in early life and may cause aberrant immune function and priming for harmful responses to postnatal triggers. Alterations in the gut microbiome have been strongly implicated in childhood malnutrition. This paper reviews the evidence linking gut microbiota, obesity, and malnutrition.