Gene-related prevalence of metabolically healthy obesity in different racio-ethnic groups

The metabolically healthy obesity (MHO) phenotype is partly influenced by race/ethnicity and genetic factors being relatively more prevalent in some groups compared to others. This review examines current evidence on the prevalence of MHO amongst children, adolescents and adults of different racio-ethnic groups; and explores gene variants and single nucleotide polymorphisms (SNPs) that may confer cardioprotection in some racio-ethnic groups compared to others. Literature search of articles published in English was conducted using PubMed, Medline and Google scholar databases, with search terms related to the prevalence of metabolically healthy obesity as well as genetic variants that decrease or increase the risk of metabolic syndrome (MetS). MHO prevalence differed across racio-ethnic groups and gene variants that confer cardioprotection were higher in some racio-ethnic groups compared to others. Lower prevalence of MHO across all ages was particularly reported in the Middle East, while high prevalence was reported in Africans, Americans and some Asian adult population. Excluding environmental and other risk factors, we observed that Caucasians were carriers of gene variants that confer protection against cardiometabolic diseases, whilst Asians showed high frequency of gene variants that increase susceptibility to MetS. A robust understanding of the role of these gene variants, their frequency distribution and racio-ethnic variations may facilitate conceptualisation of appropriate genome wide association studies (GWAS) to determine significant associations between various genetic factors and observed phenotype or disease. This will guide policy formulation and serve as a useful tool in pharmacogenomics and precision medicine. Keywords: Obesity, metabolically healthy obesity, single nucleotide polymorphism, ethnicity, race, metabolic syndrome, gene variant

Microbial dysbiosis-induced obesity: role of gut microbiota in homoeostasis of energy metabolism

The global obesity epidemic has necessitated the search for better intervention strategies including the exploitation of the health benefits of some gut microbiota and their metabolic products. Therefore, we examined the gut microbial composition and mechanisms of interaction with the host in relation to homoeostatic energy metabolism and pathophysiology of dysbiosis-induced metabolic inflammation and obesity. We also discussed the eubiotic, health-promoting effects of probiotics and prebiotics as well as epigenetic modifications associated with gut microbial dysbiosis and risk of obesity. High-fat/carbohydrate diet programmes the gut microbiota to one predominated by Firmicutes (Clostridium), Prevotella and Methanobrevibacter but deficient in beneficial genera/species such as Bacteroides, Bifidobacterium, Lactobacillus and Akkermansia. Altered gut microbiota is associated with decreased expression of SCFA that maintain intestinal epithelial barrier integrity, reduce bacterial translocation and inflammation and increase expression of hunger-suppressing hormones. Reduced amounts of beneficial micro-organisms also inhibit fasting-induced adipocyte factor expression leading to dyslipidaemia. A low-grade chronic inflammation (metabolic endotoxaemia) ensues which culminates in obesity and its co-morbidities. The synergy of high-fat diet and dysbiotic gut microbiota initiates a recipe that epigenetically programmes the host for increased adiposity and poor glycaemic control. Interestingly, these obesogenic mechanistic pathways that are transmittable from one generation to another can be modulated through the administration of probiotics, prebiotics and synbiotics. Though the influence of gut microbiota on the risk of obesity and several intervention strategies have been extensively demonstrated in animal models, application in humans still requires further robust investigation