Metabolic Syndrome (MetS) is characterized by systemic low-grade inflammation and oxidative stress and reactive oxygen species have a role in this state of inflammation. Many other key players involved in metabolic inflammation have been recognized in the recent past. Dysbiosis or an alteration of gut microbiota due to intestinal diseases and/or non-intestinal diseases like obesity and diabetes is one such factor. It may determine the reservoir of the outer membrane component of the gut microbiome, referred to as endotoxin or lipopolysaccharides (LPS), which can leak into the circulation contributing to low-grade inflammation. Enteroendocrine cells of the gut lumen secretes various gut hormones which have been implicated in metabolic homeostasis. There has also been a debate, in the recent past whether a phenotype of obesity known as Metabolically Healthy Obese (MHO), in which individuals despite meeting the criteria for obesity do not exhibit metabolic complications, are actually free of insulin resistance and unfavorable CVD outcomes or whether ‘MHO’ itself is a misnomer.
Metabolic syndrome (MetS), a prevalent pathologic condition, is characterized by a number of interconnected abnormalities including visceral obesity, dyslipidemia, hypertension, glucose intolerance and insulin resistance. The low-grade inflammation present in metabolic syndrome as well as obesity is linked with dysbiosis and gut microbiota. The role of the regulatory mechanisms of gut hormones and microbiota in maintaining metabolic homeostasis; and whether dysbiosis leads to imbalance in metabolic parameters or vice-versa are an area of research that we aim to study in this special issue. Additionally, effective therapeutic/nutritional intervention strategies to explore this cause-and-effect relationship may be explored. Besides, concluding evidences on whether there are differences in gut microbiota, dysbiosis and inflammatory markers in different phenotypes of obesity such as MHO.
This Special Issue aims to thus cover, through original investigations and up-to-date review articles, the following interesting areas which may however be extended around the study topic:
• Dysbiosis or alteration in gut microbiota in obesity and MetS;
• Adipose tissue and immune response linking dysbiosis and MetS;
• Triggers, Mechanisms, and Consequences of metabolic inflammation;
• Association analysis of inflammatory cytokines in dysbiosis and MetS;
• Pathogenesis of MetS, as well as any pharmacological, nutritional, or lifestyle treatment aimed at controlling or reversing it;
• Assessment of differences in gut microbiota and dysbiosis in MHO, MHNW and metabolically unhealthy obesity;
• Role of gut microbiota in mechanistic triggers of advancement to metabolically unhealthy obesity from MHO phenotype.
Metabolic Syndrome (MetS) is characterized by systemic low-grade inflammation and oxidative stress and reactive oxygen species have a role in this state of inflammation. Many other key players involved in metabolic inflammation have been recognized in the recent past. Dysbiosis or an alteration of gut microbiota due to intestinal diseases and/or non-intestinal diseases like obesity and diabetes is one such factor. It may determine the reservoir of the outer membrane component of the gut microbiome, referred to as endotoxin or lipopolysaccharides (LPS), which can leak into the circulation contributing to low-grade inflammation. Enteroendocrine cells of the gut lumen secretes various gut hormones which have been implicated in metabolic homeostasis. There has also been a debate, in the recent past whether a phenotype of obesity known as Metabolically Healthy Obese (MHO), in which individuals despite meeting the criteria for obesity do not exhibit metabolic complications, are actually free of insulin resistance and unfavorable CVD outcomes or whether ‘MHO’ itself is a misnomer.
Metabolic syndrome (MetS), a prevalent pathologic condition, is characterized by a number of interconnected abnormalities including visceral obesity, dyslipidemia, hypertension, glucose intolerance and insulin resistance. The low-grade inflammation present in metabolic syndrome as well as obesity is linked with dysbiosis and gut microbiota. The role of the regulatory mechanisms of gut hormones and microbiota in maintaining metabolic homeostasis; and whether dysbiosis leads to imbalance in metabolic parameters or vice-versa are an area of research that we aim to study in this special issue. Additionally, effective therapeutic/nutritional intervention strategies to explore this cause-and-effect relationship may be explored. Besides, concluding evidences on whether there are differences in gut microbiota, dysbiosis and inflammatory markers in different phenotypes of obesity such as MHO.
This Special Issue aims to thus cover, through original investigations and up-to-date review articles, the following interesting areas which may however be extended around the study topic:
• Dysbiosis or alteration in gut microbiota in obesity and MetS;
• Adipose tissue and immune response linking dysbiosis and MetS;
• Triggers, Mechanisms, and Consequences of metabolic inflammation;
• Association analysis of inflammatory cytokines in dysbiosis and MetS;
• Pathogenesis of MetS, as well as any pharmacological, nutritional, or lifestyle treatment aimed at controlling or reversing it;
• Assessment of differences in gut microbiota and dysbiosis in MHO, MHNW and metabolically unhealthy obesity;
• Role of gut microbiota in mechanistic triggers of advancement to metabolically unhealthy obesity from MHO phenotype.
