Common links between metabolic syndrome and inflammatory bowel disease: Current overview and future perspectives

Abstract

Metabolic syndrome (MS) features a constellation of central obesity, dyslipidemia, impaired glucose metabolism and often hypertension joined by insulin resistance and chronic inflammation. All these elements greatly raise patient's risk of cardiovascular disease and type 2 diabetes, resulting in an increased mortality. Metabolic syndrome affects approximately 20-25% of the world's adult population and thus it is essential to study its pathophysiology and seek new pharmacological targets. There is a thoroughly studied link between MS and inflammatory diseases of the gastrointestinal (GI) system, i.e. steatohepatitis. However, recent findings also indicate similarities in pathophysiological features between MS and inflammatory bowel disease (IBD), including adipose tissue dysregulation, inadequate immune response, and inflammation. In this review we aim to outline the pathophysiology of MS and emphasize the aspects revealed recently, such as mineralocorticoid activity, involvement of sex hormones and an accompanying increase in prolactin secretion. More importantly, we focus on the common links between MS and IBD. Finally, we describe new strategies and drug targets that may be utilized in MS therapy, namely adiponectin mimetics, GLP-1-based multi agonists, ABCA1 agonists and possible role of miRNA. We also discuss the possible utility of selected agents as adjuvants in IBD therapy.

The Microbiota and Epigenetic Regulation of T Helper 17/Regulatory T Cells: In Search of a Balanced Immune System

“…Although the exact etiology of IBD remains elusive, it is well accepted that this group of diseases preferentially affects genetically susceptible individuals and could result from a disproportionate activation of the immune system in response to changes affecting the gut microbiota [Tables 1 and 2; (44)]. Indeed, IBD is characterized by significant disturbances in the gut microbiota (83) and alterations in the balance between the dominant bacterial groups, depletion of particular bacteria, as well as a reduction in the diversity of the gut microbiota (84–86). A seminal study in the field recently identified that European children, considered to be at increased risk of IBD, were characterized by a reduced diversity in their gut microbiota and a total depletion of bacteria responsible for the digestion of dietary fibers when compared to their African counterparts (87).…”

“…Reports supporting similarities in the physiopathology of IBD and metabolic diseases have recently started to emerge and have identified dysbiosis as a common trait shared between these conditions (83, 103). Indeed, changes in the microbiota that accompany alterations in nutritional habits and the development of obesity have been identified as critical contributors to the development of metabolic complications including insulin resistance and T2D and could even precede the establishment of local and systemic inflammation (83, 103, 104). Similar to what has been reported in IBD, both a decline in diversity and a remodeling of the bacterial component of the microbiota have been observed in the early stages of the development of obesity and insulin resistance (105).…”

The link between chronic spontaneous urticaria and metabolic syndrome

“…Several immune-mediated inflammatory disorders, including rheumatoid arthritis, systemic lupus erythematosus, psoriatic disease and intestinal bowel diseases, have been associated with an elevated cardiovascular burden (25,(36)(37)(38)(39). The pathophysiological basis of such an increased risk is not completely understood, but MS and obesity in particular, with a dysregulated secretion of pro-inflammatory adipokines, could be major contributing features.…”

Polyunsaturated Fatty Acids and Their Derivatives: Therapeutic Value for Inflammatory, Functional Gastrointestinal Disorders, and Colorectal Cancer

“…Given the fact that adipose tissue inflammation plays an important role in CD (Michalak et al, 2016), these metabolites may be actively used to suppress existing inflammation or prolong remission in those patients. EPA- and DHA-derived specialized pro-resolving mediators are prime candidates for animal and clinical trials.…”