Background: Dietary fibre consists of non-digestible forms of carbohydrate, usually as polysaccharides that originate from plant-based foods. Over recent decades, our diet within Westernised societies has changed radically from that of our hominid ancestors, with implications for our co-evolved gut microbiota. This includes increased ingestion of ultra-processed foods that are typically impoverished of dietary fibre, and associated reduction in the intake of fibre-replete plant-based foods. Over recent decades, there has been a transformation in our understanding of the health benefits of dietary fibre. Objective: To explore the current medical literature on the health benefits of dietary fibre, with a focus on overall metabolic health. Data Sources: We performed a narrative review, based on relevant articles written in English from a PubMed search, using the terms ‘dietary fibre and metabolic health’. Results: In the Western world, our diets are impoverished of fibre. Dietary fibre intake associates with overall metabolic health (through key pathways that include insulin sensitivity) and a variety of other pathologies that include cardiovascular disease, colonic health, gut motility and risk for colorectal carcinoma. Dietary fibre intake also correlates with mortality. The gut microflora functions as an important mediator of the beneficial effects of dietary fibre, including the regulation of appetite, metabolic processes and chronic inflammatory pathways. Conclusions: Multiple factors contribute to our fibre-impoverished modern diet. Given the plethora of scientific evidence that corroborate the multiple and varied health benefits of dietary fibre, and the risks associated with a diet that lacks fibre, the optimization of fibre within our diets represents an important public health strategy to improve both metabolic and overall health. If implemented successfully, this strategy would likely result in substantial future health benefits for the population.

A high dietary fiber (DF) intake is emphasized in the recommendations of most diabetes and nutritional associations. It is accepted that viscous and gel-forming properties of soluble DF inhibit macronutrient absorption, reduce postprandial glucose response, and beneficially influence certain blood lipids. Colonic fermentation of naturally available high fiber foods can also be mainly attributed to soluble DF, whereas no difference between soluble and insoluble DF consumption on the regulation of body weight has been observed. However, in prospective cohort studies, it is primarily insoluble cereal DF and whole grains, and not soluble DF, that is consistently associated with reduced diabetes risk, suggesting that further, unknown mechanisms are likely to be involved. Recent research indicates that DF consumption contributes to a number of unexpected metabolic effects independent from changes in body weight, which include improvement of insulin sensitivity, modulation of the secretion of certain gut hormones, and effects on various metabolic and inflammatory markers that are associated with the metabolic syndrome. In this review, we briefly summarize novel findings from recent interventions and prospective cohort studies. We discuss concepts and potential mechanisms that might contribute to the further understanding of the involved processes.

Large prospective cohort studies consistently show associations of a high dietary fiber intake (>25 g/d in women and >38 g/d in men) with a 20–30% reduced risk of developing type 2 diabetes (T2D), after correction for confounders. It is less well recognized that these effects appear to be mainly driven by high intakes of whole grains and insoluble cereal fibers, which typically are nonviscous and do not relevantly influence postprandial glucose responses [i.e., glycemic index (GI)] or are strongly fermented by the gut microbiota in the colon. In contrast, a dietary focus on soluble, viscous, gel-forming, more readily fermentable fiber intakes derived from fruit and certain vegetables yields mixed results and generally does not appear to reduce T2D risk. Although disentangling types of fiber-rich foods and separating these from possible effects related to the GI is an obvious challenge, the common conclusion that key metabolic effects of high-fiber intake are explained by mechanisms that should mainly apply to the soluble, viscous type can be challenged. More recently, studies in humans and animal models focused on gaining mechanistic insights into why especially high-cereal-fiber (HCF) diets appear to improve insulin resistance (IR) and diabetes risk. Although effects of HCF diets on weight loss are only moderate and comparable to other types of dietary fibers, possible novel mechanisms have emerged, which include the prevention of the absorption of dietary protein and modulation of the amino acid metabolic signature. Here we provide an update of our previous review from 2008, with a focus on mechanistic insights of how HCF diets may improve IR and the risk of developing T2D.

Polycystic ovary syndrome (PCOS) is a common female condition typified by reproductive, hyperandrogenic, and metabolic features. Polycystic ovary syndrome is a genetic condition, exacerbated by obesity. There is a close link between obesity and PCOS based on epidemiological data, and more recently corroborated through genetic studies. There are many mechanisms mediating the effects of weight-gain and obesity on the development of PCOS. The metabolic effects of insulin resistance and steroidogenic and reproductive effects of hyperinsulinaemia are important mechanisms. Adipokine production by subcutaneous and visceral fat appears to play a part in metabolic function. However, given the complexity of PCOS pathogenesis, it is important also to consider possible effects of PCOS on further weight-gain, or at least on hampering attempts at weight-loss and maintenance through lifestyle changes. Possible mediators of these effects include changes in energy expenditure, mental ill health, or physical inactivity. In this brief review, we discuss the main mechanisms that underlie the association between obesity and PCOS, from divergent perspectives of weight-gain contributing to development of PCOS and vice versa. We also consider novel management options for women with obesity and PCOS.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder amongst women of reproductive age and is associated with various metabolic perturbations, in addition to chronic anovulation and factors related to androgen excess. In general, women live longer than men and develop cardiovascular disease at an older age. However, women with PCOS, as compared with age- and body mass index-matched women without the syndrome, appear to have a higher risk of insulin resistance, hyperinsulinemia, glucose intolerance, dyslipidemia, and an increased prothrombotic state, possibly resulting in a higher rate of type 2 diabetes mellitus, fatty liver disease, subclinical atherosclerosis, vascular dysfunction, and finally cardiovascular disease and mortality. Further alterations in PCOS include an increased prevalence of sleep apnea, as well as various changes in the secretion and/or function of adipokines, adipose tissue-derived proinflammatory factors and gut hormones, all of them with direct or indirect influences on the complex signaling network that regulates metabolism, insulin sensitivity, and energy homeostasis. Reviews on the cardiometabolic aspects of PCOS are rare, and our knowledge from recent studies is expanding rapidly. Therefore, it is the aim of the present review to discuss and to summarize the current knowledge, focusing on the alterations of cardiometabolic factors in women with PCOS. Further insight into this network of factors may facilitate finding therapeutic targets that should ameliorate not only ovarian dysfunction but also the various cardiometabolic alterations related to the syndrome.