The formation of advanced glycation end products (AGEs) in foods is accelerated with heat treatment, particularly within foods that are cooked at high temperatures for long periods of time using dry heat. The modern processed diet is replete with AGEs, and excessive AGE consumption is thought to be associated with a number of negative health effects. Many dietary AGEs have high molecular weight and are not absorbed in the intestine, and instead pass through to the colon, where they are available for metabolism by the colonic bacteria. Recent studies have been conducted to explore the effects of AGEs on the composition of the gut microbiota as well as the production of beneficial microbial metabolites, in particular, short-chain fatty acids. However, there is conflicting evidence regarding the impact of dietary AGEs on gut microbiota reshaping, which may be due, in part, to the formation of alternate compounds during the thermal treatment of foods. This review summarises the current evidence regarding dietary sources of AGEs, their gastrointestinal absorption and role in gut microbiota reshaping, provides a brief overview of the health implications of dietary AGEs and highlights knowledge gaps and avenues for future study.

This study shows how highly processed foods can cause innate immune inflammation that promotes chronic microvascular disease.

There is increasing evidence of the influence of the gut microbiota on hypertension and its complications, such as chronic kidney disease, stroke, heart failure, and myocardial infarction. This is not surprising considering that the most common risk factors for hypertension, such as age, sex, medication, and diet, can also impact the gut microbiota. For example, sodium and fermentable fiber have been studied in relation to both hypertension and the gut microbiota. By combining second- and, now, third-generation sequencing with metabolomics approaches, metabolites, such as short-chain fatty acids and trimethylamine N-oxide, and their producers, have been identified and are now known to affect host physiology and the cardiovascular system. The receptors that bind these metabolites have also been explored with positive findings—examples include known short-chain fatty acid receptors, such as G-protein coupled receptors GPR41, GPR43, GPR109a, and OLF78 in mice. GPR41 and OLF78 have been shown to have inverse roles in blood pressure regulation, whereas GPR43 and GPR109A have to date been demonstrated to impact cardiac function. New treatment options in the form of prebiotics (eg, dietary fiber), probiotics (eg, Lactobacillus spp.), and postbiotics (eg, the short-chain fatty acids acetate, propionate, and butyrate) have all been demonstrated to be beneficial in lowering blood pressure in animal models, but the underlying mechanisms remain poorly understood and translation to hypertensive patients is still lacking. Here, we review the evidence for the role of the gut microbiota in hypertension, its risk factors, and cardiorenal complications and identify future directions for this exciting and fast-evolving field.

Heart failure is a global health issue with significant mortality and morbidity. There is increasing evidence that alterations in the gastrointestinal microbiome, gut epithelial permeability, and gastrointestinal disorders contribute to heart failure progression through various pathways, including systemic inflammation, metabolic dysregulation, and modulation of cardiac function. Moreover, several medications used to treat heart failure directly impact the microbiome. The relationship between the gastrointestinal tract and the heart is bidirectional, termed the gut-heart axis. It is increasingly understood that diet-derived microbial metabolites are key mechanistic drivers of the gut-heart axis. This includes, for example, trimethylamine N -oxide and short-chain fatty acids. This review discusses current insights into the interplay between heart failure, its associated risk factors, and the gut microbiome, focusing on key metabolic pathways, the role of dietary interventions, and the potential for gut-targeted therapies. Understanding these complex interactions could pave the way for novel strategies to mitigate heart failure progression and improve patient outcomes.

Chronic kidney disease (CKD) has been associated with changes in gut microbial ecology, or “dysbiosis,” which may contribute to disease progression. Recent studies have focused on dietary approaches to favorably alter the composition of the gut microbial communities as a treatment method in CKD. Resistant starch (RS), a prebiotic that promotes proliferation of gut bacteria such as Bifidobacteria and Lactobacilli, increases the production of metabolites including short-chain fatty acids, which confer a number of health-promoting benefits. However, there is a lack of mechanistic insight into how these metabolites can positively influence renal health. Emerging evidence shows that microbiota-derived metabolites can regulate the incretin axis and mitigate inflammation via expansion of regulatory T cells. Studies from animal models and patients with CKD show that RS supplementation attenuates the concentrations of uremic retention solutes, including indoxyl sulfate and p-cresyl sulfate. Here, we present the current state of knowledge linking the microbiome to CKD, we explore the efficacy of RS in animal models of CKD and in humans with the condition, and we discuss how RS supplementation could be a promising dietary approach for slowing CKD progression.