Purpose In this review, we summarize current evidence on the gut microbiome and microbial metabolites in relation to obesity and obesity-associated metabolic disorders. Special emphasis is given on mechanisms interconnecting gut microbiome and microbial metabolites with metabolic disorders as well as on potential preventive and therapeutic perspectives with a "bench to bedside" approach. Recent Findings Recent data have highlighted the role of gut dysbiosis in the etiology and pathogenesis of metabolic disorders, including obesity, metabolic syndrome, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. Overall, most studies have demonstrated a reduction in gut microbiome diversity and richness in obese subjects, but there is still much debate on the exact microbial signature of a healthy or an obese gut microbiome. Despite the controversial role of an altered gut microbiome as a cause or consequence of obesity in human studies, numerous animal studies and certain human studies suggest beneficial metabolic effects of certain microbial intestinal metabolites, such as butyrate, that could be used in the prevention and treatment of obesity and its comorbidities. Summary More randomized controlled trials and larger prospective studies including well-defined cohorts as well as a multiomics approach are warranted to better identify the associations between the gut microbiome, microbial metabolites, and obesity and its metabolic complications.

Honey mainly consists of sugars and water. Apart from sugars, honey also contains several vitamins, especially B complex and vitamin C, together with a lot of minerals. Some of the vitamins found in honey include ascorbic acid, pantothenic acid, niacin and riboflavin; while minerals such as calcium, copper, iron, magnesium, manganese, phosphorus, potassium and zinc are also present. Honey has been used for its healing, nutritional and therapeutic properties since ancient times. Its antibacterial potentials even against multi-drug resistant bacteria, such as Staphylococcus aureus, Pseudomonas aeruginosa and Acinetobacterbaumanni have been proved. Honey is well known for its anti-inflammatory and antioxidant capacities, which may be useful for the prevention of chronic inflammatory process like atherosclerosis, diabetes mellitus and cardiovascular diseases. The antibacterial, antiinflammatory and antioxidant properties of honey will be reviewed here.

Chronic Kidney Disease is a growing health burden world widely. Traditional and mutual risk factors between CVD and CKD are age, hypertension, diabetes mellitus, dyslipidemia, tobacco use, family history and male gender. In this review, we will focus on whether or not early CKD is an important risk factor for the presence, severity and progression of CVD. Specifically, we will examine both traditional and novel risk factors of both CKD and CVD and how they relate to each other. We will also assess if early treatment of CKD, intensive compared to standard, has an important effect on the halt of the development of CKD as well as CVD. Insights into the pathogenesis and early recognition of CKD as well as the importance of novel kidney biomarkers will be pointed out. Also, common pathogenetic mechanisms between CKD and CVD will be discussed.

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This study investigated the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in infected and uninfected diabetic foot ulcers of 84 patients with the two types of diabetes. S. aureus was the most common pathogen among the Gram-positive bacteria isolated from ulcers, and almost 50% of S. aureus isolates were MRSA. The prevalence of MRSA was significantly higher in patients with infected foot ulcers. MRSA infection or colonisation was not associated with factors (previous hospitalisation, use of antibiotics, etc.) known to predispose to MRSA colonisation or infection. The high prevalence of MRSA in patients with foot ulcers may reflect the increased prevalence of MRSA in the community.

Diabetic neuropathy presents a major public health problem. It is defined by the symptoms and signs of peripheral nerve dysfunction in diabetic patients, in whom other causes of neuropathy have been excluded. Pathogenetic mechanisms that have been implicated in diabetic neuropathy are: a) increased flux through the polyol pathway, leading to accumulation of sorbitol, a reduction in myo-inositol, and an associated reduced Na+-K+-ATPase activity, and b) endoneurial microvascular damage and hypoxia due to nitric oxide inactivation by increased oxygen free radical activity. Alpha-lipoic acid seems to delay or reverse peripheral diabetic neuropathy through its multiple antioxidant properties. Treatment with alpha-lipoic acid increases reduced glutathione, an important endogenous antioxidant. In clinical trials, 600 mg alpha-lipoic acid has been shown to improve neuropathic deficits. This review focuses on the relationship of alpha-lipoic acid and auto-oxidative glycosylation. It discusses the impact of alpha-lipoic acid on hyperglycemia-induced oxidative stress, and examines the role of alpha-lipoic acid in preventing glycation process and nerve hypoxia.

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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. NAFLD begins as a relatively benign hepatic steatosis which can evolve to non-alcoholic steatohepatitis (NASH); the risk of cirrhosis and hepatocellular carcinoma (HCC) increases when fibrosis is present. NAFLD represents a complex process implicating numerous factors—genetic, metabolic, and dietary—intertwined in a multi-hit etiopathogenetic model. Recent data have highlighted the role of gut dysbiosis, which may render the bowel more permeable, leading to increased free fatty acid absorption, bacterial migration, and a parallel release of toxic bacterial products, lipopolysaccharide (LPS), and proinflammatory cytokines that initiate and sustain inflammation. Although gut dysbiosis is present in each disease stage, there is currently no single microbial signature to distinguish or predict which patients will evolve from NAFLD to NASH and HCC. Using 16S rRNA sequencing, the majority of patients with NAFLD/NASH exhibit increased numbers of Bacteroidetes and differences in the presence of Firmicutes, resulting in a decreased F/B ratio in most studies. They also present an increased proportion of species belonging to Clostridium, Anaerobacter, Streptococcus, Escherichia, and Lactobacillus, whereas Oscillibacter, Flavonifaractor, Odoribacter, and Alistipes spp. are less prominent. In comparison to healthy controls, patients with NASH show a higher abundance of Proteobacteria, Enterobacteriaceae, and Escherichia spp., while Faecalibacterium prausnitzii and Akkermansia muciniphila are diminished. Children with NAFLD/NASH have a decreased proportion of Oscillospira spp. accompanied by an elevated proportion of Dorea, Blautia, Prevotella copri, and Ruminococcus spp. Gut microbiota composition may vary between population groups and different stages of NAFLD, making any conclusive or causative claims about gut microbiota profiles in NAFLD patients challenging. Moreover, various metabolites may be involved in the pathogenesis of NAFLD, such as short-chain fatty acids, lipopolysaccharide, bile acids, choline and trimethylamine-N-oxide, and ammonia. In this review, we summarize the role of the gut microbiome and metabolites in NAFLD pathogenesis, and we discuss potential preventive and therapeutic interventions related to the gut microbiome, such as the administration of probiotics, prebiotics, synbiotics, antibiotics, and bacteriophages, as well as the contribution of bariatric surgery and fecal microbiota transplantation in the therapeutic armamentarium against NAFLD. Larger and longer-term prospective studies, including well-defined cohorts as well as a multi-omics approach, are required to better identify the associations between the gut microbiome, microbial metabolites, and NAFLD occurrence and progression.