The therapeutic potential of manipulating gut microbiota in obesity and type 2 diabetes mellitus.

Obesity and type 2 diabetes mellitus (T2DM) are attributed to a combination of genetic susceptibility and lifestyle factors. Their increasing prevalence necessitates further studies on modifiable causative factors and novel treatment options. The gut microbiota has emerged as an important contributor to the obesity--and T2DM--epidemic proposed to act by increasing energy harvest from the diet. Although obesity is associated with substantial changes in the composition and metabolic function of the gut microbiota, the pathophysiological processes remain only partly understood. In this review we will describe the development of the adult human microbiome and discuss how the composition of the gut microbiota changes in response to modulating factors. The influence of short-chain fatty acids, bile acids, prebiotics, probiotics, antibiotics and microbial transplantation is discussed from studies using animal and human models. Ultimately, we aim to translate these findings into therapeutic pathways for obesity and T2DM in humans.

The environment within: how gut microbiota may influence metabolism and body composition.

Obesity, diabetes and consequently atherosclerotic vascular disease have become major health and public health issues worldwide. The increasing and staggering prevalence of obesity might not only be explained by nutritional habits or the reduction of energy expenditure through decreased physical activity. In addition, recent studies have focused on intestinal microbiota as environmental factors that increase energy yield from diet, regulate peripheral metabolism and thereby increase body weight. Obesity is associated with substantial changes in composition and metabolic function of gut microbiota, but the pathophysiological processes driving this bidirectional relationship have not been fully elucidated. This review discusses the relationships between the following: composition of gut microbiota, energy extracted from diet, synthesis of gut hormones involved in energy homeostasis, production of butyrate and the regulation of fat storage.

Fecal transplant: a safe and sustainable clinical therapy for restoring intestinal microbial balance in human disease?

Recent studies have suggested an association between intestinal microbiota composition and human disease, however causality remains to be proven. With hindsight, the application of fecal transplantation (FMT) does indeed suggest a causal relation between interfering with gut microbiota composition and a resultant cure of several disease states. In this review, we aim to show the available evidence regarding the involvement of intestinal microbiota and human (autoimmune) disease. Moreover, we refer to (mostly case report) studies showing beneficial or adverse effects of fecal transplantation on clinical outcomes in some of these disease states. If these findings can be substantiated in larger randomized controlled double blind trials also implementing gut microbiota composition before and after intervention, fecal transplantation might provide us with novel insights into causally related intestinal microbiota, that might be serve as future diagnostic and treatment targets in human disease.

Low bone mineral density in COPD patients related to worse lung function, low weight and decreased fat-free mass.

UNLABELLED: Low bone mineral density is frequently seen in COPD patients. Advanced COPD, low BMI and muscle depletion are risk factors for developing low bone mineral density (BMD). Low bone mineral density is seen in 75% of the GOLD stage IV patients. INTRODUCTION: We set out to investigate the prevalence of low bone mineral density (BMD) in chronic obstructive pulmonary disease (COPD) as well as the predictors of abnormal bone mineral density. METHODS: A cross-sectional design was used to evaluate 115 subjects with COPD (GOLD stages II-IV). Bone mineral density (BMD) was measured using an ultrasound densitometer. The forced expiratory volume in 1 s (FEV(1)) was assessed and fat-free mass was measured using bioelectrical impedance analysis. Chi-square tests and logistic regression were used for analysis. RESULTS: The prevalence of a T-score < -1.0 SD and > -2.5 SD was 28.6% in GOLD stage II, 40.3% in GOLD stage III and 57.1% in GOLD stage IV. The prevalence of a T-score