The infusion of donor feces was significantly more effective for the treatment of recurrent C. difficile infection than the use of vancomycin. (Funded by the Netherlands Organization for Health Research and Development and the Netherlands Organization for Scientific Research; Netherlands Trial Register number, NTR1177.).

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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.

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.

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Summary 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 ≤−2.5 SD was 0% in GOLD stage II, 9.6% in GOLD stage III and 17.9% in GOLD stage IV. In a logistic model FFM, BMI and FEV 1 were significant predictors of abnormal bone mineral density. Patients in GOLD stage IV have a 7.6 times greater risk of abnormal bone mineral density than patients in GOLD stage II. Conclusions Low bone mineral density is frequently present in COPD patients. Low FFM, BMI and FEV 1 are risk factors for developing a low T-score. A low FFM or BMI in GOLD stage IV strongly suggests loss of BMD and warrants further examination.

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