The populations of dominant species within the human colonic microbiota can potentially be modified by dietary intake with consequences for health. Here we examined the influence of precisely controlled diets in 14 overweight men. Volunteers were provided successively with a control diet, diets high in resistant starch (RS) or non-starch polysaccharides (NSPs) and a reduced carbohydrate weight loss (WL) diet, over 10 weeks. Analysis of 16S rRNA sequences in stool samples of six volunteers detected 320 phylotypes (defined at 498% identity) of which 26, including 19 cultured species, each accounted for 41% of sequences. Although samples clustered more strongly by individual than by diet, time courses obtained by targeted qPCR revealed that 'blooms' in specific bacterial groups occurred rapidly after a dietary change. These were rapidly reversed by the subsequent diet. Relatives of Ruminococcus bromii (R-ruminococci) increased in most volunteers on the RS diet, accounting for a mean of 17% of total bacteria compared with 3.8% on the NSP diet, whereas the uncultured Oscillibacter group increased on the RS and WL diets. Relatives of Eubacterium rectale increased on RS (to mean 10.1%) but decreased, along with Collinsella aerofaciens, on WL. Inter-individual variation was marked, however, with 460% of RS remaining unfermented in two volunteers on the RS diet, compared to o4% in the other 12 volunteers; these two individuals also showed low numbers of R-ruminococci (o1%). Dietary non-digestible carbohydrate can produce marked changes in the gut microbiota, but these depend on the initial composition of an individual's gut microbiota.
Background: It has been proposed that the development of obesity in humans is influenced by the relative proportions of the two major phyla of bacteria (Bacteroidetes and Firmicutes) present in the large intestine. Objective: To examine the relationships between body mass index, weight loss and the major bacterial groups detected in fecal samples. Design: Major groups of fecal bacteria were monitored using fluorescent in situ hybridization (FISH) in obese and non-obese subjects under conditions of weight maintenance, and in obese male volunteers undergoing weight loss on two different reduced carbohydrate weight-loss diets given successively for 4 weeks each. Results: We detected no difference between obese and non-obese individuals in the proportion of Bacteroidetes measured in fecal samples, and no significant change in the percentage of Bacteroidetes in feces from obese subjects on weight loss diets. Significant diet-dependent reductions in a group of butyrate-producing Firmicutes were, however, detected in fecal samples from obese subjects on weight loss diets. Conclusions: Diets designed to achieve weight loss in obese subjects can significantly alter the species composition of the gut microbiota, but we find no evidence that the proportions of Bacteroidetes and Firmicutes among fecal bacteria have a function in human obesity.
Weight loss diets for humans that are based on a high intake of protein but low intake of fermentable carbohydrate may alter microbial activity and bacterial populations in the large intestine and thus impact on gut health. In this study, 19 healthy, obese (body mass index range, 30 to 42) volunteers were given in succession three different diets: maintenance (M) for 3 days (399 g carbohydrate/day) and then high protein/ medium (164 g/day) carbohydrate (HPMC) and high protein/low (24 g/day) carbohydrate (HPLC) each for 4 weeks. Stool samples were collected at the end of each dietary regimen. Total fecal short-chain fatty acids were 114 mM, 74 mM, and 56 mM (P < 0.001) for M, HPMC, and HPLC diets, respectively, and there was a disproportionate reduction in fecal butyrate (18 mM, 9 mM, and 4 mM, respectively; P < 0.001) with decreasing carbohydrate. Major groups of fecal bacteria were monitored using nine 16S rRNA-targeted fluorescence in situ hybridization probes, relative to counts obtained with the broad probe Eub338. No significant change was seen in the relative counts of the bacteroides (Bac303) (mean, 29.6%) or the clostridial cluster XIVa (Erec482, 23.3%), cluster IX (Prop853, 9.3%), or cluster IV (Fprau645, 11.6%; Rbro730 plus Rfla729, 9.3%) groups. In contrast, the Roseburia spp. and Eubacterium rectale subgroup of cluster XIVa (11%, 8%, and 3% for M, HPMC, and HPLC, respectively; P < 0.001) and bifidobacteria (4%, 2.1%, and 1.9%, respectively; P ؍ 0.026) decreased as carbohydrate intake decreased. The abundance of butyrate-producing bacteria related to Roseburia spp. and E. rectale correlated well with the decline in fecal butyrate.Low-carbohydrate diets in which carbohydrates are largely replaced by an increased proportion of dietary protein and/or fat have proved a popular weight loss strategy for humans (1,11,36). The potential health impacts associated with increased protein (34) or fat (27) intake have been controversial among nutritionists, but less attention has been paid to the consequences of low carbohydrate supply. It has been argued that a lower carbohydrate supply may be advantageous in ameliorating insulin insensitivity (9), although this may not occur with low-glycemic-index foods (21). Furthermore, in the context of overall dietary advice consideration also needs to be given to the role of carbohydrates in maintenance of gut health and function.Dietary carbohydrates include structural polysaccharides and oligosaccharides of plant origin plus resistant starch (14, 40) that are not digested in the small intestine and, instead, enter the colon. Here they can be fermented by the microbiota of the large intestine and normally provide the main energy supply to support microbial growth in the colon. Microbial fermentation may release as much as 10% of the dietary energy, mainly in the form of short-chain fatty acids (SCFA) that also act as energy sources for host cells (46). For example, butyrate is the preferred energy source for the epithelial cells of the colon (29, 50). Furthermore, butyr...
After 4 wk, weight-loss diets that were high in protein but reduced in total carbohydrates and fiber resulted in a significant decrease in fecal cancer-protective metabolites and increased concentrations of hazardous metabolites. Long-term adherence to such diets may increase risk of colonic disease.
There is growing interest in understanding how diet affects the intestinal microbiota, including its possible associations with systemic diseases such as metabolic syndrome. Here we report a comprehensive and deep microbiota analysis of 14 obese males consuming fully controlled diets supplemented with resistant starch (RS) or non-starch polysaccharides (NSPs) and a weight-loss (WL) diet. We analyzed the composition, diversity and dynamics of the fecal microbiota on each dietary regime by phylogenetic microarray and quantitative PCR (qPCR) analysis. In addition, we analyzed fecal short chain fatty acids (SCFAs) as a proxy of colonic fermentation, and indices of insulin sensitivity from blood samples. The diet explained around 10% of the total variance in microbiota composition, which was substantially less than the inter-individual variance. Yet, each of the study diets induced clear and distinct changes in the microbiota. Multiple Ruminococcaceae phylotypes increased on the RS diet, whereas mostly Lachnospiraceae phylotypes increased on the NSP diet. Bifidobacteria decreased significantly on the WL diet. The RS diet decreased the diversity of the microbiota significantly. The total 16S ribosomal RNA gene signal estimated by qPCR correlated positively with the three major SCFAs, while the amount of propionate specifically correlated with the Bacteroidetes. The dietary responsiveness of the individual's microbiota varied substantially and associated inversely with its diversity, suggesting that individuals can be stratified into responders and non-responders based on the features of their intestinal microbiota.
A sustainable diet that meets dietary requirements for health with lower GHGEs can be achieved without eliminating meat or dairy products or increasing the cost to the consumer.
The FTO gene has significant polymorphic variation associated with obesity, but its function is unknown. We screened a population of 150 whites (103F/47M) resident in NE Scotland, United Kingdom, for variants of the FTO gene and linked these to phenotypic variation in their energy expenditure (basal metabolic rate (BMR) and maximal oxygen consumption VO 2 max) and energy intake. There was no significant association between the FTO genotype and BMR or VO 2 max. The FTO genotype was significantly associated (P = 0.024) with variation in energy intake, with average daily intake being 9.0 MJ for the wild-type TT genotype and 10.2 and 9.5 MJ for the "at risk" AT and AA genotypes, respectively. Adjusting intake for BMR did not remove the significance (P = 0.043). FTO genotype probably affects obesity via effects on food intake rather than energy expenditure. Obesity (2008Obesity ( ) 16, 1961Obesity ( -1965Obesity ( . doi:10.1038Obesity ( /oby.2008 Obesity is a chronic condition associated with increases in the risk of type 2 diabetes, hypertension, cardiovascular disease, and various forms of cancer (1). Over the past 30 years, there has been a dramatic increase in the prevalence of obesity throughout the entire world (2). In the United States, for example, levels of obesity (BMI > 30 kg/m 2 ) in 1999-2002 were 32% of the adult population (3). Studies of mono-and di-zygotic twins have established that the variation in adult body fatness has a large genetic component (4-7).Studies of the regulation of food intake in rodent models of obesity have led to the identification of several cases where obesity is the consequence of single loss of function mutations in particularly important genes involved in regulation of body weight (8). However, these monogenic forms of obesity appear to be very rare (9). Over the past few years, several genes have been identified from wide-scale screening studies with common variants associated with differences in obesity. These studies include variants in the INSIG (10), GAD2 (11), ENPP1 (12), and FTO (13) genes. Attempts to replicate the effects of variants in the first three of these genes have met with variable success (14-16). However, the effect of polymorphic variation in the FTO gene (13), which was established in a genome-wide association study of a population of 1,924 type 2 diabetics combined with 2,938 controls, was replicated in 13 separate cohorts comprising almost 39,000 individuals. This verification lends strong support to the suggestion that this gene has common variants (the AA and AT genotypes) that predispose to obesity, relative to the wild (TT) genotype.The effect of genotype on BMI was detectable from 7 years old upward (1). Subsequent studies have confirmed the effect of the FTO variants on both obesity and diabetes (17,18).The FTO gene was originally cloned from a mutant mouse that had fused toes (Ft) (19) although the mutation in that instance included deletion of at least six separate genes, one of which was FTO. Expression studies indicate that FTO is widely expr...
With an ageing population, dietary approaches to promote health and independence later in life are needed. In part, this can be achieved by maintaining muscle mass and strength as people age. New evidence suggests that current dietary recommendations for protein intake may be insufficient to achieve this goal and that individuals might benefit by increasing their intake and frequency of consumption of high-quality protein. However, the environmental effects of increasing animal-protein production are a concern, and alternative, more sustainable protein sources should be considered. Protein is known to be more satiating than other macronutrients, and it is unclear whether diets high in plant proteins affect the appetite of older adults as they should be recommended for individuals at risk of malnutrition. The review considers the protein needs of an ageing population (>40 years old), sustainable protein sources, appetite-related implications of diets high in plant proteins, and related areas for future research.
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