Role of Colonic Short Chain Fatty Acids in Obesity: Acute Effects of Inulin and Resistant Starch on Postprandial Short Chain Fatty Acid, Glucose, Insulin, Free-fatty Acid and Gut Hormone Responses
试验速览
- 阶段
- 不适用
- 状态
- 已完成
- 入组人数
- 25
- 试验地点
- 2
- 主要终点
- Serum acetate response
研究概览
简要总结
It has been suggested that obesity occurs because the colonic microbes in obese individuals, compared to those who are lean, produce more short chain fatty acids during the fermentation of dietary fiber; this means that obese individuals obtain more energy from dietary fiber than lean. On the other hand, it is possible that the ability of colonic short chain fatty acids to improve glycemic control and suppress appetite may be reduced in obese subjects. The aim of this study was to determine the acute effects of 2 fibers commonly used as food ingredients, inulin and resistant starch, on postprandial serum responses of short chain fatty acids, glucose, insulin, free-fatty acids and selected gut hormones in lean and overweight or obese subjects.
详细描述
The human colon (large intestine) contains hundreds of species of bacteria which exist in a symbiotic (mutually beneficial) relationship with their human host. The number and type of colonic bacteria varies in different people. Recent studies show that overweight individuals have different types of bacteria in their colons than lean subjects, and that as overweight subjects lose weight their colonic bacteria change to resemble those in lean subjects. It was suggested that this was because the bacteria in overweight people more efficiently ferment dietary fiber thus producing more SCFAs and providing more energy to the body. However, this is not consistent with other studies showing that high fiber intakes are associated with reduced risk of obesity.
Some studies have shown that overweight people have higher concentrations of SCFA in their stool samples. But the reasons for the difference in stool concentrations of SCFA have not been studied. Stool concentrations of SCFA may differ in lean and overweight people because of differences in type of bacteria in their colons, differences in dietary intakes or maybe because lean and overweight people absorb SCFA produced by bacteria differently.
Therefore, the objectives of this study were to:
- determine the relationship between SCFA production and the acute effects of consuming an unabsorbed carbohydrate on blood SCFA, FFA, glucose, insulin, c-peptide and gut hormone responses in lean and overweight subjects
- determine the types of bacteria in the stools of lean and overweight subjects
- to see if the types of bacteria are correlated with body weight, the composition of the diet, breath gases, fecal SCFA and other demographic and lifestyle factors.
Healthy subjects with a BMI <25 (lean) or between 25 and 35 (overweight or obese; OWO) took part in a 2 phase study. In phase 1 subjects recorded their dietary intake for 3 days and then provided a stool sample for analysis of micro-organisms and short chain fatty acids. In phase 2 overnight fasted subjects were studied on 3 occasions separated by about a week. On each occasion subjects consumed a control test meal of dextrose, or dextrose plus inulin or dextrose plus resistant start and had breath and blood samples taken at intervals over 4 hours. Subjects were then given a standardized lunch and had more blood and breath samples taken over the next 2 hours.
研究设计
- 研究类型
- Interventional
- 分配方式
- Randomized
- 干预模型
- Crossover
- 主要目的
- Basic Science
- 盲法
- None
入排标准
- 年龄范围
- 18 Years 至 —（Adult, Older Adult）
- 性别
- All
- 接受健康志愿者
- 是
入选标准
- •over 18 years of age
排除标准
- •BMI<18 or >39.9
- •use of diuretics of beta-blockers
- •regular user of antibiotics (≥1 course per year over the last 5 years)
- •any use of antibiotics within 3 months
- •use of laxatives, weight reducing agents, pre/probiotics or supplements known to influence gastrointestinal function within 3 months
- •presence of inflammatory bowel disease, malabsorption, motility disorder, gastrointestinal infection, short bowel, or other condition affecting gastrointestinal function
- •liver or kidney disease or major medical or surgical event (within the last 6 months) requiring hospitalization
- •high fibre intake (>30g/day) or other abnormal dietary pattern
- •on a weight-loss diet or not on their habitual diet in the two months prior to the study
- •unwilling or unable to give informed consent and/or comply with study protocol
结局指标
主要结局
Serum acetate response
时间窗: 0 to 6 hours after the intervention
Incremental area under the curve of the serum acetate response from the lowest concentration achieved during the first 3 hours to the end of the study (6hr)
次要结局
- Protein intake(3 days)
- Carbohydrate intake(3 days)
- Fat intake(3 days)
- Serum propionate response(0 to 6 hours after the intervention)
- Energy intake(3 days)
- Dietary fiber intake(3 days)
- 0-2 hour Glucose response(0 to 2 hours after consuming treatment)
- Serum butyrate response(0 to 6 hours after the intervention)
- Second-meal glucose response(0 to 2 hours after lunch)
- 2-4 hour Insulin response(2-4 hours after consuming treatment)
- Post-lunch active glucagon-like peptide-1 response(0 to 2 hours after consuming lunch)
- Post-lunch ghrelin response(0 to 2 hours after consuming lunch)
- Breath hydrogen response(0 to 6 hours after the intervention)
- Fecal microbiota(1 day)
- 2-4 hour Glucose response(2 to 4 hours after consuming treatment)
- 0-2 hour Insulin response(0 to 2 hours after consuming treatment)
- Acute peptide tyrosine tyrosine response(0 to 4 hours after consuming intervention)
- Acute ghrelin response(0 to 4 hours after consuming intervention)
- Second-meal Insulin response(0-to 2 hours after lunch)
- 2-4 hour c-peptide response(2 to 4 hours after consuming treatment)
- Second-meal c-peptide response(0-2 hours after lunch)
- Post-lunch total glucagon-like peptide-1 response(0 to 2 hours after consuming lunch)
- 0-2 hour c-peptide response(0 to 2 hours after consuming treatment)
- Free-fatty acid rebound(0 to 4 hours after consuming intervention)
- Acute active glucagon-like peptide-1 response(0 to 4 hours after consuming intervention)
- Acute total glucagon-like peptide-1 response(0 to 4 hours after consuming intervention)
- Post-lunch peptide tyrosine tyrosine response(0 to 2 hours after consuming lunch)
研究者
Thomas Wolever
Professor
University of Toronto