View clinical trials related to Meal Time.
Filter by:The frequency of meals is a very important aspect of nutrition, with profound effects on human health and in life expectancy. Excessive energy consumption is totally associated with a significant increase in the incidence of chronic diseases including diabetes. That is why nutritional therapy is recommended for all people with diabetes mellitus type 1 and 2 as an effective complement to your medical treatment. For overweight or obese type 2 diabetic patients, a low-calorie diet along with healthy eating patterns are recommended for weight loss. Similarly, modest body weight decrease may provide clinical benefits in patients, such as improved blood glucose, blood pressure, lipid profile, and others. Data about the role of nutritional habits and energy density being important precursors of obesity and diabetes are well known. On the other hand, data regarding frequency and timing of meals and how these factors relate to corporal weight are not totally understood.
The interplay between diet and the gut microbiota has been implicated in the onset of cardiovascular disease. The gut microbiota displays diurnal rhythms, which may be influenced by meal timing. This study aimed to investigate the effect of main meal consumption timing on the microbiota and the cardiometabolic factors of the host using a cross-over RCT in healthy adults The main outcome measurements will be: a) changes in gut microbiota composition based on 16S rRNA gene amplicon sequencing and shotgun metagenomics, b) changes in bacterial functional capacity) and urinary/faecal metabolomics, c) changes in targeted bacterial metabolites, d)Inflammatory markers The aim of this study is to explore the effect of the timing of main meal consumption on gut microbiota and immune response in healthy adults.
Excessive fat in the liver is associated with impairments in metabolic health. Low levels of DNL and high levels of hepatic fat oxidation are considered to be protective. A decrease in glycogen stores has been causally linked to improved whole body fat oxidation. Also on an organ level, it is suggested that hepatic fat oxidation is stimulated by low hepatic glycogen stores. Next to hepatic fat oxidation, DNL may be influenced by hepatic glycogen stores. Some studies have shown that prolongation of fasting time lowers hepatic glycogen content. It is therefore hypothesized that prolonging fasting time will lower glycogen content and thereby increases fat oxidation and decreases DNL in the liver. To this end, hepatic fat oxidation (plasma marker beta-hydroxybutyrate), de novo lipogenesis, hepatic glycogen content and intrahepatic fat content, will be measured upon a short overnight fast and an extended overnight fast in 13 overweight/obese subjects with hepatic steatosis.