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Carbon stable isotope breath tests offer new opportunities to better understand gastrointestinal function in health and disease. However, it is often not clear how to isolate information about a gastrointestinal or metabolic process of interest from a breath test curve, and it is generally unknown how well summary statistics from empirical curve fitting correlate with underlying biological rates. We developed a framework that can be used to make mechanistic inference about the metabolic rates underlying a 13C breath test curve, and we applied it to a pilot study of 13C-sucrose breath test in 20 healthy adults. Starting from a standard conceptual model of sucrose metabolism, we determined the structural and practical identifiability of the model, using algebra and profile likelihoods, respectively, and we used these results to develop a reduced, identifiable model as a function of a gamma-distributed process; a slower, rate-limiting process; and a scaling term related to the fraction of the substrate that is exhaled as opposed to sequestered or excreted through urine. We demonstrated how the identifiable model parameters impacted curve dynamics and how these parameters correlated with commonly used breath test summary measures. Our work develops a better understanding of how the underlying biological processes impact different aspect of 13C breath test curves, enhancing the clinical and research potential of these 13C breath tests. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated the effect of small manipulations in carbohydrate (CHO) dose on exogenous and endogenous (liver and muscle) fuel selection during exercise.Method: Eleven trained males cycled in a double-blind randomised order on 4 occasions at 60% [Formula: see text] for 3 h, followed by a 30-min time-trial whilst ingesting either 80 g h-1 or 90 g h-1 or 100 g h-1 13C-glucose-13C-fructose [2:1] or placebo. CHO doses met, were marginally lower, or above previously reported intestinal saturation for glucose-fructose (90 g h-1). Indirect calorimetry and stable mass isotope [13C] techniques were utilised to determine fuel use.Result: Time-trial performance was 86.5 to 93%, 'likely, probable' improved with 90 g h-1 compared 80 and 100 g h-1. Exogenous CHO oxidation in the final hour was 9.8-10.0% higher with 100 g h-1 compared with 80 and 90 g h-1 (ES = 0.64-0.70, 95% CI 9.6, 1.4 to 17.7 and 8.2, 2.1 to 18.6). However, increasing CHO dose (100 g h-1) increased muscle glycogen use (101.6 ± 16.6 g, ES = 0.60, 16.1, 0.9 to 31.4) and its relative contribution to energy expenditure (5.6 ± 8.4%, ES = 0.72, 5.6, 1.5 to 9.8 g) compared with 90 g h-1. Absolute and relative muscle glycogen oxidation between 80 and 90 g h-1 were similar (ES = 0.23 and 0.38) though a small absolute (85.4 ± 29.3 g, 6.2, - 23.5 to 11.1) and relative (34.9 ± 9.1 g, - 3.5, - 9.6 to 2.6) reduction was seen in 90 g h-1 compared with 100 g h-1. Liver glycogen oxidation was not significantly different between conditions (ES < 0.42). Total fat oxidation during the 3-h ride was similar in CHO conditions (ES < 0.28) but suppressed compared with placebo (ES = 1.05-1.51).Conclusion: 'Overdosing' intestinal transport for glucose-fructose appears to increase muscle glycogen reliance and negatively impact subsequent TT performance. [ABSTRACT FROM AUTHOR]

Dietary fibers (DF) can prevent obesity in rodents fed a high-fat diet (HFD). Their mode of action is not fully elucidated, but the gut microbiota have been implicated. This study aimed to identify the effects of seven dietary fibers (barley beta-glucan, apple pectin, inulin, inulin acetate ester, inulin propionate ester, inulin butyrate ester or a combination of inulin propionate ester and inulin butyrate ester) effective in preventing diet-induced obesity and links to differences in cecal bacteria and host gene expression. Mice (n = 12) were fed either a low-fat diet (LFD), HFD or a HFD supplemented with the DFs, barley beta-glucan, apple pectin, inulin, inulin acetate ester, inulin propionate ester, inulin butyrate ester or a combination of inulin propionate ester and inulin butyrate ester for 8 weeks. Cecal bacteria were determined by Illumina MiSeq sequencing of 16S rRNA gene amplicons. Host responses, body composition, metabolic markers and gene transcription (cecum and liver) were assessed post intervention. HFD mice showed increased adiposity, while all of the DFs prevented weight gain. DF specific differences in cecal bacteria were observed. Results indicate that diverse DFs prevent weight gain on a HFD, despite giving rise to different cecal bacteria profiles. Conversely, common host responses to dietary fiber observed are predicted to be important in improving barrier function and genome stability in the gut, maintaining energy homeostasis and reducing HFD induced inflammatory responses in the liver. [ABSTRACT FROM AUTHOR]