Abstract
The metabolome and gut microbiota were investigated in a juvenile Göttingen minipig model. This study aimed to explore the metabolic effects of two carbohydrate sources with different degrees of risk in obesity development when associated with a high fat intake. A high-risk (HR) high-fat diet containing 20% fructose was compared to a control lower-risk (LR) high-fat diet where a similar amount of carbohydrate was provided as a mix of digestible and resistant starch from high amylose maize. Both diets were fed ad libitum. Non-targeted metabolomics was used to explore plasma, urine, and feces samples over five months. Plasma and fecal short-chain fatty acids were targeted and quantified. Fecal microbiota was analyzed using genomic sequencing. Data analysis was performed using sparse multi-block partial least squares regression. The LR diet increased concentrations of fecal and plasma total short-chain fatty acids, primarily acetate, and there was a higher relative abundance of microbiota associated with acetate production such as Bacteroidetes and Ruminococcus. A higher proportion of Firmicutes was measured with the HR diet, together with a lower alpha diversity compared to the LR diet. Irrespective of diet, the ad libitum exposure to the high-energy diets was accompanied by well-known biomarkers associated with obesity and diabetes, particularly branched-chain amino acids, keto acids, and other catabolism metabolites.
Highlights
The abnormal accumulation of fat in adipose tissues, i.e., obesity, is a major component in the development of metabolic syndrome (MetS) [1]
The alpha-diversity of fecal microbiota collected from pigs fed the LR diet containing high amylose maize starch (HiMaize) was reduced compared to that of HR-fed pigs at each time point tested over the 20-week intervention (Figure 1a–c)
Multi-compartmental metabolomics allowed for the identification of several pathways altered by ad libitum intake of a high-fat diet containing fructose compared to one containing HiMaize
Summary
The abnormal accumulation of fat in adipose tissues, i.e., obesity, is a major component in the development of metabolic syndrome (MetS) [1]. Obesity and MetS affect the human population through a series of co-morbidities, primarily cardiovascular disease (CVD), diabetes, and hypertension, and are nowadays considered as worldwide epidemics [2]. Fructose has been suggested as a contributing risk factor to the development of obesity and MetS [3,4]. The modern human population has been increasingly exposed to fructose, through the addition of high-fructose corn syrup to pre-processed foods and soft drinks [3,5]. Fructose only modestly stimulates insulin secretion and insulin is not necessary for the cellular uptake of this carbohydrate. Once available for hepatic metabolism, fructose is rapidly converted to fructose-1-phosphate, bypassing regulating mechanisms
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