Abstract
A dysregulation of nutrient exchange between tissues (gut, liver, muscles, adipose) occurs during overnutrition and could induce obesity and metabolic diseases. We aimed to evaluate how, in overfed mini pigs, nutrients use and partition were regulated in the gut and liver. Net nutrients fluxes were assessed in the fed (PP) and post absorptive (PA) states at 1, 14 and 60 days of adaptation to overfeeding in five adult Yucatan female multicatheterized minipigs. Pigs PA glycaemia and PP-induced hyperglycemia remained unchanged over the experimental period, suggesting that the management of the excess of energy intake allowed the maintenance of glucose levels. This was associated with (1) an increased PA plasma insulin, (2) an increased gut lactate production (increased lactate net release +89%, 1 h PP, D1 vs. D60) probably from an increased glucose oxidation, (3) a shift in utilization of gluconeogenic precursor (lactate, propionate) in the liver, and (4) a reduced gut utilization of nitrogen moieties for energy purposes (glutamine), a nitrogen sparing effect at the whole body level (decreased plasma urea in PA (−24% D1 vs. D60) and PP states) and a specific increased level of AA involved in lipids handling and bile recycling in the gut lumen (taurine and glycine).
Highlights
Prevalence of overweight and obesity has increased dramatically over the last 35 years, as well as the associated chronic diseases [1]
To address the point concerning the early steps of obesity development, we have recently investigated the whole body and tissues metabolic adaptations by analyzing genes expressions and activities of enzymes involved in the major metabolic pathways of nutrients utilization/synthesis in gut, liver, and adipose and muscle tissues in Yucatan mini pigs overfed for two months with a high fat, high sucrose diet [18,19,20]
We have confirmed specific inter-organ metabolic adaptations developed by the pigs to handle the sudden and massive dietary supply of nutrients and we have shown the development of an obese phenotype, as well as a reduced potential to phosphorylate glucose, a decreased capacity for de novo lipogenesis and an increased arterial insulin and branched chain plasma amino acids
Summary
Prevalence of overweight and obesity has increased dramatically over the last 35 years, as well as the associated chronic diseases (diabetes, cardiovascular diseases, cancers) [1]. Obesity results from an imbalance between energy supply and expenditure due to increased food intake and reduced physical activity This imbalance, when occurring over a long period of time, induces metabolic dysregulations leading firstly to metabolic adaptations capable to maintain normal homeostatic state and later to the development of metabolic disturbances such as low grade inflammation [2], insulin resistance [3] and, pathologies. These late perturbations occur when tissues and organs are no longer capable to deal with the nutrient oversupply and maintain homeostasis compatible with a healthy status. An altered gut profile of bacteria species [8] and richness [9]
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