Antimicrobial promotion of pig growth is associated with tissue-specific remodeling of bile acid signature and signaling

The spread of bacterial resistance to antimicrobials (AMA) have intensified efforts to discontinue the non-therapeutic use of AMA in animal production. Finding alternatives to AMA, however, is currently encumbered by the obscure mechanism that underlies their growth-promoting action. In this report, we demonstrate that combinations of antibiotics and zinc oxide at doses commonly used for stimulating growth or preventing post-weaning enteritis in pigs converge in promoting microbial production of bile acids (BA) in the intestine. This leads to tissue-specific modifications in the proportion of BA, thereby amplifying BA signaling in intestine, liver, and white adipose tissue (WAT). Activation of BA-regulated pathways ultimately reinforces the intestinal protection against bacterial infection and pathological secretion of fluids and electrolytes, attenuates inflammation in colon and WAT, alters protein and lipid metabolism in liver, and increases the circulating levels of the hormone FGF19. Conceivably, these alterations could spare nutrients for growth and improve the metabolic efficiency of AMA-treated animals. This work provides evidence that BA act as signaling molecules that mediate host physiological, metabolic, and immune responses to the AMA-induced alterations in gut microbial metabolism, eventually permitting the growth-promoting action of AMA. Consequently, BA emerge as a promising target for developing efficacious alternatives to AMA

Chicken or the Egg: The Reciprocal Association Between Feeding Behavior and Animal Welfare and Their Impact on Productivity in Dairy Cows

Feeding behavior in dairy cattle has a significant impact on feed efficiency, which is important for increasing the profitability of livestock and, at the same time, reducing the environmental impact. Feeding behavior can be measured by feeding time, meal duration, meal frequency, feeding rate, and rumination time. Higher feed intake is related to lower feed efficiency; whereas, an increase in feeding time facilitates chewing, reduces feed particle size and increases its digestibility. More frequent and shorter meals are usually associated with a more efficient use of feed due to improvement of feed digestibility. Rumination time is positively associated with milk production. Impaired health is associated with variations in feeding behavior, which can be used to identify and predict some diseases such as ketosis, mastitis, or lameness. Changes in rumination time are also a reliable indicator of mastitis, lameness, ketosis, abomasal displacement, and the onset of calving. In addition to the cause-effect relationship between disease and changes in feeding behavior, there are also some cases in which changes in feeding behavior may lead to an increased risk of disease, as exemplified by the relationship of feeding rate with sub-acute ruminal acidosis. Feeding behavior is regulated by internal and external factors and some of them are relevant for animal welfare. The main welfare-associated factors influencing feeding behavior are social behavior and temperament, and environmental effects. Cattle are social animals and hierarchy has a notable impact on feeding behavior, especially when access to feed is limited. Competition for feed causes a reduction in the average feeding time but increases feeding rate. Excitable animals visit the feeder more often and spend less time per meal. High environmental temperature affects feeding behavior, as heat-stressed cattle change their feeding pattern by concentrating the feeding events in crepuscular hours, leading to an increased risk of sub-acute ruminal acidosis. In conclusion, feeding behavior is a determinant feature for improving efficiency, productivity and welfare of dairy cattle. Routine assessment of feeding behavior allows monitoring of health and production status of dairy cattle at the individual and farm level, which is a useful tool to optimize the management of livestock

A comprehensive in-vitro/in-vivo screening toolbox for the elucidation of glucose homeostasis modulating properties of plant extracts (from roots) and its bioactives

Plant extracts are increasingly recognized for their potential in modulating (postprandial) blood glucose levels. In this context, root extracts are of particular interest due to their high concentrations and often unique spectrum of plant bioactives. To identify new plant species with potential glucose-lowering activity, simple and robust methodologies are often required. For this narrative review, literature was sourced from scientific databases (primarily PubMed) in the period from June 2022 to January 2024. The regulatory targets of glucose homeostasis that could be modulated by bioactive plant compounds were used as search terms, either alone or in combination with the keyword “root extract”. As a result, we present a comprehensive methodological toolbox for studying the glucose homeostasis modulating properties of plant extracts and its constituents. The described assays encompass in-vitro investigations involving enzyme inhibition (α-amylase, α-glucosidase, dipeptidyl peptidase 4), assessment of sodium-dependent glucose transporter 1 activity, and evaluation of glucose transporter 4 translocation. Furthermore, we describe a patch-clamp technique to assess the impact of extracts on KATP channels. While validating in-vitro findings in living organisms is imperative, we introduce two screenable in-vivo models (the hen’s egg test and Drosophila melanogaster). Given that evaluation of the bioactivity of plant extracts in rodents and humans represents the current gold standard, we include approaches addressing this aspect. In summary, this review offers a systematic guide for screening plant extracts regarding their influence on key regulatory elements of glucose homeostasis, culminating in the assessment of their potential efficacy in-vivo. Moreover, application of the presented toolbox might contribute to further close the knowledge gap on the precise mechanisms of action of plant-derived compounds

N-3 fatty acids combined with flavan-3-ols prevent steatosis and liver injury in a murine model of NAFLD

Non-alcoholic fatty liver disease (NAFLD) affects 25% of adults and at present no licensed medication has been approved. Despite its complex patho-physiology, dietary strategies aiming at delaying or preventing NAFLD have taken a reductionist approach, examining the impact of single components. Accumulating evidence suggests that n-3 LC-PUFAs are efficacious in regulating lipogenesis and fatty acid oxidation. In addition, plant derived flavonoids are also emerging as a dietary strategy for NAFLD prevention, with efficacy attributed to their insulin sensitising and indirect antioxidant effects. Based on knowledge of their complementary molecular targets, we aimed to demonstrate that the combination of n-3 LC-PUFA (n-3) and flavan-3-ols (FLAV) prevents NAFLD. In a high-fat high-fructose (HF/HFr) fed C57Bl/6 J mouse model, the independent and interactive impact of n-3 and FLAV on histologically defined NAFLD, insulin sensitivity, weight gain, intestinal and hepatic gene expression, intestinal bile acids were examined. Only the combination of FLAV and n-3 (FLAVn-3) prevented steatosis as evidenced by a strong reduction in hepatocyte ballooning. While FLAV reduced body (− 28–30%), adipose tissue (− 45–50%) weights and serum insulin (− 22–25%) as observed following an intra-peritoneal glucose tolerance test, n-3 downregulated the expression of Srebf1 and the lipogenic genes (Acaca, Fasn). Significant impacts of interventions on intestinal bile acid metabolism, farnesoid X receptor (Fxr) signalling in the intestine and liver, and hepatic expression of fatty acid transporters (Fabp4, Vldlr, Cd36) were also evident. FLAVn-3 may be a novel intervention for NAFLD. Future research should aim to demonstrate its efficacy in the prevention and treatment of human NAFLD