The impact of gut microbiota and its metabolites on fat metabolism have been widely reported in human and animals. However, the critical mediators and the signal transductions are not well demonstrated. As ovipara, chicken represents a specific case in lipid metabolism that liver is the main site of lipid synthesis. The aim of this study is to elucidate the linkage of gut microbiota and fat synthesis in broiler chickens. The broilers were subjected to dietary treatments of combined probiotics (Animal bifidobacterium: 4 × 10⁸ cfu/kg; Lactobacillus plantarum: 2 × 10⁸ cfu/kg; Enterococcus faecalis: 2 × 10⁸ cfu/kg; Clostridium butyrate: 2 × 10⁸ cfu/kg, PB) and guar gum (1 g/kg, GG), respectively. Results showed that dietary supplementation of PB and GG changed the cecal microbiota diversity, altered short chain fatty acids (SCFAs) contents, and suppressed lipogenesis. In intestinal epithelial cells (IECs), SCFAs (acetate, propionate, and butyrate) up-regulated the expression of glucagon-like peptide-1 (GLP-1) via mitogen-activated protein kinase (MAPK) pathways, mainly via the phospho - extracellular regulated protein kinase (ERK) and phospho-p38 mitogen activated protein kinase (p38 MAPK) pathways. GLP-1 suppressed lipid accumulation in primary hepatocytes with the involvement of (AMP)-activated protein kinase/Acetyl CoA carboxylase (AMPK/ACC) signaling. In conclusion, the result suggests that SCFAs-induced GLP-1 secretion via MAPK pathway, which links the regulation of gut microbiota on hepatic lipogenesis in chickens.

Circulating Tumor Cell (CTC) adhesion is essential in understanding the mechanism of metastasis. Although conventional methods for measuring adhesion strength have performed well on cell populations, a deeper insight into cell behavior demands new approaches for realizing non-destructive, high-resolution, in situ analysis of single cell adhesion. Here, we present a microfluidic method for adhesion strength analysis of single CTCs on a base layer of endothelial cells (ECs) to clarify cell-to-cell adhesion at single cell resolution. A confined flow in open space formed by a microfluidic device supplied a trypsin zone for the analysis of single cell adhesion. Tumor cell lines were used to model CTCs. This method was proved successful for extracting different types of CTCs from an endothelial cell layer to measure their adhesion strength by the time required for detachment. Moreover, we successfully uncovered the drug influence on the adhesion strength of single CTCs on ECs, which is promising in drug screening for tumor therapy. The current work reports a general strategy for cell-to-cell adhesion analysis for single cells.