No abstract

BackgroundChanges of gastrointestinal motility, which are important related to the food digestion and absorption in the gastrointestinal tract, may be one of the factors in obesity-formation.AimsThe changes of gastrointestinal motility were explored in the rats from diet-induced obesity (DIO), diet-induced obese resistant (DR) or control (CON) by diet intervention.MethodsAfter fed with a high fat diet (HFD), 100 male Sprague–Dawley rats were divided into DIO, DR and CON groups. The rats from DIO and DR groups were fed with HFD, and CON with a basic diet (BD) for 6 weeks. Body weight, energy intake, gastric emptying, intestinal transit, motility of isolated small intestine segments and colon’s function were measured in this study. Expression of interstitial cells of Cajal (ICCs) and enteric nervous system (ENS) - choline acetyltransferase (ChAT), vasoactive intestinal peptides (VIP), substance P (SP) and NADPH-d histochemistry of nitric oxide synthase (NOS) were determined by immunohistochemistry.ResultsBody weight and intake energy in the DIO group were higher than those in the DR group (p < 0.05). Gastric emptying of DIO group rats (78.33 ± 4.95%) was significantly faster than that of DR group (51.79 ± 10.72%) (p < 0.01). The peak value of motility in rat’s duodenum from the DR group was significantly higher than that in the DIO group (p < 0.05). In addition, the expression of interstitial cells of Cajal (ICC), choline acetyltransferase (ChAT), substance P (SP), vasoactive intestinal peptides (VIP) and neuronal nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) in the intestine of rats were significantly increased in the DIO group when compared to the DR group (p < 0.05).ConclusionA faster gastric emptying, a weaker contraction of duodenum movement, and a stronger contraction and relaxation of ileum movement were found in the rats from the DIO group. It indicated that there has effect of gastrointestinal motility on obesity induced by HFD.

Although microRNAs (miRNAs) have been intensively studied in cardiac fibrosis, their roles in drug-mediated anti-fibrotic therapy are still unknown. Previously, Pioglitazone attenuated cardiac fibrosis and increased miR-711 experimentally. We aimed to explore the role and mechanism of miR-711 in pioglitazone-treated myocardial infarction in rats. Our results showed that pioglitazone significantly reduced collagen-I levels and increased miR-711 expression in myocardial infarction heart. Pioglitazone increased the expression of miR-711 in cardiac fibroblasts, and overexpression of miR-711 suppressed collagen-I levels in angiotensin II (Ang II)-treated or untreated cells. Transfection with antagomir-711 correspondingly abolished the pioglitazone-induced reduction in collagen-I levels. Bioinformatics analysis identified SP1, which directly promotes collagen-I synthesis, as the putative target of miR-711. This was confirmed by luciferase assay and western blot analysis. Additionally, increased SP1 expression was attenuated by pioglitazone in myocardial infarction heart. Furthermore, transfection of antagomir-711 attenuated pioglitazone-reduced SP1 expression in cardiac fibroblasts with or without Ang II stimulation. We conclude that pioglitazone up-regulated miR-711 to reduce collagen-I levels in rats with myocardial infarction. The miR-711-SP1-collagen-I pathway may be involved in the anti-fibrotic effects of pioglitazone. Our findings may provide new strategies for miRNA-based anti-fibrotic drug research. pioglitazone, miR-711, cardiac fibrosis Citation:Zhao N, Yu H Y, Yu H T, et al. miRNA-711-SP1-collagen-I pathway is involved in the anti-fibrotic effect of pioglitazone in myocardial infarction.

In DIO rats, the heart mitochondrial dysfunction occurred first and the liver presented the strongest compensatory ability against oxidative stress.

The aim of the present study was to examine the interactions of fructose and fat on glucose regulation and lipid metabolism in CD-1 mice. Mice were assigned in five groups. The control group was provided with tap water and a gavage of vehicle; four experimental groups were treated with 150 g/l fructose solution (FS1), fat emulsion (FE), 150 g/l fructose solution and fat emulsion (FS1+FE), or 70 g/l fructose solution and fat emulsion (FS2+FE) for 12 weeks. At the end of the 8th week, both oral glucose tolerance test and insulin tolerance test were conducted. Lipid profiles in serum, liver, and red gastrocnemius muscle, and serum insulin and glucose concentrations were assessed. The FS1+FE group showed combined glucose intolerance (CGI) and decrease of insulin sensitivity. The low-density lipoprotein cholesterol (LDL-C) concentrations were elevated in all experimental groups (p<0.05). The combined diet groups showed statistically significant (p<0.01) increase in total cholesterol (TC) level in comparison with the control FE (p<0.05), or FS1 (p<0.05) group. Triglyceride levels in liver and red gastrocnemius muscle were significantly increased in FE and combined groups. In conclusion, combination of FE and 150 g/l fructose solution for 8 weeks led to CGI. Fructose enhanced the adverse effect of FE on glucose regulation with increasing percentage in the diet. Furthermore, there was a synergistic effect of fructose and fat on elevating the serum TC level.