Metabolic Disorders Induced by Fructosedrinking Water Affect Angiotensin II-mediated Intestinal Contractility in Male Wistar Rats.

INTRODUCTION: The high-fructose diet in rats has been reported to cause metabolic disorders such as impaired fasting glucose levels, in-sulin resistance, dyslipidemia, and dysregulation of the renin-angiotensin system. This could lead to further complications, for instance, to the smooth muscle dysfunction. AIM: The present study aimed at developing fructose-induced metabolic perturbations in rats and the investigation of their impact on angiotensin II-induced smooth muscle intestinal motility. MATERIALS AND METHODS: Mature Wistar rats were randomly divided into two groups (9 rats per group): control group (drinking tap water) and fructose-drinking group (15% fructose, dissolved in tap water). At the end of the experimental period (11 weeks), the plasma levels of insulin, renin, angiotensin II and creatinine, as well as the lipid profile were assessed. Morphometric analysis and lipid index calculation were also performed. The contractile properties of ileum, colon and rectum were studied using stimulation with angiotensin II in the isolated tissue bath system. RESULTS: Our experiment showed that drinking 15% fructose solution induced dyslipidaemia accompanied by elevated lipid indexes as well as an increase in creatinine and renin plasma levels in the rats. CONCLUSIONS: Fructose drinking and consequently the developed metabolic disorders modified the Ang II-induced intestinal activity causing a gradual alteration in the distal direction with the rectum being the most strongly affected organ.

Fructose-induced metabolic disturbances in rats and its impact on stomach endocrine cell number and smooth muscle contractility.

Context: Gastric ghrelin-positive endocrine cells (GHR + EC) were most dense in the oxyntic mucosa.Objective: We evaluated ECs and contractile activity in rat stomach with metabolic disorders.Materials and methods: Male Wistar rats were divided into two groups: Control (n = 9) received tap water and Fructose (n = 9) drank 15% fructose solution for 12 weeks. Streptozotocin was applied in a dose of 20 mg/kg b.w. two weeks after the beginning of the experiment on Fructose group. Smooth-muscle strips from the stomach were influenced by Angiotensin II for analysis of parameters of contractions. Stomach samples were elaborated with immunohistochemistry for ghrelin, somatostatin, gastrin antibodies and with double immunofluorescence.Results: In treated animals, GHR + EC were significantly increased in the corpus where somatostatin-positive cells were decreased. Contractile activity was decreased.Conclusions: The increase number of GHR + EC was discussed in the context of Somatostatin and Gastrin-positive ECs variations and correlated with the decrease of smooth muscle contraction.

Hepatoprotective properties of Curcuma longa L. extract in bleomycin-induced chronic hepatotoxicity.

Curcuma longa L. (CLL) extract has previously been reported to alleviate liver damage. The current study examined the antioxidant activity of CLL by which the extract protects the liver against bleomycin (BLM)-induced hepatotoxicity in mice. The hypothesis was that CLL extract would protect the liver by reducing oxidative stress (induced superoxide dismutase (SOD) and catalase (CAT) activity), inhibiting lipid peroxidation, lowering biochemical parameters, and decreasing ROS production. Hepatic toxicity was induced by intraperitoneal injection of mice once daily with BLM (0.069 U/mL; 0.29 U/kg bw.) for a period of 4 weeks. The CLL was administered once a day for 4 weeks, 2 h prior at dose (40 mg/mL; 0.187 mg/kg/day). CLL extract significantly protected the liver, it decreased plasma bilirubin (BL) and gamma glutamyl transpeptidase (GGT), and it reduced lipid peroxidation levels. BLM intoxication produced oxidative stress, in which the antioxidant system functioned incorrectly and ROS production significantly increased. The CLL extract provided significant hepatic protection against BLM toxicity by improving SOD, CAT (p < 0.05), and MDA levels and decreasing ROS in the group receiving BLM (p < 0.05), leading to reduced membrane lipid peroxidation. Throughout this study, the CLL extract facilitated recovery from BLM-induced hepatic injury by suppressing oxidative stress. Therefore, the CLL extract has the potential to serve as an antioxidant compound to treat chronic hepatotoxicity.