chondroitin-sulfates and Weight-Gain

A nutrient retention study and a growth study were conducted with broiler chickens to evaluate the nutritive value and potential toxicity of 2 hairless canary seed products-hulled seed and groats (cultivar CDC Maria), and one hairy hulled canary seed (cultivar Keet). Each treatment was replicated 6 times (6 groups of 4 birds each). The hairless canary seed groat, hairless hulled canary seed, and the hairy hulled canary seed contained 24.5, 21.8, and 16.3% CP; 7.1, 5.8, and 6.6% ether extract; 1.5, 14.2, and 12.3% acid detergent fiber, and 3,867, 3,205 and 3,292 kcal/kg of AME(n), on a DM basis, respectively. The hairless canary seed groat, hairless hulled canary seed, and the hairy hulled canary seed protein comprised, respectively, 0.49, 0.33, and 0.33% lysine (DM basis), which was 79, 78, and 67% digestible (apparent ileal); 0.65, 0.53, and 0.60% cysteine (DM basis), which was 86, 87, and 85% apparent ileal digestible; and 0.40, 0.30, and 0.25% methionine (DM basis), which was 89, 90, and 86% apparent ileal digestible. In the second study, a 35-d feeding study with male broiler chickens was conducted. The canary seed products were compared with a Canadian Western Red Spring wheat control. Each treatment was replicated 6 times (6 groups of 4 birds each). The test ingredients comprised 50% of the corn/soybean diets. The birds fed the hulled canary seed (hairy or hairless) had similar weight gain, feed intake, and G:F to those fed wheat. There were no statistically significant (P = 0.05) differences in the weights of the bursa, heart, kidneys, liver, spleen, or the pancreas, nor was there any effect on serum lactate dehydrogenase or creatine kinase. The data indicated that feeding hulled canary seed increased the number of gizzard ulcers (P < 0.01). It was concluded that canary seed does not contain anti-nutritional components that negatively affect broiler performance or bird health. However, the canary seed hulls may damage the gizzard lining.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Chickens; Chondroitin Sulfates; Dermatan Sulfate; Diet; Digestion; Eating; Gastrointestinal Tract; Heparitin Sulfate; Male; Phalaris; Weight Gain

This study investigated the effects of fucosylated chondroitin sulfate (CHS) isolated from sea cucumber on glucose metabolism and insulin signaling in the liver of insulin-resistant C57BL/6 mice fed a high-fat, high-sucrose diet (HFSD). Male C57BL/6J mice were randomly assigned into six groups: control; HFSD; 1 mg RSG/kg·body weight (RSG); 80 mg CHS/kg · body weight (CHS); 20 mg CHS+1 mg RSG/kg · body weight (20 CHS+RSG); and 80 mg CHS+1 mg RSG/kg · body weight (80 CHS+RSG). Blood glucose, insulin parameters, glucose metabolism-related enzymes activities and insulin-signaling transducers in the liver were analyzed at 19 weeks. Results showed that CHS significantly decreased body weight gain, adipose tissue weight, and fasting blood glucose and serum insulin levels in insulin-resistant mice. Rosiglitazone (RSG) is an effective thiazolidinedione hypoglycemic agent, and CHS synergistically enhanced the effect of RSG. CHS feeding normalized the activities of hexokinase, pyruvate kinase, glycogen phosphorylase, glucose-6-phosphatase, and increased glycogen reserves in the liver. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis showed that CHS promoted the mRNA expression of insulin receptors (IR), insulin receptor substrate 2 (IRS-2), phosphatidylinositol 3 kinase (PI3K), protein kinase B (PKB), and glycogen synthase (GS) in the liver of insulin resistant mice, and inhibited glycogen synthase kinase-3 (GSK-3β) mRNA expression. The results suggested that CHS treatment improved glucose metabolism by modulating metabolic enzymes and promoting the PI3K/PKB/GSK-3β signaling pathway mediated by insulin at the transcriptional level. These results provided strong justification for the development of CHS as a functional food.

Topics: Adipose Tissue; Animals; Blood Glucose; Carbohydrate Metabolism; Chondroitin Sulfates; Diet, High-Fat; Dietary Sucrose; Drug Synergism; Glycogen; Glycogen Synthase; Hypoglycemic Agents; Insulin; Insulin Receptor Substrate Proteins; Liver; Male; Mice; Mice, Inbred C57BL; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Real-Time Polymerase Chain Reaction; Rosiglitazone; Sea Cucumbers; Signal Transduction; Thiazolidinediones; Weight Gain