Polysaccharide-Rich Red Algae ( Gelidium amansii ) Hot-Water Extracts Alleviate Abnormal Hepatic Lipid Metabolism without Suppression of Glucose Intolerance in a Streptozotocin/Nicotinamide-Induced Diabetic Rat Model

• Published in: Molecules (Basel, Switzerland) Switzerland), 2022-02, Vol.27 (4), p.1447
• Main Authors: Liu, Shing-Hwa, Ku, Chia-Yu, Chiang, Meng-Tsan
• Format: Article
• Language: English
• Subjects: Adipose tissue; Adipose Tissue - drug effects; Adipose Tissue - metabolism; Algae; Animals; Biomarkers; Blood Glucose - drug effects; Body fat; Body weight; Chemical Fractionation; Cholesterol; Diabetes; Diabetes mellitus; Diabetes Mellitus, Experimental; diabetic rats; Diet; Disease Models, Animal; Drinking water; Enzymes; Experiments; Flavonoids; Food; Gelidium amansii; Glucose; Glucose Intolerance - drug therapy; Glucose Intolerance - metabolism; Glucose metabolism; Glucose tolerance; Glycogen; Glycogens; Insulin; Intolerance; Kinases; Lipid metabolism; Lipid Metabolism - drug effects; Lipids; Lipolysis; Liver; Liver - drug effects; Liver - metabolism; Male; Metabolism; Nicotinamide; Obesity; Phosphatase; Phosphorylation; polysaccharide-rich; Polysaccharides; Polysaccharides - chemistry; Polysaccharides - isolation & purification; Polysaccharides - pharmacology; Proteins; Rats; red algae hot-water extracts; Rhodophyta - chemistry; Rodents; Solvents; Streptozocin
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules27041447

This study was designed to investigate the effects of polysaccharide-rich red algae ( ) hot-water extracts (GHE) on lipid and glucose metabolism in rats with streptozotocin (STZ)/nicotinamide (NA)-induced diabetes. Rats were divided into three groups: NC-normal control group), DM-diabetic group, and DG-diabetic group supplemented with GHE (5%). The experimental diet and drinking water were available ad libitum for 10 weeks. After the 10-week feeding duration, the body weight, liver weight, total adipose tissue weight, and hepatic TBARS and cholesterol levels were significantly increased, and hepatic glycogen content and adipose lipolysis rate were significantly decreased in the DM group, which could be effectively reversed by supplementation of GHE. However, GHE supplementation could not improve the glucose intolerance in DM rats. It was interesting to note that GHE supplementation could decrease the liver glucose-6-phosphotase activity, which was increased in DM rats. Taken together, these results suggested that GHE feeding may ameliorate abnormal hepatic lipid metabolism, but not glucose intolerance, in diabetic rats induced by STZ/NA.