The anti-obesity and anti-diabetic effects of the edible seaweed Gloiopeltis furcata (Postels et Ruprecht) J. Agardh in mice fed a high-fat diet.
Shigeru MurakamiChihiro HirazawaToshiki MizutaniRina YoshikawaTakuma OhyaNing MaYutaka OwakiToyohiro OwakiTakashi ItoChiaki MatsuzakiPublished in: Food science & nutrition (2022)
Obesity and diabetes are serious, chronic medical conditions associated with a wide range of life-threatening conditions. The aim of this study was to investigate the effects of the edible red seaweed Gloiopeltis furcata (Postels et Ruprecht) J. Agardh ( G. furcata ) on the development of obesity, diabetes and related metabolic diseases in mice. Male C57BL/6J mice were fed a high-fat (HF) diet (60% energy as fat), or an HF diet containing 2% (w/w) or 6% powdered G. furcata for 13 weeks. Polysaccharides of G. furcata were isolated and their anti-inflammatory effects were evaluated in lipopolysaccharide-stimulated RAW264.7 cells. The HF diet group showed greater weight gain, lipid accumulation in the body and liver, and increased serum levels of glucose and cholesterol in comparison to the normal group fed a normal diet (10% energy as fat). The treatment of HF diet mice with G. furcata reduced these changes and stimulated the fecal excretion of fat. In addition, G. furcata suppressed the HF diet-induced elevation of inflammation and oxidative stress markers in the serum and liver. The isolated sulfated polysaccharide from G. furcata inhibited pancreatic lipase activity and decreased the production of nitric oxide and TNF-α in the murine macrophage cell line RAW264.7. These results show that G. furcata treatment can attenuate obesity, diabetes, hepatic steatosis, and dyslipidemia in mice fed an HF diet, which is associated with inhibited intestinal fat absorption and reduced inflammation and oxidative stress by a sulfated polysaccharide.
Keyphrases
- high fat diet induced
- weight loss
- insulin resistance
- weight gain
- adipose tissue
- oxidative stress
- type diabetes
- high fat diet
- physical activity
- glycemic control
- metabolic syndrome
- nitric oxide
- induced apoptosis
- cardiovascular disease
- body mass index
- birth weight
- acute heart failure
- dna damage
- skeletal muscle
- healthcare
- ischemia reperfusion injury
- wild type
- heart failure
- inflammatory response
- hydrogen peroxide
- endoplasmic reticulum stress
- cell proliferation
- diabetic rats
- blood pressure
- nitric oxide synthase
- gestational age
- signaling pathway
- atrial fibrillation
- pi k akt