Caulerpa lentillifera extract ameliorates insulin resistance and regulates glucose metabolism in C57BL/KsJ-db/db mice via PI3K/AKT signaling pathway in myocytes

Abstract

BackgroundGlucose homeostasis is distorted by defects of the PI3K/AKT and AMPK pathways in insulin-sensitive tissues, allowing the accumulation of glucose in the blood. The purpose of this study was to assess the effects and mechanisms by which ethanol extract of Caulerpa lentillifera (CLE) regulates glucose metabolism in C57BL/KsJ-db/db (db/db) mice.MethodsMice were administered CLE (250 or 500 mg/kg BW) or rosiglitazone (RSG, 10 mg/kg BW) for 6 weeks. Then, oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT) were performed, and blood glucose was measured in db/db mice. Levels of insulin and insulin resistance factors in plasma, glycogen content in the liver, and IRS, PI3K, AKT, and GLUT4 expressions in skeletal muscles were measured in db/db mice. Glucose uptake and insulin signaling molecules were measured in L6 myocytes, using fluorometry and Western blotting.ResultsCLE significantly decreased fasting blood glucose, glucose level in OGTT and IPITT, plasma insulin, homeostatic model assessment-insulin resistant (HOMA-IR), TNF-α, IL-6, FFA, TG and TC levels, and hepatic glycogen content in db/db mice. CLE significantly increased the activation of IRS, AKT, PI3K, and GLUT4, which are the key effector molecules of the PI3K/AKT pathway in L6 myocytes and the skeletal muscles of db/db mice. The enhanced glucose uptake by CLE was abolished by treatment with a PI3K inhibitor (LY294002), but not by an AMPK inhibitor (compound C) in L6 myocytes. CLE regulated glucose uptake and homeostasis via the PI3K/AKT pathway in myocytes and db/db mice, respectively.ConclusionOur results suggest that CLE could be a potential candidate for the prevention of diabetes.

Role of the PI3K-Akt Signaling Pathway in the Pathogenesis of Polycystic Ovary Syndrome

“…Sharma et al used C57BL/KsJ-db/db mice and gave them Caulerpa lentillifera (CLE) extract. 53 After 6 weeks, oral glucose tolerance test and intraperitoneal insulin tolerance test were performed and IRS, PI3K, AKT, and GLUT4 were assessed. It was found that CLE regulated glucose uptake and homeostasis via the PI3K-Akt signaling pathway in myocytes and db/db mice, respectively.…”

“…It was found that CLE regulated glucose uptake and homeostasis via the PI3K-Akt signaling pathway in myocytes and db/db mice, respectively. 53 Gandhi et al 54 showed that gallic acid could reduce IR. Gallic acid attenuated IR through adipose-specific partial agonism of peroxisome proliferator-activated receptor g and enhanced insulin-dependent glucose uptake through translocation and activation of GLUT4 in the PI3K-Akt signaling pathway in epididymal adipose tissue of insulin-resistant animal model.…”

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