This study investigated the effect and mechanism of pre-germinated brown rice (PGBR) prevented hyperglycemia in C57BL/6J mice fed high-fat-diet (HFD). Normal six-week-old mice were randomly divided into three groups. Group 1 was fed standard-regular-diet (SRD) and group 2 was fed HFD for 16 weeks. In group 3, the mice were fed a HFD with its carbohydrate replaced with PGBR for 16 weeks. Comparing the SRD and HFD groups, we found the HFD group had higher blood pressure, higher concentrations of blood glucose and HbA1c. The HFD group had less protein expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), phosphatidylinositol-3-kinase (PI3K), glucose transporter-4 (GLUT-4) and glucokinase (GCK) and greater expression of glucogen synthase kinase (GSK) in skeletal muscle. The HFD group also had less expression of IR, serine/threonine kinase PI3K-linked protein kinase B (Akt/PKB), AMP-activated protein kinase (AMPK), GCK and peroxisome proliferator-activated receptor γ (PPARγ) in liver. In the HFD + PGBR group, the PGBR could reverse the disorders of blood pressure, blood glucose, HbA1c and increase insulin concentration. PGBR increased the IR, IRS-1, PI3K, Akt, GLUT-1 and GLUT-4 proteins, and ameliorated AMPK, GCK, GSK and PPARγ proteins. Together, PGBR prevented HFD-induced hyperglycemia through improving insulin levels, insulin receptor, glucose transporters and enhancing glucose metabolism.

Seven new sesquiterpenoids, lochmolins A–G (1–7), were isolated from a Taiwanese soft coral Sinularia lochmodes. The structures of these metabolites were elucidated by extensive spectroscopic study. Compounds 1–4 were found to inhibit the accumulation of the LPS-induced pro-inflammatory COX-2 protein in RAW264.7 macrophage cells.

Pre-germinated brown rice (PGBR) can ameliorate hyperlipidemia, but the action mechanism is not clear. We focus the mechanisms of PGBR prevented hyperlipidemia. Six-week-old mice were divided into: standard-regular diet (SRD), high-fat diet (HFD) and HFD with PGBR (HFD + PGBR) groups for 16 weeks. The HFD group has higher concentrations of TG, TC, HDL and Non-HDL in the blood, and a higher atherosclerosis index (AI). The TG levels in the liver, and TG, bile acid levels in the feces were enhanced; and the total adipocytokines level in adipose tissue was reduced. The HFD group had higher protein expressions of SREBP-1, SCD-1, FAS, LDLR, and CYP7α1 in the liver. Moreover, the greater expressions of SREBP-1, SCD-1, FAS and the less expressions of PPAR-α and adiponectin were in adipose tissue. In the HFD + PGBR group, the PGBR regulated the levels of TG, TC, HDL, Non-HDL, AI and adipocytokines. PGBR increased more cholesterol and bile acid exhaust in feces. The SREBP-1, SCD-1, FAS, HMGCR, LDLR, CYP7α1 and PPAR-α proteins in the liver; and the SREBP-1, SCD-1, FAS, PPAR-α and adiponectin proteins in adipose tissue were reversed by PGBR. Taken together, PGBR can improve lipid synthesis and metabolism, and we suggest PGBR is a recommendable food for controlling hyperlipidemia.

This study examined the effect of pre‐germinated brown rice extract (PGBRE), containing no dietary fibers, but γ‐oryzanol, γ‐aminobutyric acid (GABA), flavonoids, and anthocyanidin, on high‐fat‐diet (HFD)‐induced metabolic syndrome. C57BL/6 mice were divided into five groups: regular diet, HFD, HFD with oral PGBRE 30, 300, or 600 mg/kg per day for 18 weeks. In the HFD group, higher body and liver weight gain, hyperglycemia, HbA1c, and insulin; higher TG, TC, LDL‐C, non‐HDL, atherosclerosis index, lower HDL, adiponectin in blood; higher TG in the liver; higher TG, bile acid in feces; and lower protein levels of AMP‐activated protein kinase, insulin receptor, insulin receptor substrate‐1, insulin receptor substrate‐2, peroxisome proliferator‐activated receptor‐γ, phosphatidylinositol‐3‐kinase, Akt/PKB, glucose transporter‐1, glucose transporter‐4, glucokinase in the skeletal muscle; lower glucagon‐like peptide 1 (GLP‐1) in the intestine; higher sterol regulatory element‐binding protein‐1 (SREBP‐1), stearoyl‐CoA desaturase 1 (SCD‐1), fatty acid synthase (FAS), 3‐hydroxy‐3‐methylglutaryl‐CoA reductase, proprotein convertase subtilisin/kexin type 9 (PCSK9), and lower PPAR‐α, low‐density lipoprotein receptor, cholesterol‐7α‐hydroxylase in the liver; higher SREBP‐1, SCD‐1, FAS, and lower PPAR‐α, adiponectin in the adipose tissue were found. In HFD + PGBRE groups, the above biochemical parameters were improved. Practical applications According to the results, we suggested that dietary fibers played a minor role in this study. Extract of PGBR, excluding dietary fiber, showed beneficial activity to ameliorate metabolic syndrome. γ‐oryzanol, GABA, flavonoids, and anthocyanidin in PGBRE can inhibit HFD‐induced metabolic syndrome and we demonstrated clearly its action mechanisms. This is the first report to examine the relation between PGBRE, GLP‐1, and PCSK9. Taken together, PGBRE can potentially be used to develop a good supplement to control metabolic syndrome.

In this study the effects of low-dose aspirin (5 mg/kg) on adhesion molecule and chemokine expression in a hyperlipidemic rat model. Six-week-old Sprague-Dawley (SD) rats were assigned to two control groups receiving either a regular diet or high-fat diet (HFD) and a treatment group fed HFD with 5 mg/kg aspirin for a 10-week period. Compared with the regular diet control group, the HFD control group had higher body weight, lower levels of high-density lipoprotein, higher concentrations of insulin, triglyceride, total cholesterol, and low-density lipoprotein, but no differences in blood glucose and glycated hemoglobin. The prothrombin time (PT) and activated partial thromboplastin time (aPTT) were clearly shortened in the HFD group. That group also had increased expression of intercellular adhesion molecule-1 (ICAM-1), ICAM-2, ICAM-3, vascular cell adhesion molecule (VCAM), platelet endothelial cell adhesion molecule (PECAM) and P-selectin in platelets and vascular adhesion protein-1 in lymphocyte and in aorta increased expressions of ICAM-1, ICAM-2, ICAM-3, VCAM, PECAM, E-selectin, monocyte chemoattractant protein-1 (MCP-1) and CCR2. The HFD rats also had increased PKCα, IκB kinase α (IKKα), p65, mitogen-activated protein kinases (MAPKs) (p38, c-Jun N-terminal kinases 1, extracellular signal-regulated kinase 1/2), and their phosphorylated forms. Low-dose aspirin improved HFD-induced hyperinsulinemia and hyperlipidemia, recovered PT and aPTT, inhibited upregulation of adhesion molecules and chemokines and reduced expression of PKCα, IKKα, p65, and MAPKs. Low-dose aspirin ameliorates HFD-induced hyperlipidemia and hyperinsulinemia, and prevents HFD-induced expression of adhesion molecules and chemokine formation.