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We have identified the effects of oligonol, a low-molecular polyphenol derived from lychee fruit, on oxidative stress and lipid metabolism in a type 2 diabetic model. Oligonol was orally administered at 10 or 20 mg per kg body weight per d for 8 weeks to db/db mice, and its effects were compared with those of the vehicle in db/db and m/m mice. Serum and hepatic biochemical factors, and protein and mRNA expression related to lipid metabolism were measured. In the oligonol-administered group, there were significant reductions of reactive oxygen species (ROS), lipid peroxidation, and the TAG and total cholesterol concentrations in both the serum and liver. Additionally, oligonol attenuated oxidative stress through the inhibition of advanced glycation endproduct formation and its receptor expression. Furthermore, augmented expressions of NF-kBp65 and inducible NO synthase were down-regulated to the levels of m/m mice in the group treated with oligonol at 20 mg/kg. Regarding lipid metabolism, lower hepatic lipid resulted from the down-regulation of sterol regulatory element-binding protein-1 and its target gene of lipogenic enzymes in the liver of db/db mice. The present results suggest that oligonol has protective effects against ROS-related inflammation and excess lipid deposition in the type 2 diabetic liver.Key words: Oligonol: Type 2 diabetes: Oxidative stress: Dyslipidaemia: Steatosis Type 2 diabetes is associated with oxidative stress and abnormal lipid metabolism due to hyperglycaemia and hyperlipidaemia. Increased reactive oxygen species (ROS) generation and lipid peroxidation activate stress-sensitive intracellular signalling pathways such as the transcription of NF-kB, which plays a central role in inflammation-related disease (1) . In addition, hyperglycaemia accelerates the formation of advanced glycation endproducts (AGE), which are proteins produced from non-enzymic glycation reactions (2) . AGE and their binding with receptors, such as the receptor for AGE (RAGE), galectin-3 and CD36, induce free radical formation. They accumulate during the normal ageing process and at accelerated rates during the course of diabetes, and are associated with the pathogenesis of chronic diseases such as arthritis, atherosclerosis, liver cirrhosis and diabetic nephropathy (3) . Therefore, the attenuation of oxidative stress during the initiation and propagation of type 2 diabetes is important to prevent a vicious cycle of inflammatory responses and tissue damage. Moreover, insulin resistance in type 2 diabetes leads to a marked disruption of lipid dynamics, often reflected by elevated levels of circulating NEFA and TAG, together with excess fat deposition in various tissues (4) . Lipid homeostasis is regulated by a transcription factor, sterol regulatory elementbinding protein (SREBP), which is highly expressed in the presence of metabolic disorders such as obesity and diabetes. In particular, up-regulated SREBP-1 has been suggested to play a central role in the development of hepatic steatosis in an insulin-res...

This study investigated the anti-obesity effects of collagen peptide derived from skate skin on lipid metabolism in high-fat diet (HFD)-fed mice. All C57BL6/J male mice were fed a HFD with 60% kcal fat except for mice in the normal group which were fed a chow diet. The collagen-fed groups received collagen peptide (1050 Da) orally (100, 200, or 300 mg/kg body weight per day) by gavage, whereas the normal and control groups were given water (n = 9 per group). The body weight gain and visceral adipose tissue weight were lower in the collagen-fed groups than in the control group (p < 0.05). Plasma and hepatic lipid levels were significantly reduced by downregulating the hepatic protein expression levels for fatty acid synthesis (sterol regulatory element binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)) and cholesterol synthesis (SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)) and upregulating those for β-oxidation (peroxisome proliferator-activated receptor alpha (PPAR-α) and carnitine palmitoyltransferase 1 (CPT1)) and synthesis of bile acid (cytochrome P450 family 7 subfamily A member 1 (CYP7A1)) (p < 0.05). In the collagen-fed groups, the hepatic protein expression level of phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK) and plasma adiponectin levels were higher, and the leptin level was lower (p < 0.05). Histological analysis revealed that collagen treatment suppressed hepatic lipid accumulation and reduced the lipid droplet size in the adipose tissue. These effects were increased in a dose-dependent manner. The findings indicated that skate collagen peptide has anti-obesity effects through suppression of fat accumulation and regulation of lipid metabolism.

Vegetable-based diets have generally focused on their health benefits including negative associations with the serum cholesterol concentrations. The aim of this study was to investigate whether serum lipid concentrations are influenced by the amount of kimchi intake. For the study, 100 volunteers were assigned to 2 dietary groups, low (15 g/day, n = 50) and high (210 g/day, n = 50) kimchi intake, and were housed together in a dormitory for 7 days. Identical meals except with different amount of kimchi were provided and subjects were instructed to maintain their normal physical activity. Concentrations of fasting blood glucose (FBG), total glucose, total cholesterol and low density lipoprotein (LDL)-C significantly decreased in both groups after 7 days of kimchi intake, but the effects were dose dependent. Lipid lowering effects of kimchi were more profound in the subjects with total cholesterol and LDL-C level over 190 and 130 mg/dL, respectively, in both groups. FBG was significantly decreased in the high kimchi intake as compared to the low intake group (P = .003). In conclusion, greater consumption of kimchi improved FBG and serum total cholesterol in young healthy adults.

The present study was conducted to examine whether morroniside has an ameliorative effect on diabetes-induced alterations such as oxidative stress, inflammation, and apoptosis in the liver of type 2 diabetic db/db mice. Morroniside (20 or 100 mg/kg body weight/d, per os ( p.o.)) was administered every day for 8 weeks to db/db mice, and its effect was compared with vehicle-treated db/db and m/m mice. The administration of morroniside decreased the elevated serum glucose concentration in db/db mice, and reduced the increased oxidative biomarkers including the generation of reactive oxygen species and lipid peroxidation in the liver. The db/db mice exhibited the up-regulation of nicotinamide adenine dinucleotide phosphate oxidase subunits, NF-E2-related factor 2 (Nrf2), heme oxygenase-1, nuclear factor-kappa B, cyclooxygenase-2, inducible nitric oxide synthase, monocyte chemotactic protein-1, and intracellular adhesion molecule-1 levels in the liver; however, morroniside treatment significantly reduced those expressions. Moreover, the augmented expressions of apoptosis-related proteins, Bax and cytochrome c, were down-regulated by morroniside administration. Hematoxylin-eosin staining showed that the increased hepatocellular damage in the liver of db/db mice improved on morroniside administration. Taking these into consideration, our findings support the therapeutic evidence for morroniside ameliorating the development of diabetic hepatic complications via regulating oxidative stress, inflammation, and apoptosis.