Antihyperglycemic effect of extra virgin sacha inchi oil in type 2 diabetic rats: Mechanisms involved in pancreatic ß-cell function and apoptosis.

Background and aim: The purpose of the study was to investigate the anti-hyperglycemic effect of extra virgin sacha inchi oil (EVSIO) and its possible mechanisms and actions against pancreatic ß-cell death and dysfunction in type 2 diabetic (T2D) rats. Experimental procedure: T2D rats were induced with a high-fat diet and low-dose of streptozotocin. The rats were then treated for 5 weeks with EVSIO (0.5, 1, and 2 ml/kg), or pioglitazone. Biochemical and histopathological studies, oxidative and inflammatory markers, and expression of apoptotic-related proteins were then evaluated. Results: EVSIO treatment exhibited a dose-dependent reduction of fasting blood glucose, area under the curve of glucose, total cholesterol, and triglyceride levels in the diabetic rats, while improved pancreatic ß-function was demonstrated by increasing pancreatic and serum insulin levels. EVSIO treatment effectively lowered atrophic pancreatic islets and reduced the level of serum and pancreatic MDA in the diabetic rats. In addition to serum and pancreatic GPx activities in the diabetic rats, EVSIO also augmented serum SOD. Increased levels of NF-κB, TNF-α and IL-6 present in the diabetic rats were greatly reduced by EVSIO treatment. Furthermore, EVSIO revealed an anti-apoptotic effect on the diabetic rat pancreas by upregulating Bcl-2, and downregulating Bax and cleaved caspase-3 protein expression. Conclusion: The overall study results demonstrated the potential anti-hyperglycemic effect of EVSIO in the diabetic rats. The beneficial effects of EVSIO may be attributed to its ability to improve pancreatic ß-cell function and ameliorate ß-cell apoptosis by inhibiting oxidative stress and inflammatory cytokines.

Papaya improves non-alcoholic fatty liver disease in obese rats by attenuating oxidative stress, inflammation and lipogenic gene expression.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a global health issue that is correlated with obesity and oxidative stress. AIM: To evaluate the anti-NAFLD effect of papaya in high fat diet induced obesity in rats. METHODS: Four-week-old male Sprague-Dawley rats were divided into four groups after 1 wk of acclimatization: Group 1 was the rats fed a normal diet (C); group 2 was the rats fed a high fat diet (HFD); group 3 was the rats fed a HFD with 0.5 mL of papaya juice/100 g body weight (HFL), and group 4 was the rats fed a HFD with 1 mL of papaya juice/100 g body weight (HFH) for 12 wk. At the end of the treatment, blood and tissue samples were collected for biochemical analyses and histological assessment. RESULTS: The results of the HFH group showed significantly reduced body weight (HFH vs HFD, P < 0.01), decreased NAFLD score (HFH vs HFD, P < 0.05), and reduced hepatic total cholesterol (HFL vs HFD, P < 0.01; HFH vs HFD, P < 0.001), hepatic triglyceride (HFH vs HFD, P < 0.05), malondialdehyde (HFL, HFH vs HFD, P < 0.001), tumour necrosis factor-α (HFH vs HFD, P < 0.05) and interleukin-6 (HFH vs HFD, P < 0.05) when compared to the HFD group. However, the liver weight showed no significant difference among the groups. The activities of catalase and superoxide dismutase significantly increased in HFH when compared with the HFD group (P < 0.05 and P < 0.001, respectively). The suppression of transcriptional factors of hepatic lipogenesis, including sterol regulatory element-binding protein 1c and fatty acid synthase, were observed in the papaya treated group (HFH vs HFD, P < 0.05). These beneficial effects of papaya against HFD-induced NAFLD are through lowering hepatic lipid accumulation, suppressing the lipogenic pathway, improving the balance of antioxidant status, and lowering systemic inflammation. CONCLUSION: These current results provide experimental-based evidence suggesting papaya is an efficacious medicinal fruit for use in the prevention or treatment of NAFLD.

Hibiscus sabdariffa L. calyx extract prevents the adipogenesis of 3T3-L1 adipocytes, and obesity-related insulin resistance in high-fat diet-induced obese rats.

Roselle (Hibiscus sabdariffa) is reported to be beneficial in treating obesity which can develop into a range of metabolic disorders. The molecular mechanisms by which roselle extract works to prevent obesity-related insulin resistance remains poorly understood. We hypothesized that the roselle extract can decrease lipid accumulation and improve insulin resistance by downregulating adipogenesis. The aim of this study is to investigate the protective effect of roselle extract on the mechanism of adipogenesis and prevent complications of the obesity-related insulin resistance in high-fat diet-induced obese rats for 8 weeks. Male Sprague Dawley rats were divided into 4 groups: control (C), high-fat diet (HFD), high-fat diet supplemented with 250 mg/kg BW of roselle (R250), and high-fat diet supplemented with 500 mg/kg BW of roselle (R500). The results demonstrated that roselle had the potential to reduce body weight, food intake, lipid profiles, inflammatory cytokines, lipid peroxidation, serum leptin, insulin and duodenal glucose absorption, while significantly increased glucose uptake of adipose tissue and muscle when compared to the HFD group. Roselle can prevent lipid accumulation by suppressing differentiation of 3T3-L1 adipocyte by downregulating the adipogenic gene expression. The results of this study demonstrated that the molecular mechanism underlying the protective effect of roselle, could be an alternative approach for obesity-related insulin resistance prevention.

Anti-adipogenesis and antioxidative defense status of a crude extract of 'Kalasin 2' peanut sprouts in 3T3-L1 mouse adipocytes.

The aim of this study was to investigate the effects of extracts from germinated (GPE) and non-germinated peanuts (NGPE) on adipogenesis and oxidative status in normal and oxidative-stress-induced 3T3-L1 mouse adipocytes. The treated cells were analysed for cell growth, lipid accumulation, levels of intracellular reactive oxygen species (ROS), and the expression levels of mRNAs and proteins related to adipogenesis and antioxidative defense systems. The results indicated that an extract from peanuts made 9 days after germination (9GPE) reduced lipid contents and mRNA expression of adipogenesis-related genes to a greater extent than an extract from peanuts made 1-day after germination (1GPE) or from NGPE, respectively. In oxidative-stress-induced adipocytes, 9GPE decreased ROS levels, lipid content, and the protein expression of peroxisome-proliferator-activated receptor gamma, and also increased the protein expression of antioxidants. These results illustrate the anti-adipogenic capacity and oxidative status improvement achievable with GPE, and that it could be used as a putative therapeutic agent in the prevention of and (or) treatment of obesity and diseases associated with oxidative stress.

Antioxidative and neuroprotective activities of peanut sprout extracts against oxidative stress in SK-N-SH cells

Objective: To evaluate the protective effect of peanut sprout extract (PSE) against paraquat (PQ) induced SK-N-SH cells. Methods: Three groups of cells were used in the experiment, together with a fourth, control group. One group was treated with PQ, the second group was treated with PSE, and the third group was pre-treated with PSE. The control group was untreated. Cell viability and toxicity were detected by MTT assay, cellular reactive oxygen species (ROS) was detected by Muse Cell Analyzer, quantitative RT-PCR was applied to investigate the expression of SIRT1 and a-synuclein genes, and Ab42 was detected by western blot. Results: The 50% effective concentration of PQ was 0.75 mmol/L. PSE had no sig-nificant cytotoxicity at a concentration of 1.5 mg/mL. In the group of cells pre-treated with PSE, cell death was significantly inhibited. In the PQ treated group, PQ was increased in the intracellular ROS in the cells. Intracellular ROS was significantly decreased in the cells treated with PSE and also those pre-treated with PSE. PSE significantly downregulated the expression of SIRT1 and a-syn genes, and it was found that PQ significantly increased b-amyloid 42 levels whereas this action was inhibited by PSE. Conclusions: PSE has neuroprotective activities against oxidative stress in SK-N-SH cells induced by PQ, suggesting that PSE is a highly promising agent in the preven-tion of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.

Antioxidant activity, total phenolic, and resveratrol content in five cultivars of peanut sprouts

Objective:To investigate the change in total phenolic compounds,antioxidant activity,and resveratrol content of five different germinated peanut cultivars.Methods:The germinated sprouts of five peanut cultivars (Kalasinl,Kalasin2,Konkaen,Konkaen4,and Tainan9) were extracted with 80％ ethanol and collected as crude extract.The antioxidant capacities were determined with 2,2-diphenyl-l-picrylhydrazyl and ferric ion reducing antioxidant power method.The total phenolic compound was measured using the Folin-Ciocalteau assay.The qualification and quantification of resveratrol was performed by high performance liquid chromatography method.Results:Among the five cultivars,a three-day germination of Kalasinl showed the highest phenolic content [(40.67 ± 2.62) μg gallic acid/g dry weight],expressed the highest 2,2-diphenyl-l-picrylhydrazyl antioxidant value [(80.51 ± 1.47) mmol/L Trolox/g dry weight],and ferric ion reducing antioxidant power antioxidant value [(171.33 ± 8.59)mmol/L ascorbic acid/g dry weight].However,the high performance liquid chromatography result of Kalasin2 significantly increased to the highest resveratrol content of (6.44 ± 1.26) μg/g dry weight on the second day of germination.Conclusions:The variation of phytochemical content in the peanut sprout is due to the effect of the peanut cultivar and the germination period.

Differential regulation of metabolic genes in skeletal muscle during starvation and refeeding in humans.

This study investigated the molecular alterations underlying the physiological adaptations to starvation and refeeding in human skeletal muscle. Forty-eight hours' starvation reduced whole-body insulin sensitivity by 42% and produced marked changes in expression of key carbohydrate (CHO) regulatory genes and proteins: SREBP1c and hexokinase II (HKII) were downregulated 2.5- and 5-fold, respectively, whereas the pyruvate dehydrogenase kinase 4 (PDK4) was upregulated 4-fold. These responses were not dependent on the phosphorylation status of Akt and FOXO1. On the other hand, starvation and the concomitant increase in circulating free fatty acids did not upregulate the expression of transcription factors and genes involved in fat metabolism. Twenty-four hours' refeeding with a CHO-rich diet completely reversed the changes in PDK4, HKII and SREBP1c expression in human skeletal muscle but failed to fully restore whole-body insulin sensitivity. Thus, during starvation in healthy humans, unlike rodents, regulation of fat metabolism does not require an adaptive response at transcriptional level, but adaptive changes in gene expression are required to switch off oxidative glucose disposal. Lack of effect on key proteins in the insulin-signalling pathway may indicate that changes in intracellular substrate availability/flux may be responsible for these adaptive changes in glucose metabolism. This may represent an important aspect of the molecular basis of the development of insulin resistance in metabolic conditions characterized by energy restriction.