Obesity and diabetes are major public health concerns in the US and worldwide. A high fat diet contributes significantly in the development of these diseases. Momordica charantia (MC), also known as bitter melon, is a widely consumed vegetable in Asia and has hypoglycemic properties. This study compared the effects of freeze‐dried MC with the PPARγ agonist‐ rosiglitazone (rosi), and the known PPARα agonist‐ fenofibrate (feno), on body weight and glucose using a mouse model of diet‐induced obesity. Eight wk old male C57BL/6 mice were randomized to 8 dietary treatment groups (n=20/group): control diet (ad lib), control diet (pair fed), high fat (HF) diet, HF + 1% MC (w/w), HF + 10% MC (w/w), HF+1% MC seeds (w/w), HF + rosi (50mg/kg diet), and HF + feno (500mg/kg diet) for 8 wks. Significant differences in body weights were observed within one week of beginning the experimental diet. The final body weights of mice receiving the 10% MC were similar to the mice receiving the control diet (ad lib). Rosiglitazone and 1% MC were not able to reduce body weight; however, fenofibrate and MC seeds mildly reduced body weight. HF fed mice exhibited the highest percent body fat. Interestingly, 10% MC prevented the increase in adiposity due to high fat diet. A high fat diet containing 10% MC, similar to rosiglitazone, normalized blood glucose after a glucose tolerance test. Fenofibrate caused an enlargement of liver which was not observed in other treatment groups. The mechanism by which MC modulates glucose and body weight warrants further investigation. (Supported by USDA, #2008‐35200‐18692)Grant Funding SourceUSDA
Our earlier study showed that flaxseed prevents vascular lesion development in ovariectomized hamsters. Flaxseed contains significant amounts of phenolic compounds, lignan, which are metabolized by colonic microflora to enterodiol (END) and enterolactone (ENL). The objective of this study was to evaluate and compare the anti‐inflammatory effects of END and ENL using the murine Raw 264.7 macrophage cell line. Cells were incubated in DMEM containing 10% FBS and 1% penicillin and then treated with increasing concentrations (0, 1, 10, 100, 500, 1000, 2500 and 5000μM) of END or ENL for 24 hrs. Subsequently, cells were challenged with LPS (500 ng/mL) for 24 hrs to induce an inflammatory response. Nitric oxide (NO) and cell viability were assessed using the Griess and Resazurin assays, respectively. Cell viability was not affected by any concentrations of END and ENL used in the study. As expected, the addition of LPS induced a significant increase in the production of NO and both END and ENL significantly decreased NO production. However, lower concentrations of ENL compared to END were required to significantly reduce NO production. These findings may in part explain the anti‐atherosclerotic effect of flaxseed and suggest that ENL may have more potent anti‐inflammatory properties.
Bitter melon or Momordica Charantia is a widely consumed vegetable in South Asia. One of the most notable health benefits of bitter melon is its role in lowering blood glucose as demonstrated in both animal and clinical studies. These effects on glucose appear to be mediated by activation of peroxisome proliferator‐activated receptor (PPAR)‐α and ‐γ, members of the steroid hormone nuclear receptor family involved in the regulation of lipid and glucose homeostasis. The objective of this research was to explore the anti‐inflammatory properties of bitter melon using the RAW 264.7 murine macrophage cell line. Bitter melon was deseeded, the edible portion was blended, and the pulp was separated to obtain the juice. Cells were plated at a density of 10,000 cells/well in a 96‐well plate and then treated with bitter melon at concentrations of 0, 0.125, 0.25, 0.5, 1% (v/v) for 24 hours. Cells were then stimulated with 500 ng/mL of LPS for another 24 hours and the supernatants were collected for determination of nitric oxide (NO), prostaglandin E2 (PGE2) and interleukin (IL)‐6. All experiments were repeated three times and cell viability was assessed using the resazurin‐based assay. Cell viability was not affected by any of the bitter melon juice concentrations used in the study. The LPS‐induced increase in NO production was dose‐dependently down‐regulated by bitter melon. PGE2 and IL‐6 were also elevated by LPS and bitter melon also reduced these inflammatory molecules. Bitter melon, which has been reported to activate both PPAR‐α and PPAR‐γ, suppresses the production of inflammatory mediators brought about by LPS and these anti‐inflammatory effects should be further evaluated using in vivo models. (Supported by College of Human Environmental Sciences, Oklahoma State University)
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