BACKGROUND: A significant body of research demonstrates that intake of berries and berry phytochemicals favorably influence metabolism via a number of different biological mechanisms. However, raspberries and select phytochemicals present in raspberries have been less studied than several other berry fruits. OBJECTIVE: The current study tested the relative effect of whole raspberry products or raspberry phytochemicals using the C57BL/6J mouse fed a high-fat, high-sucrose diet as a model for the obesigenic Western diet. The development of obesity and related metabolic complications were measured. METHODS: C57BL/6J mice were fed experimental diets for ten weeks. Diets were formulated to include a typical dietary level of whole raspberry food products, or for the case of ellagic acid (EA) and raspberry ketone (RK), levels that could be reasonably achieved with typical dietary supplement use. In week nine, a glucose tolerance test was conducted. After ten weeks, animals were sacrificed, serum collected, and liver tissue saved for histology and lipid accumulation measurements. RESULTS: Addition of raspberry food products and phytochemicals to high-fat diet reduced body weight gain significantly when raspberry juice and puree concentrates (RJC and RPC), and the EA+RK combination were added. Food efficiency values reflected these weight changes, with the same three groups having food efficiencies similar to normal-weighted low-fat fed mice. Serum insulin and resistin levels were measured and resistin levels were reduced in the two groups fed high fat diets with RPC or RJC added. A histological evaluation of liver tissue was completed and some differences were impacted by diet. CONCLUSIONS: When added to a high-fat diet, raspberry juice and puree concentrates and the combination of EA+RK decreased weight gain and food efficiency obesity associated with consumption of the obesigenic high-fat, high-calorie diet. Future studies are required to determine mechanisms that may be responsible for these changes.
The study is designed to determine whether consumption of the soy isoflavones, genistein and daidzein, differentially influence metabolic syndrome, and to further investigate the involvement of Liver X Receptor (LXR) regulation. C57BL/6J mice were fed diets as follows: low fat diet (LF), western-style diet (WD), and WD containing 0.16% (w/w) of genistein (WD + G) or daidzein (WD + D) for 10 weeks. Intake of WD + G and WD + D produced a robust decrease in body weight gain by 40% and 19%, respectively (p < 0.05). Genistein reduced energy intake by 26%, and daidzein decreased energy intake by 8% (p < 0.05). A glucose tolerance test indicated that genistein consumption significantly decreased the incremental areas under the curve (AUC) from 60–120 min, compared to WD-fed mice. Gene array profiling of hepatic mRNA, and cell studies utilizing transiently-transfected HepG2 cells and mouse embryonic fibroblast cells devoid of or expressing LXRα, indicate that genistein and daidzein induce LXR-mediated pathways. In summary, addition of genistein, compared to daidzein, to a western-style diet, more profoundly decreased food intake, body weight gain, while both appear to regulate LXR-mediated pathways.
Background: Watermelon intake has demonstrated effects on blood pressure regulation along with other health benefits. Objective: We hypothesized that intake of whole watermelon and products made from watermelon rind (WR) and watermelon skin (WS) would remediate metabolic complications in C57BL/6 J male mice fed a diet modeling a Western-style diet. Methods: Ten-week-old male C57BL/6 J mice were provided either a low-fat (LF) diet [10% fat (by energy), 8% sucrose (by energy) and no added cholesterol], a high-fat (HF) diet [45% fat (by energy), 20% kcal sucrose (by energy), and 1% (w/w) cholesterol], or an HF diet plus WS, WR, or watermelon flesh (WF) for 10 wk. Dried WF was provided at 8% of total energy (equivalent to 2 servings/d) and watermelon skin and rind were added at 2.25% (w/w, dry weight of additives) of diet. Animals were provided experimental diets ad libitum. Body weights, food intake, and glucose tolerance were determined. Serum insulin, inflammatory markers, microbiome, and the relative hepatic concentrations of 709 biochemicals were measured postmortem. Results: The final body weight of the LF control group was significantly lower than that of the HF-fed control group (32.8 +/- 0.9 g compared with 43.0 +/- 1.7 g, P <= 0.05). Mice in treatment groups fed HF supplemented with watermelon products had final body weights similar to those of the HF-fed control mice. Serum insulin concentrations were reduced by similar to 40% in mice fed an HF diet with WR supplementation compared with mice fed an HF diet alone (P <= 0.05). Depending on the individual species or group, microbiome populations changed significantly. Supplementation with WF resulted in a return to the basal hepatic concentrations of monohydroxy fatty acids and eicosanoids observed in LF-fed mice (P <= 0.05). Conclusions: In obese male mice, supplementation with each of the watermelon products to an HF diet improved fasting blood glucose, circulating serum insulin concentrations, and changes in hepatic metabolite accumulation. At a modest level of supplementation to an HF diet, fiber-rich additives made from WR and WS further improved glucose metabolism and energy efficiency and shifted the microbiome composition.
Using an animal model for diet-induced metabolic disease, we have shown previously that the addition of raspberry juice concentrate (RJC) and raspberry puree concentrate (RPC) at a level of 10% of kcal, equivalent to four servings per day, to an obesogenic high-fat, western-style diet (HF) significantly reduced body weight gain, serum resistin levels, and altered the expression of hepatic genes related to lipid metabolism and oxidative stress. This study was designed to examine the effect of a lower level of RJC or RPC consumption, at a level representing a single serving of food per day (2.5% of kcal). For ten weeks, four groups of C57BL/6J mice (n = 8 ea.) were fed: low fat (LF), HF, HF + RJC, or HF + RPC diets. Intake of RJC and RPC decreased final body weight. Hepatic lipid accumulation was significantly decreased in HF + RPC- and HF + RJC-fed mice, compared to HF-fed mice. Further, the relative expression of hepatic genes including Heme oxygenase 1 (Hmox1) and Hormone sensitive lipase (Lipe), were altered by RPC or RJC consumption. In this mouse model of diet-induced metabolic disease, consumption of the equivalent of a single daily serving of either RPC or RJC improved metabolism in mice fed HF diet. We hypothesize that the phytochemicals contained in raspberries, and/or their subsequent metabolites, may be acting to influence gene expression and other regulatory pathways, to produce the metabolic improvements observed in this study.