'Saba' banana (Musa acuminata x balbisiana BBB Group) peel pectin supplementation improves biomarkers of obesity and associated blood lipid disorders in obese hypercholesterolemic mice.

'Saba' banana peel contains significant amounts of pectin but with very limited commercial use. To increase its value, the present study investigated the effect of 'saba' peel pectin (SPP) on biomarkers of obesity and associated blood lipid disorders in vivo and identified its potential mechanism via in vitro lipid lowering assays. ICR male mice were induced with obesity and hypercholesterolemia using 45% high fat diet (HFD) for three weeks. The mice were then randomly allocated to four groups fed various diets ad libitum for nine weeks as follows: (1) normal diet (ND), (2) high-fat diet (HFD), (3) HFD with 10% w/w commercial citrus pectin (HFD-CCP), and (4) HFD with 10% w/w SPP (HFD-SPP). For the in vitro study, lipid lowering assays were carried out using published protocols with some modifications. Results showed that the mean endline body weight of HFD-CCP and HFD-SPP were significantly lower than HFD group despite having comparable feed intake. The pectin-supplemented groups also had lower blood total cholesterol than HFD group. Necropsy results showed no significant treatment-related difference in the relative organ weights, except for the liver of HFD group being pale, enlarged, and heavier than the other mice groups. This is consistent with the microscopic observations of liver sections from HFD-CCP and HFD-SPP which had occasional fat deposits only whereas HFD group showed mild necrosis and fat infiltration. In terms of body fat, the adiposity index was significantly lower among HFD-SPP and HFD-CCP than the HFD group, with both pectin-supplemented groups showing lesser extent of increase in adipocyte diameter. Meanwhile, HFD-CCP and HFD-SPP groups were significantly comparable in terms of body weight, blood lipids, organ and adipose tissue weights, adiposity index, and liver morphology. In vitro assays revealed that SPP had significantly higher cholesterol and bile acid binding capacities at 60 µg/mL and 20 µg/mL, respectively than CCP and bile acid-binding drug, cholestyramine. These showed that SPP supplementation improves biomarkers of obesity and associated blood lipid disorders at par with commercially-available citrus pectin possibly via cholesterol and bile acid binding pathways, suggesting that SPP may be a potential functional ingredient with anti-obesity and anti-hypercholesterolemic properties.

Dark Sweet Cherry (Prunus avium) Phenolics Enriched in Anthocyanins Induced Apoptosis in MDA-MB-453 Breast Cancer Cells through MAPK-Dependent Signaling and Reduced Invasion via Akt and PLCγ-1 Downregulation.

Dark sweet cherries (DSCs) are rich source of phenolics known to exert anticancer and anti-invasive activities. This study elucidated the molecular mechanisms underlying the activity of DSC phenolics against MDA-MB-453 breast cancer cells In Vitro. Cells were treated with DSC phenolics in whole extract (WE), and fractions enriched in anthocyanins (ACN) and proanthocyanidins (PCN) at concentrations that inhibited cell growth by 50%. Results showed that DSC phenolics suppressed Akt and PLCγ-1 activation, and inhibited cell motility and invasion, but only ACN reached significance. The extrinsic and intrinsic apoptotic pathways were also activated by DSC phenolics via caspase-8 cleavage and increased Bax/Bcl-2 ratio, with ACN exhibiting significant activation and stronger PARP-1 cleavage. Furthermore, sustained activation of mitogen-activated protein kinases (MAPKs) ERK1/2 and p38 was observed wherein ERK1/2 (U0126) and p38 (SB203580) inhibitors confirmed crosstalk ERK1/2-Akt and MAPK intrinsic mitochondrial pathways. In conclusion, DSC phenolics inhibited MDA-MB-453 breast cancer cells by targeting cell signaling pathways that induce apoptosis and suppress cell invasion, with ACN showing enhanced chemopreventive activities.

Antitumor potential of dark sweet cherry sweet (Prunus avium) phenolics in suppressing xenograft tumor growth of MDA-MB-453 breast cancer cells.

This study investigated in vivo the antitumor activity of dark sweet cherry (DSC) whole extracted phenolics (WE) and fractions enriched in anthocyanins (ACN) or proanthocyanidins (PCA) in athymic mice xenografted with MDA-MB-453 breast cancer cells. Mice were gavaged with WE, ACN or PCA extracts (150 mg/kg body weight/day) for 36 days. Results showed that tumor growth was suppressed at similar levels by WE, ACN and PCA compared to control group (C) without signs of toxicity or significant changes in mRNA oncogenic biomarkers in tumors or mRNA invasive biomarker in distant organs. Tumor protein analyses showed that WE, ACN and PCA induced at similar levels the stress-regulated ERK1/2 phosphorylation, known to be linked to apoptosis induction. However, ACN showed enhanced antitumor activity through down-regulation of total oncogenic and stress-related Akt, STAT3, p38, JNK and NF-kB proteins. In addition, immunohistochemistry analysis of Ki-67 revealed inhibition of tumor cell proliferation with potency WE ≥ ACN ≥ PCA. Differential quantitative proteomic high-resolution nano-HPLC tandem mass spectrometry analysis of tumors from ACN and C groups revealed the identity of 66 proteins associated with poor breast cancer prognosis that were expressed only in C group (61 proteins) or differentially up-regulated (P<.05) in C group (5 proteins). These findings revealed ACN-targeted proteins associated to tumor growth and invasion and the potential of DSC ACN for breast cancer treatment. Results lead to a follow-up study with highly immunodeficient mice/invasive cell line subtype and advanced tumor development to validate the anti-invasive activity of DSC anthocyanins.

Red raspberry (Rubus idaeus L.) intake decreases oxidative stress in obese diabetic (db/db) mice.

Red raspberry fruit intake was investigated on obese diabetic (db/db) mice for 8weeks. Animals fed isocaloric diets (5.3% freeze-dried raspberry, or control) were assessed for obesity-diabetes-disease risk biomarkers. Results showed that raspberry intake improved antioxidant status and lessened plasma interleukin (IL)-6 (0.3-fold of control, p<0.1); most likely through enhancing glutathione peroxidase (GPx) activity in liver (4.3-fold of control), and in blood (2.1-fold of control). Other disease-risk biomarkers were similar between groups (p>0.05). Plasma levels of total cholesterol (T-CHL), low density lipoprotein-cholesterol (LDL-CHL), and resistin were higher in the raspberry group. Overall, the enhanced detoxifying cell defenses exerted by raspberry intake might be due to its polyphenolics and fibre. This study demonstrates in vivo that raspberry intake, at a dose that can be achieved by human consumption, might protect against diabetes-induced oxidative stress.