Dietary Plant Lectins Appear to Be Transported from the Gut to Gain Access to and Alter Dopaminergic Neurons of Caenorhabditis elegans, a Potential Etiology of Parkinson’s Disease

© Copyright © 2016 Zheng, Wang, Wei, Keller, Adhikari, King, King, Peng and Laine. Lectins from dietary plants have been shown to enhance drug absorption in the gastrointestinal tract of rats, be transported trans-synaptically as shown by tracing of axonal and dendritic paths, and enhance gene delivery. Other carbohydrate-binding protein toxins are known to traverse the gut intact in dogs. Post-feeding rhodamine- or TRITC-tagged dietary lectins, the lectins were tracked from gut to dopaminergic neurons (DAergic-N) in transgenic Caenorhabditis elegans (C. elegans) [egIs1(Pdat-1:GFP)] where the mutant has the green fluorescent protein (GFP) gene fused to a dopamine transport protein gene labeling DAergic-N. The lectins were supplemented along with the food organism Escherichia coli (OP50). Among nine tested rhodamine/TRITC-tagged lectins, four, including Phaseolus vulgaris erythroagglutinin (PHA-E), Bandeiraea simplicifolia (BS-I), Dolichos biflorus agglutinin (DBA), and Arachis hypogaea agglutinin (PNA), appeared to be transported from gut to the GFP-DAergic-N. Griffonia Simplicifolia and PHA-E, reduced the number of GFP-DAergic-N, suggesting a toxic activity. PHA-E, BS-I, Pisum sativum (PSA), and Triticum vulgaris agglutinin (Succinylated) reduced fluorescent intensity of GFP-DAergic-N. PHA-E, PSA, Concanavalin A, and Triticum vulgaris agglutinin decreased the size of GFP-DAergic-N, while BS-I increased neuron size. These observations suggest that dietary plant lectins are transported to and affect DAergic-N in C. elegans, which support Braak and Hawkes’ hypothesis, suggesting one alternate potential dietary etiology of Parkinson’s disease (PD). A recent Danish study showed that vagotomy resulted in 40% lower incidence of PD over 20 years. Differences in inherited sugar structures of gut and neuronal cell surfaces may make some individuals more susceptible in this conceptual disease etiology model

Oat consumption reduced intestinal fat deposition and improved health span in Caenorhabditis elegans model

© 2015 The Authors. In addition to their fermentable dietary fiber and the soluble β-glucan fiber, oats have unique avenanthramides that have anti-inflammatory and antioxidant properties that reduce coronary heart disease in human clinical trials. We hypothesized that oat consumption will increase insulin sensitivity, reduce body fat, and improve health span in Caenorhabditis elegans through a mechanism involving the daf-2 gene, which codes for the insulin/insulin-like growth factor-1-like receptor, and that hyperglycemia will attenuate these changes. Caenorhabditis elegans wild type (N2) and the null strains sir-2.1, daf-16, and daf-16/daf-2 were fed Escherichia coli (OP50) and oat flakes (0.5%, 1.0%, or 3%) with and without 2% glucose. Oat feeding decreased intestinal fat deposition in N2, daf-16, or daf-16/daf-2 strains (P \u3c.05); and glucose did not affect intestinal fat deposition response. The N2, daf-16, or sir-2.1 mutant increased the pharyngeal pumping rate (P \u3c.05), a surrogate marker of life span, following oat consumption. Oat consumption increased ckr-1, gcy-8, cpt-1, and cpt-2 mRNA expression in both the N2 and the sir-2.1 mutant, with significantly higher expression in sir-2.1 than in N2 (P \u3c.01). Additional glucose further increased expression 1.5-fold of the 4 genes in N2 (P \u3c.01), decreased the expression of all except cpt-1 in the daf-16 mutant, and reduced mRNA expression of the 4 genes in the daf-16/daf-2 mutant (P \u3c.01). These data suggest that oat consumption reduced fat storage and increased ckr-1, gcy-8, cpt-1, or cpt-2 through the sir-2.1 genetic pathway. Oat consumption may be a beneficial dietary intervention for reducing fat accumulation, augmenting health span, and improving hyperglycemia-impaired lipid metabolism

Lower Doses of Fructose Extend Lifespan in Caenorhabditis elegans

© 2017, Copyright © Taylor & Francis Group, LLC. Epidemiological studies indicate that the increased consumption of sugars including sucrose and fructose in beverages correlate with the prevalence of obesity, type-2 diabetes, insulin resistance, hyperinsulinemia, hypertriglyceridemia, and hypertension in humans. A few reports suggest that fructose extends lifespan in Saccharomyces cerevisiae. In Anopheles gambiae, fructose, glucose, or glucose plus fructose also extended lifespan. New results presented here suggest that fructose extends lifespan in Caenorhabditis elegans (C. elegans) wild type (N2). C. elegans were fed standard laboratory food source (E. coli OP50), maintained in liquid culture. Experimental groups received additional glucose (111 mM), fructose (55 mM, 111 mM, or 555 mM), sucrose (55 mM, 111 mM, or 555 mM), glucose (167 mM) plus fructose (167 mM) (G&F), or high fructose corn syrup (HFCS, 333 mM). In four replicate experiments, fructose dose-dependently increased mean lifespan at 55 mM or 111 m Min N2, but decreased lifespan at 555 mM (P \u3c 0.001). Sucrose did not affect the lifespan. Glucose reduced lifespan (P \u3c 0.001). Equal amount of G&F or HFCS reduced lifespan (P \u3c 0.0001). Intestinal fat deposition (IFD) was increased at a higher dose of fructose (555 mM), glucose (111 mM), and sucrose (55 mM, 111 mM, and 555 mM). Here we report a biphasic effect of fructose increasing lifespan at lower doses and shortening lifespan at higher doses with an inverse effect on IFD. In view of reports that fructose increases lifespan in yeast, mosquitoes and now nematodes, while decreasing fat deposition (in nematodes) at lower concentrations, further research into the relationship of fructose to lifespan and fat accumulation in vertebrates and mammals is indicated

Delivery of alpha-tocopherol through soluble dietary fibre-based nanofibres for improving the life span of Caenorhabditis elegans

The effect of alpha-tocopherol (α-TOC) delivered by soluble dietary fibre-based nanofibres (α-TOC-SDNF) on the life span of nematode Caenorhabditis elegans N2 (wild type) and TK22 (mev-1 mutants) with and without heat shock was investigated. Without heat shock, the wild-type and mev-1 mutants maintained in the 100 µg/mL of α-TOC-SDNF had longer life spans than their respective blank control groups. With heat shock, the wild-type N2 in the 200 µg/mL of α-TOC-SDNF had a survival rate of 5% at day 49, while no nematodes survived in the blank control group. An increased pharyngeal pumping rate was observed in the α-TOC-SDNF treated mev-1 mutants worms compared to the blank control group. Encapsulating α-TOC in SDNF yielded protective effects and the life span and pumping rate of C. elegans was increased with α-TOC delivered by SDNF

A resistant-starch enriched yogurt: fermentability, sensory characteristics, and a pilot study in children [v1; ref status: indexed, http://f1000r.es/5cb]

The rising prevalence of obesity and the vulnerability of the pediatric age group have highlighted the critical need for a careful consideration of effective, safe, remedial and preventive dietary interventions.  Amylose starch (RS2) from high-amylose maize (HAM) ferments in the gut and affects body weight.   One hundred and ten children, of 7-8 (n=91) or 13-14 (n=19) years of age scored the sensory qualities of a yogurt supplemented with either HAM-RS2 or an amylopectin starch.  The amylopectin starch yogurt was preferred to the HAM-RS2-enriched yogurt by 7-8 year old panelists (P<0.0001).  Appearance, taste, and sandiness scores given by 13- to 14-year-old panelists were more favorable for the amylopectin starch yogurt than for HAM-RS2-enriched yogurt (P<0.05).  HAM-RS2 supplementation resulted in acceptable (≥6 on a 1-9 scale) sensory and hedonic ratings of the yogurt in 74% of subjects.  Four children consumed a HAM-RS2-enriched yogurt for four weeks to test its fermentability in a clinical trial.  Three adolescents, but not the single pre-pubertal child, had reduced stool pH (P=0.1) and increased stool short-chain fatty acids (SCFAs) (P<0.05) including increased fecal acetate (P=0.02), and butyrate (P=0.089) from resistant starch (RS) fermentation and isobutyrate (P=0.01) from protein fermentation post-treatment suggesting a favorable change to the gut microbiota.  HAM-RS2 was not modified by pasteurization of the yogurt, and may be a palatable way to increase fiber intake and stimulate colonic fermentation in adolescents.  Future studies are planned to determine the concentration of HAM-RS2 that offers the optimal safe and effective strategy to prevent excessive fat gain in children