Glucose-rich diet aggravates monocrotophos-induced dopaminergic neuronal dysfunction inCaenorhabditis elegans

Abstract

The present study aimed to obtain insights into the mechanism(s) by which glucose-rich diet aggravates monocrotophos (MCP)-induced dopaminergic neuronal dysfunction in Caenorhabditis elegans. In this study, we exposed three different strains of worms (wild-type N2, CB1112 (cat-2(e1112)II, tyrosine hydroxylase-deficient mutant, catecholamine absent) and the transgenic BZ555 (egls1-dat-1p::green fluorescent protein [GFP]) (in which bright GFP is tagged to the dopamine neuronal soma and processes) grown and maintained in normal nematode growth medium or 2% glucose enriched-nematode growth medium to MCP (0.75 mm) for 48 h. After the exposure, dopamine-mediated behaviors such as repulsion to nonanone, chemotaxis index and basal slowing response were determined in worms. Dopamine, 3,4-dihydroxy phenyl acetic acid and homovanillic acid content were quantified in N2 worms. The extent of neurodegeneration was visualized and quantified in dat-1::GFP worms. Basal slowing response study clearly indicated that cat-2 worms exposed to MCP and glucose were less affected compared to N2 of the same treatment. Learning and memory were affected by MCP and glucose. While MCP-treated worms showed lesser repulsion to nonanone compared to control worms, MCP-treated, glucose-fed worms showed a greater reduction in repulsion to nonanone. Further, MCP-treated, glucose-fed worms exhibited a marked reduction in dopamine content and an increase in 3,4-dihydroxy phenyl acetic acid and homovanillic acid levels compared to that in control. Dat-1::GFP showed a significant degeneration of dopaminergic neurons when exposed to glucose and MCP. Thus, our results clearly demonstrate that glucose-rich diet aggravates the dopaminergic neuronal dysfunction induced by MCP in C. elegans. Copyright © 2016 John Wiley & Sons, Ltd.

Metabolic shift from glycogen to trehalose promotes lifespan and healthspan in Caenorhabditis elegans

“…Recent studies in mice found that a high-glucose diet significantly impaired healing following a tendon injury (65,66), demonstrating that high-sugar diets have far-reaching effects. Similar to previous studies (5)(6)(7)(8)(10)(11)(12)(13) and data in Fig. 1, we found that addition of glucose to the C. elegans diet leads to shortened lifespan, diminished healthy aging or healthspan, and increased AGEs.…”

“…According to the US Department of Agriculture, the average individual consumed almost 100 pounds of sugar in 2015, more than double the amount consumed in 1900 (4). The effects of a high-sugar diet can be modeled in Caenorhabditis elegans, as the addition of glucose to the standard Escherichia coli diet has been shown to cause glucose toxicity, which results in a decrease in lifespan (5)(6)(7)(8), an increase in triglycerides (7,8), neuronal defects (9,10), and a decrease in locomotion (11,12). Intracellularly, excess glucose can also lead to a greater incidence of advanced glycation end products (AGEs) in both humans and C. elegans (13).…”

High-Glucose Diet Attenuates the Dopaminergic Neuronal Function in C. elegans, Leading to the Acceleration of the Aging Process

“…Therefore, worm’s dopaminergic behaviors including BSR and alcohol avoidance are more deteriorated by high-glucose-diet-induced specific and early degeneration of ADE neurons. More deterioration of ADE than CEP was also found in the previous study focusing on a synergetic effect of a glucose-rich diet on insecticide-induced dopaminergic neuronal dysfunction in C. elegans.…”

“…Therefore, worm's dopaminergic behaviors including BSR and alcohol avoidance are more deteriorated by highglucose-diet-induced specific and early degeneration of ADE neurons. More deterioration of ADE than CEP was also found in the previous study 59 focusing on a synergetic effect of a glucose-rich diet on insecticide-induced dopaminergic neuronal dysfunction in C. elegans. Without insecticides, we here found that a high-glucose diet independently induced dopaminergic neuronal dysfunction in C. elegans through the reduction of dopamine synthesis and transport.…”

Chronic high-sugar diet in adulthood protectsCaenorhabditis elegansfrom 6-OHDA induced dopaminergic neurodegeneration

“…Possessing 8 dopaminergic neurons and high genetic tractability, several transgenics have been generated to assist with visualization of dopamine neuron morphology (21, 22). High glucose exposure studies in C. elegans showed increased susceptibility to organophosphate pesticide-induced neurodegeneration in dopaminergic, GABAergic, and cholinergic neurons (17, 18, 23). These studies, however, were mostly performed with acute, developmental exposures to glucose.…”