ABSTRACT
The use of many psychotropic drugs (PDs) is associated with increased caloric intake, significant weight gain, and metabolic disorders. The nematode Caenorhabditis elegans (C. elegans) has been used to study the effects of PDs on food intake. However, little is known about PDs effects on the body fat of C. elegans. In C. elegans, feeding behavior and fat metabolism are regulated through independent mechanisms. This study aims to evaluate the body fat and food intake of C. elegans in response to treatment olanzapine and fluoxetine. Here we report that, with careful consideration to the dosage used, administration of fluoxetine and olanzapine increases body fat and food intake in C. elegans.
ABSTRACT
BACKGROUND: We previously showed that cocoa, a rich source of polyphenols improved the age-associated health and extended the lifespan in C. elegans when supplemented starting from L1 stage. AIM: In this study, we aimed to find out the effects of timing of cocoa exposure on longevity improving effects and the mechanisms and pathways involved in lifespan extension in C. elegans. METHODS: The standard E. coli OP50 diet of wild type C. elegans was supplemented with cocoa powder starting from different larval stages (L1, L2, L3, and L4) till the death, from L1 to adult day 1 and from adult day 1 till the death. For mechanistic studies, different mutant strains of C. elegans were supplemented with cocoa starting from L1 stage till the death. Survival curves were plotted, and mean lifespan was reported. RESULTS: Cocoa exposure starting from L1 stage till the death and till adult day 1 significantly extended the lifespan of worms. However, cocoa supplementation at other larval stages as well as at adulthood could not extend the lifespan, instead the lifespan was significantly reduced. Cocoa could not extend the lifespan of daf-16, daf-2, sir-2.1, and clk-1 mutants. CONCLUSION: Early-start supplementation is essential for cocoa-mediated lifespan extension which is dependent on insulin/IGF-1 signaling pathway and mitochondrial respiration.
ABSTRACT
BACKGROUND: The antidepressant Mianserin has been shown to extend the lifespan of Caenorhabditis elegan (C. elegan), a well-established model organism used in ageing research. The extension of lifespan in C. elegan was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegan elegan in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. OBJECTIVE: To investigate the effect of glucose added to the diet of C. elegan on the lifespan-extension effect of mianserin. METHODS: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 µM mianserin, (G) 73 mM glucose, and (M50G) 50 µM mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. RESULTS: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. CONCLUSION: The addition of glucose to the diet of C. elegan abolishes the lifespan-extension effects of mianserin.
