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Measuring Food Intake and Nutrient Absorption in Caenorhabditis elegans.

Gomez-Amaro RL, Valentine ER, Carretero M, LeBoeuf SE, Rangaraju S, Broaddus CD, Solis GM, Williamson JR, Petrascheck M - Genetics (2015)

Bottom Line: Caenorhabditis elegans has emerged as a powerful model to study the genetics of feeding, food-related behaviors, and metabolism.We show that serotonin-increased feeding leads to increased protein synthesis in a SER-7-dependent manner, including proteins known to promote aging.Protein content in the food has recently emerged as critical factor in determining how food composition affects aging and health.

View Article: PubMed Central - PubMed

Affiliation: Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California 92037 Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037 Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, California 92037.

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Modulation of food intake by serotonergic signaling. (A) Dose–response curve for wild-type N2 animals treated with serotonin. Food intake expressed relative to control treatment (water). Tukey-style box plots, unless otherwise stated, depict food intake over the D1:D4 interval. Data are representative of three independent experiments, nwells = 20. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Food intake of pre- and post-reproductive wild-type N2 animals treated with water or serotonin (2 mM). Food intake is expressed relative to the D1:D4 interval of control water-treated N2 animals. Data are representative of three independent experiments, n = 18. ***P < 0.0001, Student’s t-test. (C) Food intake in response to serotonin (2 mM) for wild-type N2 animals and serotonin receptor mutants. Data for each strain are representative of a minimum of three independent experiments. Data as depicted in graph represent two independent experiments, nwells ≥ 42. ***P < 0.001, two-way ANOVA with Bonferroni post-test comparing response to serotonin for each genotype. ###P < 0.001, one-way ANOVA with Dunnett’s multiple correction post-test comparing serotonin-treated animals of each genotype to wild-type serotonin-treated animals. (D) Basal food intake of serotonin-synthesis-deficient tph-1 mutants. Food intake is expressed relative to wild-type N2. Data represent three independent experiments, nwells ≥ 95. Student’s t-test was used to establish significance. Note: For a version of graphs in A and C showing S.E.M. and thus reproducibility between experiments, see Figure S2.
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fig3: Modulation of food intake by serotonergic signaling. (A) Dose–response curve for wild-type N2 animals treated with serotonin. Food intake expressed relative to control treatment (water). Tukey-style box plots, unless otherwise stated, depict food intake over the D1:D4 interval. Data are representative of three independent experiments, nwells = 20. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Food intake of pre- and post-reproductive wild-type N2 animals treated with water or serotonin (2 mM). Food intake is expressed relative to the D1:D4 interval of control water-treated N2 animals. Data are representative of three independent experiments, n = 18. ***P < 0.0001, Student’s t-test. (C) Food intake in response to serotonin (2 mM) for wild-type N2 animals and serotonin receptor mutants. Data for each strain are representative of a minimum of three independent experiments. Data as depicted in graph represent two independent experiments, nwells ≥ 42. ***P < 0.001, two-way ANOVA with Bonferroni post-test comparing response to serotonin for each genotype. ###P < 0.001, one-way ANOVA with Dunnett’s multiple correction post-test comparing serotonin-treated animals of each genotype to wild-type serotonin-treated animals. (D) Basal food intake of serotonin-synthesis-deficient tph-1 mutants. Food intake is expressed relative to wild-type N2. Data represent three independent experiments, nwells ≥ 95. Student’s t-test was used to establish significance. Note: For a version of graphs in A and C showing S.E.M. and thus reproducibility between experiments, see Figure S2.

Mentions: Thus far, we have established that we can determine reductions in food intake. We next set out to measure increases in food intake. The neurotransmitter serotonin (5-HT) is a conserved regulator of energy balance (Noble et al. 2013). Treatment with exogenous serotonin increases the rate of pharyngeal pumping in a manner dependent on the G-protein coupled receptors (GPCRs) ser-1, ser-5, or ser-7 (Srinivasan et al. 2008; Cunningham et al. 2012). As expected, treating C. elegans with serotonin increased bacterial clearance in a dose-dependent manner (Figure 3, A and B).


Measuring Food Intake and Nutrient Absorption in Caenorhabditis elegans.

Gomez-Amaro RL, Valentine ER, Carretero M, LeBoeuf SE, Rangaraju S, Broaddus CD, Solis GM, Williamson JR, Petrascheck M - Genetics (2015)

Modulation of food intake by serotonergic signaling. (A) Dose–response curve for wild-type N2 animals treated with serotonin. Food intake expressed relative to control treatment (water). Tukey-style box plots, unless otherwise stated, depict food intake over the D1:D4 interval. Data are representative of three independent experiments, nwells = 20. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Food intake of pre- and post-reproductive wild-type N2 animals treated with water or serotonin (2 mM). Food intake is expressed relative to the D1:D4 interval of control water-treated N2 animals. Data are representative of three independent experiments, n = 18. ***P < 0.0001, Student’s t-test. (C) Food intake in response to serotonin (2 mM) for wild-type N2 animals and serotonin receptor mutants. Data for each strain are representative of a minimum of three independent experiments. Data as depicted in graph represent two independent experiments, nwells ≥ 42. ***P < 0.001, two-way ANOVA with Bonferroni post-test comparing response to serotonin for each genotype. ###P < 0.001, one-way ANOVA with Dunnett’s multiple correction post-test comparing serotonin-treated animals of each genotype to wild-type serotonin-treated animals. (D) Basal food intake of serotonin-synthesis-deficient tph-1 mutants. Food intake is expressed relative to wild-type N2. Data represent three independent experiments, nwells ≥ 95. Student’s t-test was used to establish significance. Note: For a version of graphs in A and C showing S.E.M. and thus reproducibility between experiments, see Figure S2.
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Related In: Results  -  Collection

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fig3: Modulation of food intake by serotonergic signaling. (A) Dose–response curve for wild-type N2 animals treated with serotonin. Food intake expressed relative to control treatment (water). Tukey-style box plots, unless otherwise stated, depict food intake over the D1:D4 interval. Data are representative of three independent experiments, nwells = 20. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Food intake of pre- and post-reproductive wild-type N2 animals treated with water or serotonin (2 mM). Food intake is expressed relative to the D1:D4 interval of control water-treated N2 animals. Data are representative of three independent experiments, n = 18. ***P < 0.0001, Student’s t-test. (C) Food intake in response to serotonin (2 mM) for wild-type N2 animals and serotonin receptor mutants. Data for each strain are representative of a minimum of three independent experiments. Data as depicted in graph represent two independent experiments, nwells ≥ 42. ***P < 0.001, two-way ANOVA with Bonferroni post-test comparing response to serotonin for each genotype. ###P < 0.001, one-way ANOVA with Dunnett’s multiple correction post-test comparing serotonin-treated animals of each genotype to wild-type serotonin-treated animals. (D) Basal food intake of serotonin-synthesis-deficient tph-1 mutants. Food intake is expressed relative to wild-type N2. Data represent three independent experiments, nwells ≥ 95. Student’s t-test was used to establish significance. Note: For a version of graphs in A and C showing S.E.M. and thus reproducibility between experiments, see Figure S2.
Mentions: Thus far, we have established that we can determine reductions in food intake. We next set out to measure increases in food intake. The neurotransmitter serotonin (5-HT) is a conserved regulator of energy balance (Noble et al. 2013). Treatment with exogenous serotonin increases the rate of pharyngeal pumping in a manner dependent on the G-protein coupled receptors (GPCRs) ser-1, ser-5, or ser-7 (Srinivasan et al. 2008; Cunningham et al. 2012). As expected, treating C. elegans with serotonin increased bacterial clearance in a dose-dependent manner (Figure 3, A and B).

Bottom Line: Caenorhabditis elegans has emerged as a powerful model to study the genetics of feeding, food-related behaviors, and metabolism.We show that serotonin-increased feeding leads to increased protein synthesis in a SER-7-dependent manner, including proteins known to promote aging.Protein content in the food has recently emerged as critical factor in determining how food composition affects aging and health.

View Article: PubMed Central - PubMed

Affiliation: Department of Chemical Physiology, The Scripps Research Institute, La Jolla, California 92037 Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037 Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, California 92037.

No MeSH data available.


Related in: MedlinePlus