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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.

No MeSH data available.


Related in: MedlinePlus

Body size influences food intake. (A) Food intake of long-lived eat mutants. Food intake expressed relative to wild-type N2 (D1:D4). Data represent three independent experiments, nwells ≥ 88. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Small animals eat less. Data represent three independent experiments, nwells ≥ 43. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (C) Body length of animals in B. Body length as measured on day 4 of adulthood. Data represent three independent experiments, nwells ≥ 28. ***P < 0.001, one-way ANOVA with Dunnett’s multiple comparison post-test. (D) Interaction of animal size and food intake. Food intake and body length measurements expressed relative to wild-type N2 on day 4 of adulthood. Data represent three independent experiments. Linear regression line (dashed red line) and the 95% confidence interval (dashed gray lines) are shown. Goodness of fit statistic, R2 = 0.753 (P < 0.002).
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fig2: Body size influences food intake. (A) Food intake of long-lived eat mutants. Food intake expressed relative to wild-type N2 (D1:D4). Data represent three independent experiments, nwells ≥ 88. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Small animals eat less. Data represent three independent experiments, nwells ≥ 43. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (C) Body length of animals in B. Body length as measured on day 4 of adulthood. Data represent three independent experiments, nwells ≥ 28. ***P < 0.001, one-way ANOVA with Dunnett’s multiple comparison post-test. (D) Interaction of animal size and food intake. Food intake and body length measurements expressed relative to wild-type N2 on day 4 of adulthood. Data represent three independent experiments. Linear regression line (dashed red line) and the 95% confidence interval (dashed gray lines) are shown. Goodness of fit statistic, R2 = 0.753 (P < 0.002).

Mentions: In C. elegans, mutations in the eat genes disrupt the function of the pharynx, leading to reduced pharyngeal pumping and a starved appearance (Avery 1993; Lakowski and Hekimi 1998). However, the cumulative food intake of any eat mutant has not been determined. We compared the food intake of wild-type animals with different eat-2 and eat-18 alleles. While the food intake of all eat mutants was reduced compared to wild type (Figure 2A), the magnitude of the decrease was considerably smaller than predicted, given that their pharyngeal pumping rates are ∼10% of wild type (Raizen et al. 1995; Petrascheck et al. 2007). The food intake of eat-2 and eat-18 mutants was 80% and 60% that of wild-type animals, respectively. This was much higher than we expected, but in the case of eat-2(ad1116), correlates well with its brood size (∼60% of wild type) (Hughes et al. 2007). Interestingly, the reduction in food intake we describe in long-lived eat mutants is very close to the reduction in food intake necessary to extend lifespan in mammals (Taormina and Mirisola 2014).


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)

Body size influences food intake. (A) Food intake of long-lived eat mutants. Food intake expressed relative to wild-type N2 (D1:D4). Data represent three independent experiments, nwells ≥ 88. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Small animals eat less. Data represent three independent experiments, nwells ≥ 43. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (C) Body length of animals in B. Body length as measured on day 4 of adulthood. Data represent three independent experiments, nwells ≥ 28. ***P < 0.001, one-way ANOVA with Dunnett’s multiple comparison post-test. (D) Interaction of animal size and food intake. Food intake and body length measurements expressed relative to wild-type N2 on day 4 of adulthood. Data represent three independent experiments. Linear regression line (dashed red line) and the 95% confidence interval (dashed gray lines) are shown. Goodness of fit statistic, R2 = 0.753 (P < 0.002).
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig2: Body size influences food intake. (A) Food intake of long-lived eat mutants. Food intake expressed relative to wild-type N2 (D1:D4). Data represent three independent experiments, nwells ≥ 88. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (B) Small animals eat less. Data represent three independent experiments, nwells ≥ 43. ***P < 0.01, one-way ANOVA with Dunnett’s multiple comparison post-test. (C) Body length of animals in B. Body length as measured on day 4 of adulthood. Data represent three independent experiments, nwells ≥ 28. ***P < 0.001, one-way ANOVA with Dunnett’s multiple comparison post-test. (D) Interaction of animal size and food intake. Food intake and body length measurements expressed relative to wild-type N2 on day 4 of adulthood. Data represent three independent experiments. Linear regression line (dashed red line) and the 95% confidence interval (dashed gray lines) are shown. Goodness of fit statistic, R2 = 0.753 (P < 0.002).
Mentions: In C. elegans, mutations in the eat genes disrupt the function of the pharynx, leading to reduced pharyngeal pumping and a starved appearance (Avery 1993; Lakowski and Hekimi 1998). However, the cumulative food intake of any eat mutant has not been determined. We compared the food intake of wild-type animals with different eat-2 and eat-18 alleles. While the food intake of all eat mutants was reduced compared to wild type (Figure 2A), the magnitude of the decrease was considerably smaller than predicted, given that their pharyngeal pumping rates are ∼10% of wild type (Raizen et al. 1995; Petrascheck et al. 2007). The food intake of eat-2 and eat-18 mutants was 80% and 60% that of wild-type animals, respectively. This was much higher than we expected, but in the case of eat-2(ad1116), correlates well with its brood size (∼60% of wild type) (Hughes et al. 2007). Interestingly, the reduction in food intake we describe in long-lived eat mutants is very close to the reduction in food intake necessary to extend lifespan in mammals (Taormina and Mirisola 2014).

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