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In vitro and in vivo studies uncovered a molecular link between elevated mitochondrial ceramide levels, coenzyme Q depletion, and insulin resistance.

Germ cell ablation delays C. elegans aging, in part, because unconsumed fat triggers activation of the detoxification factor SKN-1/Nrf, which is regulated by lipid signals and maintains lipid homeostasis.

Analysis of molecular signatures of lifespan variation across wild yeast isolates revealed how Nature employs environment to modify genotype, gene expression, and metabolome to arrive at different lifespan, while preserving fitness in various ecological niches.

Differential agonist-induced phosphorylation of free fatty acid receptor 2 is shown in different tissues of transgenic mice engineered to express variant forms of the human ortholog of the receptor.

In response to starvation, C. elegans converts a favorable pheromone that induces aggregation to an unfavorable one that induces a stress-resistant larval stage, thereby altering its chemical message without having to synthesize new pheromones de novo.

High-fat ingestion triggers microglial metabolic activation within a single feeding cycle, and enhances whole-body metabolism and memory by converting fatty acids into protective substrates for surrounding neurons.

The essential function of ACP is not related to mitochondrial fatty acid and lipoic acid synthesis, but rather an evolutionarily-conserved role in iron sulfur cluster biogenesis.

Isotope tracing, mathematical modeling, and single-cell ATP analysis reveal changes in blood cell metabolism under various conditions, showing stressed hematopoietic stem cells support hematopoiesis through glycolytic ATP production via PFKFB3.

A novel dimethylsulfoniopropionate lyase was identified, which catalyzes dimethyl sulfide releasing by a new mechanism and is found in several bacterial lineages, revealing its important roles in global sulfur cycling.

Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.