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Insulin signaling couples growth and early maturation to cholesterol intake in Drosophila. | LitMetric

Insulin signaling couples growth and early maturation to cholesterol intake in Drosophila.

Curr Biol

Department of Biology, Section for Cell and Neurobiology, University of Copenhagen, Universitetsparken 15, Building 3, 2100 Copenhagen, Denmark. Electronic address:

Published: April 2022

AI Article Synopsis

  • Nutrition significantly influences growth and maturation timing in mammals and insects, with childhood obesity positively linked to early puberty, though the mechanisms remain unclear.
  • Cholesterol, a vital dietary lipid, impacts growth and maturation by enhancing insulin-like peptide production, linking nutrient intake to hormonal changes that facilitate the transition from juvenile to adult stages.
  • The study reveals that the Npc1-TOR signaling pathway regulates cholesterol sensing in specific tissues, influencing overall growth and maturation timing, potentially clarifying the relationship between cholesterol levels, obesity, and premature puberty.

Article Abstract

Nutrition is one of the most important influences on growth and the timing of maturational transitions including mammalian puberty and insect metamorphosis. Childhood obesity is associated with precocious puberty, but the assessment mechanism that links body fat to early maturation is unknown. During development, the intake of nutrients promotes signaling through insulin-like systems that govern the growth of cells and tissues and also regulates the timely production of the steroid hormones that initiate the juvenile-adult transition. We show here that the dietary lipid cholesterol, which is required as a component of cell membranes and as a substrate for steroid biosynthesis, also governs body growth and maturation in Drosophila via promoting the expression and release of insulin-like peptides. This nutritional input acts via the nutrient sensor TOR, which is regulated by the Niemann-Pick-type-C 1 (Npc1) cholesterol transporter, in the glia of the blood-brain barrier and cells of the adipose tissue to remotely drive systemic insulin signaling and body growth. Furthermore, increasing intracellular cholesterol levels in the steroid-producing prothoracic gland strongly promotes endoreduplication, leading to an accelerated attainment of a nutritional checkpoint that normally ensures that animals do not initiate maturation prematurely. These findings, therefore, show that a Npc1-TOR signaling system couples the sensing of the lipid cholesterol with cellular and systemic growth control and maturational timing, which may help explain both the link between cholesterol and cancer as well as the connection between body fat (obesity) and early puberty.

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Source
http://dx.doi.org/10.1016/j.cub.2022.02.021DOI Listing

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