Many insects, amphibians, molluscs, crustaceans, cnidarians, echinoderms and tunicates undergo metamorphosis, which is generally accompanied by changes in habitat and behaviour. Metamorphosis is a set of biological processes through which an animal develops from birth (preceded by embryonic development) to maturity, undergoing profound structural and physiological changes. Not only are there changes in size and an increase in the number of cells, but there are also changes in cellular differentiation. Metamorphosis is an ancestral characteristic of all chordates and is present in cephalochordates (acraniates).

Insect metamorphoses:

Whereas in amphibians metamorphosis generally involves the remodelling of pre-existing tissues, in insects this process involves the breakdown of larval tissues and their replacement by a different population of cells. Metamorphosis usually proceeds through several stages, beginning with the larva or nymph, possibly passing through a pupal stage, and ending with the adult. Throughout these stages, growth is produced by processes of shedding and forming a new cuticle as body size increases.

There are mainly two types of metamorphosis in insects:

 - hemimetabolous species with simple or incomplete metamorphosis. 

 - holometabolous species with complex or complete metamorphosis.

Some insects, such as silverfish, show direct development and are therefore referred to as ametabolous. A pronymphal stage occurs just before hatching, during which the structures required for hatching have already developed. In this case, as the insect develops, its size increases without a substantial change in form.

Insect growth and metamorphosis are regulated by effector hormones controlled by neurohormones of the brain. Moulting and metamorphosis are regulated by two effector hormones: 20-hydroxyecdysone (ecdysone) and juvenile hormone (JH). Hydroxyecdysone initiates and coordinates each moult and regulates changes in gene expression during metamorphosis. Juvenile hormone prevents the ecdysone-induced changes in gene expression required for metamorphosis, thereby preventing premature larval development while allowing the moults necessary for growth.

The moulting process begins in the brain, where neurosecretory cells release prothoracicotropic hormone (PTTH) in response to neuronal, hormonal or environmental signals. This hormone stimulates the production of ecdysone in the prothoracic gland. Once the hormone has been produced, PTTH release ceases, and metamorphosis then becomes independent of the brain. In peripheral tissues, this hormone is converted into its active form, 20-hydroxyecdysone, which is released into the haemolymph. This stimulates epidermal cells to synthesise enzymes that digest and recycle cuticular components. The concentration of 20-hydroxyecdysone increases during apolysis and reaches a maximum during epicuticle deposition; its production ceases shortly before ecdysis (in hemimetabolous insects) or emergence (in holometabolous insects). The hormonal concentrations required for moulting differ along the epidermis; the final phase of decreasing concentration controls late events of adult development. If hormone levels are artificially increased during this phase, emergence of the imagos is interrupted.

20-Hydroxyecdysone binds to nuclear receptors (EcR) that form an active molecule by binding to the ultraspiracle protein (Usp). This protein binds to ecdysone-responsive genes and inhibits their transcription; when EcR binds to Usp, transcription is activated. Three receptor isoforms exist, each playing an important role during metamorphosis by activating different groups of genes of the same hormone, although it is known that cells giving rise to the imago have a higher concentration of the EcR-A isoform. Usp is also a juvenile hormone receptor, through which this binding can inhibit the formation of 20-hydroxyecdysone.

Juvenile hormone (JH) is secreted by the corpora allata, whose cells are active during larval moults but not during metamorphic moults. In the presence of juvenile hormone, 20-hydroxyecdysone stimulates a moult that generates new larval stages. At the final larval stage, the brain inhibits juvenile hormone production in the corpora allata, and the hormone is degraded in the tissues. This results in a decrease in juvenile hormone levels below a threshold value, triggering the release of prothoracicotropic hormone (PTTH) in the brain. This response stimulates ecdysone synthesis which, in the absence of high juvenile hormone levels, induces the development of the nymph.

The processes of ecdysis and emergence are linked to the circadian rhythm of each species and are controlled by the eclosion hormone (EH), which is secreted by nerve cells and acts directly on the nervous system by inducing behaviours and movements that allow the insect to free itself from the puparium or exuviae, and to fully expand its wings to become functional. The final stage of metamorphosis is sclerotisation (hardening of the cuticle), which, like the previous stages, is hormonally controlled. The hormone responsible is called bursicon and has physiological effects regulating the mechanical properties of the cuticle. The chemical structure of bursicon has been studied in Drosophila melanogaster.

Knowledge of growth hormones is used in the control of pest insects. It is possible to use chemical products that interfere with the function of these hormones and prevent normal insect development.