Introduction

The phenomenon of catch-up growth has long been recognized in the clinic (Prader, Tanner & von Harnack, 1963; Tanner, 1963) and in the laboratory (Hatai, 1907; Osborne & Mendel, 1914) (Figure 1), but the mechanism controlling it remains unknown (see reviews: Tanner, 1979; Tanner, 1981; Van den Brande, 1986). One of the principal unresolved problems in catch-up growth has been the question whether the phenomenon is controlled by a central mechanism or whether it occurs by multicentric mechanisms in peripheral tissues. Tanner (1963) has suggested a model for the central control of catch-up growth which requires a sensor of the degree of growth deficit and a regulator of growth rate according to the deficit. Alternatively, cells may be ‘programmed for a certain amount of growth’ and simply follow the program if inhibiting factors are removed (Prader, 1978). However, the hypothesis for a central control is attractive for its ability to account for fine-tuning of growth recovery under varying conditions (Tanner, 1981) as well as for offering opportunities for experimental attack.

In the present report we describe experiments which test the hypothesis of central control. In addition, we summarize work which delineates factors limiting catch-up growth.

Experimental models

In most of our experiments we have used the black-hooded Long–Evans strain of rat because it has a larger body size and a relatively vigorous constitution in comparison with other strains of domesticated rats. Fasting has been carried out by withholding food for 24 to 72 hours at 40 days of age with the animals housed in hanging cages to prevent coprophagia.