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M.a ELVIRA LÓPEZ-OLIVA Y COLS. AN. R. ACAD. NAC. FARM.

de la masa grasa, similar al determinado por el crecimiento que sigue a la reali-
mentación después de malnutrición, lo que puede coexistir con un estado de resis-
tencia del tejido adiposo a la GH. Sin embargo el efecto anabólico de la somato-
tropa parece manifestarse, en los animales bien nutridos, por un mayor depósito
de la proteína muscular al incrementar la tasa fraccional de síntesis proteica, que
permite la aparición de un fenómeno de hipertrofia compensadora. Por lo tanto,
la administración de rhGH en el momento del destete parece interferir con los
delicados mecanismos de adaptación a la alimentación sólida característicos de
este periodo, e inducir el cese del crecimiento entre los 21 y 30 días, generando
más tarde un crecimiento de carácter compensador que se inicia a partir de los 35
días de vida.

Palabras clave: GH.— Destete.— Proteína de la dieta.— Crecimiento compen-
sador.

ABSTRACT

Growth hormone, weaning and nutritional status

The GH-IGF-I system constitutes the major determinant of body size, specially
in postnatal growth. It is well established that exogenous GH increases muscle
mass and decreases lipid content, leading to the alteration of nutrients repartitio-
ning. The mechanism involves, at least, an increase in the protein synthesis and
creates a status of positive nitrogen balance by increasing nitrogen retention and
decreasing protein catabolism in animals fed an adequate diet. GH can act directly
on tissues inducing these metabolic changes and can also stimulate IGF-I in an
endocrine, autocrine or paracrine fashion. Body fat decreases by the increase of
triglycerides hydrolysis and the decrease of free fatty acid re-esterification. The
magnitude of the response to exogenous GH is variable and at least partly attribu-
table to the nutritional status and to the growth stage of animal. The action of
growth hormone is minimal between the 2nd and the 3rd week of age and is mani-
fested at 31 days of age, increasing its efficacy at puberty. The reason for this
refractoriness to GH treatment is unknown but it can be related to the biphasic
response developed in mice fed two dietary protein levels between 21 to 50 days
of age, when administered with rhGH. The GH-induced fall of feed intake in mice
between 21 and 30 days old provokes a loss of body and skeletal muscle compo-
nents due to the lack of nutrients leading to the impairment of growth. Later on
(35-50 days) the self-controlled increase of feed intake let the recovery of the body
weight, through of a catch-up growth phenomenon, characterized by a higher lipid
body accretion, similar to the compensatory growth developed during refeeding
after protein-energy malnutrition, and possibly contemporary of a GH-resistance
status of the fat mass. However, the GH anabolic action is clearly seen on the
muscle mass, specially in the well-nourished mice, with increased fractional pro-
tein synthesis rate that allows higher both muscle protein deposit and muscle
cellular size. Thus, GH administration throughout weaning seems to interfere with
the delicate adaptive mechanisms to the solid diet, impeding normal growth bet-

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