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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catch-up (compensatory) growth following transient growth retardation due to illness or starvation has long been recognized in biology and in clinical medicine. This report summarizes work utilizing experimental models in rats in efforts to elucidate the control of catch-up growth. The results support the hypothesis that the catch-up growth mechanism includes a set-point or reference for body size appropriate for age and that the control resides in the central nervous system. Growth hormone (GH) secretion is increased during catch-up growth, although the results also show that increased GH secretion is not required for catch-up growth acceleration. Environmental light modulates the effect of catch-up growth on GH secretion. The mechanisms for sensing a deficit in body size and for stimulating catch-up growth acceleration remain unknown.
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PMID:The control of catch-up growth. 287 34

Groups of female mice were starved or exposed to hypobaric hypoxia during pregnancy. A significantly lower weight gain during pregnancy occurred in the mothers starved or exposed to hypoxia compared to controls. Hypoxia also decreased maternal food intake. Therefore, the hypoxic groups included a combination of hypoxia and starvation. Body weight, brain weight, brain DNA (deoxyribonucleic aid) and total protein were investigated in the offspring at birth and at 20 and 70 days of age. Starvation and hypoxia impaired fetal growth, with reduction in body weight, brain weight, brain cell number (DNA content) and brain total protein content in a dose-related manner. In the most severely starved fetuses brain cell size (brain weight/DNA and total protein/DNA) was also reduced. Long-term effects were observed with lower body weight, brain weight and brain DNA content at adult age in the most severely malnourished and hypoxic offspring. Catch-up growth took place after a more moderate starvation and hypoxic exposure. It is concluded that intrauterine malnutrition interferes with fetal cellular mitotic rate. This may give rise to growth-retarded fetuses because of a decreased cell number. Depending o the degree of malnutrition a cell deficit may persist at adult age. Intrauterine hypoxia may aggravate these effects of fetal starvation.
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PMID:Somatic growth and brain development. Effects of intrauterine malnutrition and hypoxia in mice. 726 Feb 11

Catch-up or compensatory growth is known as a physiological phenomenon. However, most studies of catch-up growth were based on measurements of body weight, whereas changes in longitudinal bone growth remained largely undescribed. The present study describes the dynamics of both weight and longitudinal bone growth using mikro-knemometry, during normal feeding, severe food restriction (starvation), and refeeding of 14 intact and 28 GH-deficient male rats. Starvation induced rapid weight loss (P < 0.001), and stunted leg growth (P < 0.001). Refeeding led to rapid catch-up in weight of up to 4 times above normal daily weight gain, both in intact and GH-deficient animals, whereas an equivalent compensation of lower leg growth remained undetectable. Intact and GH-deficient animals show a circaseptan spontaneous variation of growth velocity (mini growth spurts). During starvation, mini growth spurts disappear, and return to normal after refeeding with no evidence of catch-up. In GH-deficient animals, GH (1 IU/rat, administered twice daily s.c. at 10:00 hand 16:00 h) was capable of augmenting catch-up in weight and, to a lesser extent, in leg length increment.
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PMID:Differential catch-up in body weight and bone growth after short-term starvation in rats. 897 52

In 1963, Prader, Tanner, and von Harnack published a landmark article describing catch-up growth in children after illness or starvation. That same year, Tanner proposed a theory about catch-up growth based on a central regulatory principle that is 'informed' about an organism's height by means of a humoral factor. This led to the assumption that, when dissociation between a central age-appropriate set point for body size and actual body size occurs, an efferent signal is transmitted to growth tissue to stimulate growth that corresponds to age-appropriate body size. Catch-up growth has been observed in a wide range of endocrinological, nutritional, medical, and emotional disturbances, and the underlying causes are complex and not always well understood. Recently, catch-up growth in four situations has attracted the attention of endocrinologists, as these situations provide useful lessons for the clinician: hypothyroidism, growth hormone deficiency, intrauterine growth retardation, and adoption of children born in developing countries and raised in Western societies.
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PMID:Catch-up growth: new lessons for the clinician. 1251 Sep 76