Showing papers on "Compensatory growth (organism) published in 1985"

Reduced and compensatory growth: endocrine and metabolic changes during food restriction and refeeding in steers.

Abstract: Effects of food restriction, followed by refeeding, on energy and nitrogen metabolism, growth rates and blood levels of hormones and metabolites were studied in steers. During the restriction period, which lasted for almost 5 mo, allowance for energy and nitrogen were close to maintenance requirements. Heat production and growth rates were markedly lowered. In response to reduced food intake concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3), insulin (IRI), glucose and alpha-amino-acid nitrogen (AAN) were reduced, those of growth hormone (GH) and nonesterified fatty acids (NEFA) were elevated, whereas 3,3',5'-triiodothyronine (rT3) and albumin were not different from levels measured in nonrestricted animals. During refeeding heat production and energy balances increased, nitrogen balances were transiently elevated and the animals exhibited compensatory growth. In response to refeeding, concentrations of T4, T3 and IRI increased within days. In contrast, GH decreased whereas rT3 did not change. Within 2 d of refeeding there was a rapid fall of NEFA, and an increase of glucose, and beta-hydroxybutyrate within 2 and 12 d, respectively. The data demonstrate the ability of growing ruminants to adapt rapidly to variations in food intake by closely linked metabolic and endocrine changes, which are associated with shifts in energy and nitrogen metabolism and, finally, by reduced or compensatory growth.

Compensatory growth in infants with severe failure to thrive.

Abstract: :We studied compensatory growth and caloric intake during an accelerated growth period of ten infants with severe failure to thrive (FTT). The mean age at diagnosis was 7.1 months (range 1.5 to 16.0 months). The average percentage of normal weight for age in this group was 54.9%, mean length

Growth of adipose tissue following lipectomy

Abstract: Publisher Summary This chapter discusses regrowth of adipose tissue and the nature of that regrowth following lipectomy. Hypothetically, there are four possible responses to lipectomy: (1) adipose tissue may regenerate, (2) there may be compensatory growth of non-excised depots, (3) the adipose mass of the body may diminish even further, and (4) there may be no response. In lipectomized experimental animals, adipose tissue regeneration is considered to have occurred if adipose tissue reappears in the dead space created by lipectomy. This reappearance is not the result of migration of tissue formed elsewhere prior to surgery. In man, proper surgical technique requires the elimination of dead space, so lipectomy—more usually dermo-lipectomy—leaves no such dead space. Compensatory growth of adipose tissue has two forms: compensatory hyperplasia and compensatory hypertrophy. There are several types of regrowth or accelerated growth of adipose tissue that occurs after lipectomy in man under certain conditions. However, the nature of the surgery, the small percentage of body fat removed in such lipectomies, and the difficulties associated with measuring changes in adipose mass in man, make it unlikely that any of these responses can be detected easily. Furthermore, lipectomy patients are fully developed, non-growing adults, while practically all animal experiments in which regrowth had been seen were performed on young growing animals. It is therefore possible that regeneration and compensatory hyperplasia do not occur in most patients. People who, for genetic reasons, have a high propensity for adipocyte multiplication—for example, the severely obese—can also have a high propensity for adipose tissue regeneration, while people who regain weight lost prior to lipectomy can experience compensatory growth in remaining adipose tissue.

Skeletal changes and some muscle-skeletal relationships during growth and undernutrition in sheep

Abstract: A serial slaughter experiment was conducted with sheep under continuous growth and during realimentation following body weight stasis at c. 20 kg for 56 days. Undernutrition resulted in negative protein and energy balance. Skeletal remodelling facilitated growth in linear dimensions while protein, water and ash decreased or remained unchanged in bone. Bone weight increases were solely attributable to large increases in bone fat. Protein appeared to be depleted in similar proportions from muscle, bone and the whole body. Realimentation resulted in a trend for compensatory growth of muscle mass relative to bone length and protein content. Within bone there was a trend for restoration of bone protein content rather than growth in bone length. Bone weight was inadequate in describing these phenomena.