Plasma TGFbeta1 is not a useful marker of CFLD. The increased plasma TGFbeta1 and PF4 in CFPD patients are of interest both as possible noninvasive markers of pulmonary fibrosis and because the increased values suggest that platelet activation may play a pathogenetic role in CFPD.
During the 3rd wk of postnatal life in the rat, dramatic maturational changes occur in the structure and function of the small intestine, enabling the animal to make the transition from milk to solid food. To investigate the role of GH in the regulation of this complex process, we studied postnatal intestinal maturation in the spontaneous dwarf rat, a strain of Sprague-Dawley rats with an autosomal recessive mutation in the GH gene resulting in complete but isolated GH deficiency. GH-deficient and GH-normal littermates were studied at d 7 and 14 (suckling) and d 23 (postweaned). The body weight of GH-deficient animals was inhibited by 60% at each age. Longitudinal growth of the small intestine was not inhibited, suggesting that longitudinal small bowel growth is independent of GH regulation. Mucosal cell mass was significantly lower in GH deficiency at all ages studied, and digestive hydrolase capacity per cm of intestine was significantly lower in GH-deficient postweaned animals. However, epithelial cell mass increased markedly in association with weaning and the maturation of lactase, sucrase, and aminooligopeptidase proceeded normally in GH deficiency. These data suggest that, although GH is not required for normal postnatal intestinal maturation, the mucosal epithelial hypoplasia found in GH-deficient animals suggests that GH or GH-dependent factors act as an intestinal mucosal growth factor whose function is to promote the homeostatic or steady-state regulation of mucosal epithelial growth.
The residual small bowel undergoes profound adaptive alterations after surgical resection. GH is considered to have a role in regulation of these adaptive changes, but its precise role is unknown. We investigated the role of GH by studying the response to intestinal resection in rats with isolated GH deficiency. Spontaneous dwarf rats, a strain of rats with congenital isolated GH deficiency, underwent 60% resection of the small intestine and parameters of the response of the intestinal remnant were compared with age-matched GH-deficient rats undergoing transection, GH-normal rats undergoing 60% resection, and nonmanipulated GH-normal rats. Deficiency of GH did not inhibit hyperplasia of the mucosal mass of the intestinal remnant, indicating that GH is not required for regulation of this aspect of the adaptive response. However, GH deficiency resulted in lack of accumulation of mucosal protein, including lack of accumulation of digestive hydrolases. In addition, GH deficiency resulted in alterations in processing of digestive hydrolases of the distal intestine, indicating that GH may have region-specific effects on small intestinal function. We conclude that GH is required for the normal expression of specific components of the adaptive response to massive small intestinal resection, but not for all aspects. The aspects that require GH appear to involve protein synthesis and processing. Abbreviations: SDR, spontaneous dwarf rats dr, adult GH deficient rats undergoing intestinal resection ds, adult GH deficient rats undergoing intestinal transection dc, adult GH deficient rats not surgically manipulated Dr, adult GH normal rats undergoing intestinal resection Dc, adult GH normal rats not surgically manipulated AOP, aminooligopeptidase Surgical resection of the small intestine provokes a profound adaptive response in the intestinal remnant characterized by dramatic hyperplasia of the mucosal epithelium and enhanced segmental absorption of nutrients (1-4). These changes result in increased functional capacity of the residual intestine.Multiple lines of evidence suggest GH may be essential for the marked increase in intestinal growth seen in adaptation to surgical resection. Our group has shown that GH administration is required for normalization of intestinal growth in rats hypophysectomized in early infancy (5). Receptors for GH have been identified on crypt and villus epithelial cells of the small intestine (6). Small bowel growth has been shown to be enhanced in transgenic mice overexpressing GH (7). Finally, GH is the major regulator of IGF-I, administration of which has been shown to result in enhanced intestinal adaptation after resection (8, 9). Few studies have been performed to investigate the role of GH in adaptation of the residual small bowel after surgical resection in which exogenous human recombinant GH was administered to GH-sufficient rats after small bowel resection. However, contradictory results were obtained, rendering the role of GH in this setting unclear (10 -12).To clarify the specific role ...
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