scholarly journals Prenatal over‐ and undernutrition differentially program small intestinal growth, angiogenesis, absorptive capacity, and endocrine function in sheep

2020 ◽  
Vol 8 (12) ◽  
Author(s):  
Prabhat Khanal ◽  
Anne Marie D. Axel ◽  
Sina Safayi ◽  
Vibeke S. Elbrønd ◽  
Mette O. Nielsen

1997 ◽  
Vol 273 (4) ◽  
pp. E815-E820 ◽  
Author(s):  
Kirk D. Fischer ◽  
Savita Dhanvantari ◽  
Daniel J. Drucker ◽  
Patricia L. Brubaker

Glucagon-like peptide 2 (GLP-2) has recently been identified as a novel intestinal growth factor. Because experimental diabetes is associated with bowel growth, we examined the relationship between GLP-2 and intestinal growth in rats made diabetic by streptozotocin (STZ) injection and treated with or without insulin for 3 wk. Ileal concentrations of the intestinal proglucagon-derived peptides, i.e., glicentin + oxyntomodulin, and GLPs 1 and 2, were increased by 57 ± 20% above those of controls in untreated STZ diabetes ( P < 0.05–0.001). Similar increases in plasma concentrations of glicentin + oxyntomodulin (77 ± 15% above controls, P < 0.01) and GLP-2 (91 ± 32% above controls, P < 0.05) were seen in untreated STZ diabetes. Both wet and dry small intestinal weight increased by 74 ± 20% above controls ( P < 0.01) in STZ diabetes, and macromolecular analysis indicated parallel increases in both protein ( P < 0.001) and lipid ( P < 0.05) content. Villus height ( P < 0.001) and crypt depth ( P < 0.01) were also increased in untreated diabetic rat intestine. Insulin therapy prevented the changes in plasma GLP-2 and intestinal mass seen in untreated STZ diabetes. Thus STZ diabetes is associated with both increased production of GLP-2 and enhanced bowel weight, thereby suggesting a role for GLP-2 in diabetes-associated bowel growth.



1997 ◽  
Vol 8 (4) ◽  
pp. 327-332 ◽  
Author(s):  
RA Sherwood ◽  
JT Marsden ◽  
CA Stein ◽  
S Somasundaram ◽  
C Aitken ◽  
...  

3′-Azido-3′-deoxythymidine (AZT; zidovudine) either alone or in combination with didanosine or another nucleoside analogue is the first-line treatment for patients with human immunodeficiency virus (HIV) infection, many of whom have concurrent gastrointestinal (GI) disease. This study assessed whether the absorption of AZT was affected by GI disease. The absorption and pharmacokinetics of AZT in 23 HIV-infected individuals was measured after a single dose of AZT and was related in 12 patients to small intestinal function. Levels of AZT and its metabolite 5′-glucopyranuronosylthymidine (G-AZT) were measured by radioimmunoassay. Intestinal permeability was assessed by differential urinary excretion of orally administered lactulose/1-rhamnose; absorptive capacity was measured simultaneously by the urinary excretion of 3-o-methyl-D-glucose, d-xylose and 1-rhamnose. Small intestinal inflammation was assessed by faecal excretion of indium-labelled neutrophils. Peak levels of AZT in serum varied between 170 and 1820 ng mL−1. The metabolite G-AZT was present in serum at peak concentrations varying from 1020 to 9930 ng mL−1. There was up to a sevenfold variation in the area under the curve (AUC). The time to maximum serum concentration for AZT was between 30 and 120 min, with an absorption half-life of between 2 and 38 min. The median elimination half-life was 57 min (range 46–72 min), close to the predicted half-life of 60 min. Intestinal permeability was increased in six of the 12 subjects studied and eight had evidence of reduced absorptive capacity. Ten of the 12 patients had evidence of small intestinal inflammation. We concluded that neither changes in permeability nor absorptive capacity influenced the absorption of AZT. There was no relationship between the presence of intestinal inflammation and AZT absorption. This study showed a significant intra-individual variation of serum AZT levels which cannot be explained on the basis of altered intestinal absorptive capacity or intestinal inflammatory changes.



2000 ◽  
Vol 130 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Ruhong Jiang ◽  
Xiaoyan Chang ◽  
Barbara Stoll ◽  
Ming Z. Fan ◽  
John Arthington ◽  
...  


1996 ◽  
Vol 270 (5) ◽  
pp. R1085-R1091 ◽  
Author(s):  
D. G. Burrin ◽  
T. J. Wester ◽  
T. A. Davis ◽  
S. Amick ◽  
J. P. Heath

Our objective was to determine the potentially anabolic effects of orally administered recombinant human insulin-link growth factor I (rhIGF-I)on small intestinal growth in formula-fed neonatal pigs. Unsuckled neonatal pigs received formula or formula containing added rhIGF-I (3.5 mg.kg-1.day-1) from birth to 4 days of age. Pigs in both groups were fed 30 ml/kg formula every 2 h on day 1 and then every 4 h on days 2-4, and blood was sampled daily. Oral administration of rhIGF-I to formula-fed neonatal pigs increased small intestinal weight, protein, and DNA content,but not length. Jejunal and ileal villus height, but not crypt depth or muscularis thickness, also were increased by oral rhIGF-I administration. Neither the circulating concentration of IGF-I nor the IGF-binding proteins differed between control and oral rhIGF-treated pigs, suggesting that the absorption of orally administered rhIGF-I from the intestinal lumen into the peripheral circulation was limited. Our results demonstrate that oral administration of rhIGF-I during the first 4 days after birth significantly increased small intestinal mucosal growth in formula-fed neonatal pigs. These results suggest that oral administration of rhIGF-I may be a viable therapeutic approach to enhance intestinal growth in neonates.





1993 ◽  
Vol 104 (6) ◽  
pp. 1669-1677 ◽  
Author(s):  
John G. Banwell ◽  
Richard Howard ◽  
Iqbal Kabir ◽  
Thomas E. Adrian ◽  
Robert H. Diamond ◽  
...  


1993 ◽  
Vol 70 (1) ◽  
pp. 333-345 ◽  
Author(s):  
Y. C. Ge ◽  
R. G. H. Morgan

Pancreatic and intestinal growth rates were measured in mice fed on raw soya-bean flour (RSF) for up to 24 weeks. Control animals were fed on standard chow. The effects of RSF on the mouse pancreas resembled that seen in rats, showing hypertrophy with some hyperplasia. A marked increase in small intestinal weight was also found in mice fed on RSF but not in rats fed on this diet. Histological studies showed an increase in both villous and crypt thicknesses in the small intestine from these mice, and DNA, RNA and protein measurements indicated that the increase in intestinal weight was due to hypertrophy and hyperplasia of the mucosal layer. To determine whether the intestinal growth in mice fed on RSF was purely a response to the trypsin inhibitor (TI) component of the diet, pancreatic and intestinal growth rates were also determined in mice fed on the synthetic trypsin inhibitor camostate, at levels of 0·5 or 2 g/kg in rat chow, for periods of 1–8 weeks. Control animals were fed on standard chow. RSF and 0·5 g camostate/kg had similar trypsin inhibitor activities (measured against bovine trypsin), and both caused similar increases in pancreatic weight, DNA, RNA and protein content. However, 0·5 g camostate/kg did not affect small intestinal weight. Chow containing 2 g camostate/kg contained twice as much TI activity as the RSF diet but produced only a small increase in small intestinal weight at 2 and 8 weeks. This intestinal growth was significantly less than that seen with RSF. The present study shows that, in the mouse, RSF or a diet containing camostate in the appropriate dose produces pancreatic growth comparable to that seen in the rat. RSF also causes intestinal growth, but camostate-containing diets have little or no effect on the growth of the intestine.



2018 ◽  
Vol 96 (1) ◽  
pp. 306-317 ◽  
Author(s):  
Daming Sun ◽  
Hongwei Li ◽  
Shengyong Mao ◽  
Weiyun Zhu ◽  
Junhua Liu


1988 ◽  
Vol 66 (2) ◽  
pp. 574 ◽  
Author(s):  
K. R. Cera ◽  
D. C. Mahan ◽  
R. F. Cross ◽  
G. A. Reinhart ◽  
R. E. Whitmoyer


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