When male rats were given single i.p. injection of 500 mg of L-arginine/100 g body weight, the pancreatic acinar cells were destroyed selectively, without any morphological change of Langerhans' islets. As early as 24 hours after the injection, loss of basophilia, zymogen degranulation, and vacuolar and necrotic changes of the acinar cells were noted. After 3 days, fibroblastic activity and atrophy of pancreatic lobuli were evident. Early electron microscopic findings were changes of the endoplasmic reticulum, such as partial dilatation or vacuolation of the cisternae, usually with loss of ribosomes attached to the membrane. The effect of arginine excess may be ascribed to imbalance of amino acids and subsequent to decrease of protein synthesis in the acinar cells. In the course of this study, fat necrosis with marked infiltration of leucocytes was observed in adipose tissues in peripancreatic, epididymal, omental and retroperitoneal areas. This change correlated closely with the marked necrosis of the pancreas. An increase in the level of lipase in the blood was also demonstrated.

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SummaryTransfer of lipid to the lymph by the intestine was studied in rats fed on choline-deficient or choline-supplemented diet for 2 weeks. In choline-deficient rats, lymph output was reduced. Choline deficiency impaired the incorporation of glycerol tri[1-14C]oleate into triglyceride in the lymph. The triglyceride level in lymph lipoproteins was lower in choline-deficient rats than in controls. Ultrastructural studies suggested that impaired release of lipoproteins was responsible for accumulation of fat in intestinal absorptive cells. These defects are probably related to changes in the membrane system of the intestine and to a failure in lipid droplet movement within absorptive cells, resulting from alterations in the microfilaments. Oral administration of phosphatidylcholine to rats on choline-deficient diet rapidly improved the decreased lymph output and the impaired incorporation of glycerol tri[l-14C]oleate into triglyceride and reduced fat deposition in intestinal epithelial cells. In conclusion, phos pholipids such as choline are confirmed as being extremely important in the absorption of fat by the possible mechanism of fat transport across the membrane.

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SummarySurfactant protein A (SP-A) is a major apo-protein of pulmonary surfactant, which lines the alveolar walls, lowering the surface tension to prevent lung collapse. Pregnant rats were divided into two groups which received a diet with either 5% or 20% protein from gestational day 9. By a sensitive immunoassay, SP-A levels in the fetal lungs and the amniotic fluid showed a dramatic increase with advancing gestation after the initial appearance on gestational day 18 in both diet groups. Significantly lower levels of SP-A in pregnant rats fed 5% protein diet than those in pregnant rats fed 20% protein diet were observed in the fetal lungs on gestational day 21 and in the amniotic fluid on gestational days 20 and 21. The profiles of increased SP-A levels in the amniotic fluid reflected those in the fetal lungs during gestation. Immunohistochemical examination with anti-rat SP-A antibody at 21 days of gestation showed that the immunoreactive staining of bronchiolar epithelial Clara cells and alveolar type II cells were weaker in the fetal lung sections from pregnant rats fed 5% protein diet than in those from pregnant rats fed 20% protein diet. It is concluded that protein malnutrition in pregnant rats affects the biosynthesis of SP-A in the fetal lungs, which may have important consequences for prematurity and decreased respiratory functions in the neonatal lungs at birth.