Using a specific RIA technique, we have determined the somatostatin-like immunoreactivity (SLI) concentrations in acid extracts of pancreatic and gastrointestinal tissues and studied their relationships to feeding in fed and 15-h-fasted immature (less than 24 days old) rats. Mean pancreatic SLI concentrations per unit of protein were low before and immediately after birth before the initiation of feeding. They increased 7-fold during the first 3 days and remained high for the next 2 weeks. Gastric SLI concentrations were also low before and immediately after birth and increased progressively with age up to day 21 (time of weaning), followed by an abrupt increase at day 24, especially in 15-h-fasted rats. The mean SLI concentrations in the duodenum and jejunum were 4.9-6.3 times higher than that in the gastric antrum 1 day before birth and were also significantly higher than those in the gastric antrum for the first 3-7 days. No significant difference was found by age in the gel filtration patterns of tissue extracts from the pancreas, gastric antrum, and duodenum in fetal and fasted 3- and 24-day-old rats. I conclude from these findings that: 1) the developmental patterns of pancreatic and gastrointestinal SLI show a close relationship with feeding, suggesting the important role of somatostatin in the digestive functions and nutrition in immature rats, and 2) the quantitative distribution of somatostatin in the gastrointestinal tract markedly differs so that there is intestinal predominance in fetal or neonatal rats, and predominance in the stomach in adult rats.
Postprandial peripheral plasma concentrations of somatostatin-like immunoreactivity (SLI) were measured by RIA after extraction with acetone-petroleum ether in 98 normal newborns and infants. In 62 subjects, plasma concentrations of gastrin were determined simultaneously. The plasma levels of SLI increased progressively with age during the neonatal period. The mean plasma levels of SLI increased significantly from 19.5 +/- 7.5 (+/- SD) pg/ml in 29 cord blood samples to 29.0 +/- 17.2 pg/ml in 36 newborns aged 1-5 days. The mean postprandial level of plasma SLI was significantly higher in 18 infants aged 1-3 months (45.5 +/- 25.8 pg/ml) than in newborns and tended to decrease in infants aged 7-10 months after weaning (31.6 +/- 7.9 pg/ml). The mean postprandial levels of plasma SLI were significantly higher in newborns and infants less than 10 months old than in older children aged 8-12 yr (10.2 +/- 3.7 pg/ml). The gel filtration patterns of SLI of plasma extracts were similar in infants and older children. The changing pattern of mean plasma gastrin with age was similar to that of SLI, and individual plasma levels of SLI were significantly correlated with those of gastrin during the neonatal period. High concentrations of SLI are present in the peripheral circulation during the first 10 months of life. Thus, this peptide may play a significant role as a hormone in nutrient homeostasis in infants.
Background. Familial hypercholesterolemia (FH) is a genetic disorder characterized by high levels of low-density lipoprotein cholesterol (LDL-C). Because of underdiagnosis, acute coronary syndrome (ACS) is often the first clinical manifestation of FH. In Japan, there are few reports on the prevalence and diagnostic ratios of FH and the proportion of ACS among FH patients in clinical settings. Methods. This retrospective, observational study used anonymized data from electronic healthcare databases between April 2001 and March 2015 of patients who had ≥2 LDL-C measurements recorded after April 2009. The index date was defined as the date of the first LDL-C measurement after April 2009. The primary endpoint was the prevalence of definite or suspected FH; secondary endpoints included the proportion of FH patients hospitalized for ACS, the proportion of patients using lipid-lowering drugs (LLDs), and LDL-C levels. Results. Of the 187,781 patients screened, 1547 had definite or suspected FH (0.8%) based on data from the entire period; 832 patients with definite (n=299, 0.16%) or suspected FH (n=533, 0.28%) before the index date were identified in the main analysis cohort. LLDs were used in 214 definite FH patients (71.6%) and 137 suspected FH patients (25.7%). Among definite or suspected FH patients with ACS (n=84) and without ACS (n=748), 32.1% and 30.1% with definite FH and 3.2% and 2.4% with suspected FH had LDL-C levels<2.6 mmol/L (<100 mg/dL), respectively. Sixty patients (7.2%) were hospitalized due to ACS at the index date. Conclusions. The prevalence of FH in this Japanese cohort of patients with ≥2 LDL-C measurements at hospitals was 0.8%, which is higher than that currently reported in epidemiological studies (0.2–0.5%). Patients with suspected FH, with or without ACS, had poorly controlled LDL-C levels and were undertreated. The proportion of FH patients who were hospitalized due to ACS was 7.2%.
SUMMARY Plasma renin activity (PRA) and aldosterone concentration (PAC) were determined in normal infants aged 20 days to 1 year as well as in normal neonates and older children. The responses of PRA and PAC to five intramuscular injections of synthetic ACTH‐Z at 6‐hour intervals while on replacement cortisol therapy were also studied in nine infants with salt‐losing type of congenital adrenal hyperplasia due to 21‐hydroxylase deficiency (CAH) of varying severity, using the data obtained in normal infants as control. The mean PRA and PAC decreased with age from the neonatal period, but in infants aged 20 days to 3 months these variables remained as high as those in newborns. They were also remarkably higher in infants aged 4 to 12 months than in older children. In two cases of CAH (cases 1 and 2) where salt wasting symptoms had been only transiently observed during the neonatal period, PAC was markedly elevated in response to ACTH administration, while in the remaining seven infants with CAH (cases 3–9) with persistent salt wasting symptoms, PAC was not elevated at all or only slightly so. PRA, on the other hand, increased with time during the ACTH stimulation in cases 3–9, while it increased and then decreased in cases 1 and 2. These findings suggest that the salt‐wasting symptoms in CAH may arise where there is a tendency toward renal salt loss due to the overproduction of ACTH‐dependent steroids characteristic of this disease, and cannot be compensated for by sufficient secretion of aldosterone. In cases 3–9, the maximal PAC under the ACTH stimulation was 17–44 ng/dl. These levels are comparable to or even higher than the normal range for control older children aged 2–8 years, but the levels were inappropriately low for the marked elevation of PRA in all of them when compared with the mean level in normal infants. Therefore, these data also seem to explain at least in part the well known clinical fact that the salt wasting symptoms in CAH are severe during infancy, requiring the administration of mineralocorticoids in addition to cortisol. However, beyond infancy only the replacement cortisol therapy is necessary to remit the symptoms.
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