PubMed Health⌕ Search

Biomedical subjects

S S Fajans

Publications and source records attributed to S S Fajans.

At least 55 records · Page 3Linked to original sources
PubMed1982

Glucose tolerance in two unacculturated Indian tribes of Brazil.

Plasma levels of glucose, insulin, growth hormone, and pancreatic polypeptide in response to a standard oral glucose load were studied in the Yanomama and the Marubo, two relatively unacculturated Amerindian tribes of the Brazilian Amazon. The findings in the two tribes differed significantly from each other and in the degree of deviation from control subjects. The average responses in both tribes differed significantly from those of age- and sex-matched Caucasoid control subjects studied in Ann Arbor, Michigan; however, of the two tribes, the Marubo, the more acculturated group, resembled the controls more closely. Plasma concentrations of glucose and the hormones at three time points (fasting, 1 h, 2 h) were compared by means of a multivariate analysis. When the Marubo were compared with the control subjects, the only highly significant difference was in the plasma glucose concentrations (all three points were higher in the Marubo); however, the Yanomama differed significantly from the control subjects with respect to all four plasma indicators (p less than 0.05). Unlike the Marubo, the Yanomama showed no significant rise in plasma glucose at 1 h and no decrease at 2 h. Neither tribe exhibited the bimodality of the 2 h glucose value characteristic of acculturated Amerindians, such as the Pima, but the samples studied were small.

Adolescent↗
PubMed1982

Identifying risk factors for diabetes in first degree relatives of non-insulin dependent diabetic patients.

Glucose tolerance test data on 794 first-degree relatives of diabetics in pedigrees ascertained through non-insulin dependent diabetes mellitus from southeastern Michigan were used to identify risk factors for diabetes. The general risk factors, age and obesity, were important in predicting diabetes at initial visit, although the predicted risk curves were very different from males and females. In predicting diabetes at initial visit, the number of affected sibs contributed more to the logistic regression than did the number of affected parents. Among a group of 393 individuals who were followed up for a mean of eight years, the initial glucose tolerance test response was the best single predictor of being diabetic on follow-up. These results suggest there may be a strong within-generational component which influences both the quantitative test response and the risk to diabetes. This component may reflect environmental factors influencing glucose tolerance among sibs and, as such, should be considered when studying the genetics of diabetes.

Adolescent↗
PubMed1982

Estimating genetic and non-genetic components of variance for fasting glucose levels in pedigrees ascertained through non-insulin dependent diabetes.

Fasting glucose levels measured on 337 individuals in 14 pedigrees ascertained through a proband with non-insulin dependent diabetes were used to estimate genetic and non-genetic components of variance under a multifactorial model of inheritance. In this sample genetic factors were important in controlling variation in basal carbohydrate metabolism, as represented by age-adjusted log-fasting glucose. There was no evidence that arbitrary sib common environments or arbitrary parent common environments accounted for significant portions of the variability in fasting glucose in these data. An arbitrary environment shared by parent and offspring, however, had a marginally significant impact on the likelihood. Parameter estimates obtained from multifactorial models analysed in this manner are sensitive to extreme phenotypic values, however, and caution must be exercised in estimating total genetic variation. While additive genetic factors did account for a significant proportion of the total variation in fasting glucose, a large proportion remained unexplained.

Adolescent↗
PubMed1982

Localization of the source of hyperinsulinism: percutaneous transhepatic portal and pancreatic vein catheterization with hormone assay.

Insulin concentrations were measured in the portal venous system through the percutaneous transhepatic approach in 12 patients with organic hyperinsulinism. Single insulinomas were found in 10, an adenoma and islet cell hyperplasia in one, and nesidioblastosis in one patient. Angiography localized adenomas in two. Local step-ups of insulin levels in the portal venous system, found in all patients with insulinomas, corresponded to tumor sites at surgery. Multiple step-ups were found in the portal venous system of the patient with nesidioblastosis and the patient with an adenoma with islet cell hyperplasia. Three tumors were localized in the head of the pancreas which would indicate the primary surgical approach rather than blind resection of the body and tail. Three of the 10 adenomas were not identifiable by palpation after pancreatic mobilization during surgery. In all patients, organic hyperinsulinism was cured after surgery. Percutaneous transhepatic portal and pancreatic vein catheterization with measurement of radioimmunoactive insulin concentrations is a safe and reliable method and may play an important role in the localization of adenomas in patients with normal angiographic studies and previous negative surgical explorations.

Adenoma↗
PubMed1981

Nesidioblastosis in adults. A surgical dilemma.

Nesidioblastosis is the leading cause of hyperinsulinemia in newborns and infants. To our knowledge, it has not been previously reported in adults unless associated with other diseases. Three males and three females, aged 11 to 57 years, are described. Pancreatic resections ranged from 50% to 100%. Postoperatively, three patients were normoglycemic, two were insulin-dependent diabetics, and one had recurrent hypoglycemia controlled by drugs. The histologic findings in adults were very similar to those in infants with nesidioblastosis. It appears that a minimum resection of 75% to 80% of the pancreas will benefit the majority of patients, alleviating hypoglycemia and preventing the development of diabetes.

Adult↗
PubMed1981

Gastrointestinal/pancreatic hormone concentrations in the portal venous system of nine patients with organic hyperinsulinism.

Percutaneous transhepatic sampling of blood in the portal venous system (TPVS) was used to; (1) localize hormone secreting tumors and help in differentiating tumors from diffuse disease (nesideoblastosis and hyperplasia with adenomata) in 9 patients with fasting hypoglycemia and hyperinsulinism, and (2) study the concentration an distribution of the immunoreactive peptides: insulin (IRI), gastrin (IG), glucagon (IRG), pancreatic polypeptide (hPP), and somatostatin (SRIF-LI), in the venous drainage of the uninvolved portion of the pancreas and GI tract. Localized elevations of IRI (64-920 microunits/ml) predicted tumor localization in 6 patients with single tumors that were not demonstrable angiographically. In one patient with nesideoblastosis and another with islet cell hyperplasia with adenoma, elevated IRI concentrations at multiple locations suggested a diffuse or multicentric process. Elevations of SRIF-LI in the same region as IRI elevations in one patient and of IRG in another patient suggested that these tumor produced two hormones. Some problems in the interpretation of portal venous insulin concentrations are discussed. The locations of maximum portal venous system plasma concentrations and portal-arterial gradients (mean +/- SE pg/ml) in five patients with small single insulinomas were: IG, gastrocolic trunk (126 +/- 27, 46 +/- 22); IRG, proximal splenic vein (130 +/- 30, 47 +/- 13) and gastrocolic trunk (131 +/- 23, 60 +/- 13); hPP, portal vein (164 +/- 48, 49 +/- 22); SRIF-LI, superior mesenteric vein (186 +/- 50, 57 +/- 20) and gastrocolic trunk (178 +/- 59, 55 +/- 21). It is concluded; (1) TPVS can be used successfully to localize single insulin-secreting tumors of the pancreas and to help distinguish them from diffuse disease but problems in such differentiation do occur, (2) circulating SRIF-LI and IRG are derived from both the pancreas and the gut, IG predominantly from the proximal gut and hPP from the head of the pancreas, and (3) The data provide new information for the interpretation of portal insulin concentrations in patients with organic hyperinsulinism and of hormone concentrations for localization of peptide-producing tumors of the pancreas other than insulinomas.

Adenoma↗
PubMed1980

The effect of adrenergic receptor blockade on the exercise-induced rise in pancreatic polypeptide in man.

The effect of adrenergic receptor-blocking agents upon plasma levels of human pancreatic polypeptide (hPP), human GH (hGH), immunoreactive insulin, and glucose during graded submaximal exercise was ascertained in six healthy nonobese males. Subjects exercised from 0--27 min on a motor-driven treadmill and received infusions from -10 to 40 min of either 1) saline, 2) saline plus phentolamine (0.5 mg/min; alpha-adrenergic blockade), or 3) propranolol (3 mg) from -10 to -5 min, followed by saline plus propranolol (0.08 mg/min; beta-adrenergic blockade). During saline-exercise, mean plasma hPP rose from a mean (+/-SE) basal level of 45 +/- 11 to 149 +/- 51 pg/ml at 27 min, whereas with phentolamine-exercise, the maximal level reached by mean plasma hPP (305 +/- 28 pg/ml) was significantly greater than that with saline (P less than 0.05). During propranolol-exercise, mean plasma hPP did not rise significantly above the basal level. The incremental area under the hPP curve for phentolamine-exercise also was significantly greater than that for saline-exercise or propranolol-exercise. The changes in plasma hGH during and after saline-exercise correlated with those of hPP, but the effects of phentolamine and propranolol upon exercise-induced increases in hGH were opposite to the effects upon hPP. The exercise-induced fall in immunoreactive insulin was accentuated with propranolol and abolished with phentolamine. It is concluded that 1) submaximal exercise stimulates secretion of hPP and hGH, 2) adrnergic mechanisms participate in exercise-induced increased secretion of hPP (beta-adrenergic stimulation augments secretion and alpha-adrenergic stimulation inhibits secretion), and 3) adrenergic effects which modulate exercise-induced secretion of hPP and insulin are in parallel but are opposite to those that modulate the secretion of hGH.

Adult↗
PubMed1979

Clinical and etiological heterogeneity of idiopathic diabetes mellitus. The banting memorial lecture.

We have presented and reviewed evidence for the heterogeneous nature of diabetes mellitus in terms of genetics, environmental factors, insulin responses to glucose and vascular disease. We have reviewed evidence for heterogeneity between juvenile-onset diabetes (JOD) and maturity-onset diabetes (MOD) and maturity-onset diabetes of young (MODY) and for heterogeneity within groups of JOD and MOD and MODY patients. Although much remains to be learned, a beginning has been made and suggests that primary diabetes mellitus is not a single specific disease but a syndrome comprised of a variety of diseases all characterized by hyperglycemia and tissue changes that result from heterogeneous etiologic and pathogenetic factors. Future classifications of primary diabetes mellitus will undoubtedly be lengthy, as are for other diseases and syndromes also caused by a variety of etiologic and pathogenetic mechanisms.

Adenoma, Islet Cell↗
PubMed1978

Effect of age on fasting plasma levels of pancreatic hormones in man.

The effect of age and adiposity on fasting plasma levels of pancreatic polypeptide (HPP), glucagon (IRG), insulin (IRI) and glucose was examined in 263 healthy subjects between the ages of 20-69 yr. Mean plasma levels of hPP rose continuously from the third through the seventh decades. Mean plasma levels of IRG rose within the third and fourth decades but failed to rise further thereafter. Mean plasma levels of IRI did not change with age. Mean plasma levels of glucose rose by approximately 2 mg/dl . decade. The correlations of age with hPP, IRG, glucose, and adiposity were 0.47, 0.35, 0.25 (all P less than 0.01) and 0.15 (P less than 0.05), respectively. When adjustments were made for adiposity, the correlations of age with hPP, IRG, and glucose remained. Adiposity correlated with IRI, IRG, and glucose but when age correction was made, only the correlation of adiposity with IRI persisted. We conclude that: 1) age has a significant effect on fasting plasma levels of hPP and IRG; 2) the patterns of the age-related changes in hPP and IRG are not the same, suggesting that there are differences in the mechanism(s) by which age influences plasma levels of these two pancreatic hormones; and 3) age should be considered in the interpretation of fasting plasma levels of hPP and IRG.

Adult↗
PubMed1977

Ectopic production of chorionic gonadotropin and its subunits by islet-cell tumors. A specific marker for malignancy.

We measured human chorionic gonadotropin (hCG) and its subunits in 76 patients with islet-cell tumors. Seventeen of 27 patients with functioning islet-cell carcinomas had elevated plasma levels of hCG or one of its subunits (hCG-alpha and hCG-beta). Secretion was often discordant; the most frequent finding was an elevated level of hCG-alpha alone. In one patient responding to streptozocin, changes in hCG-alpha correlated with the clinical course. Studies of tumor extracts suggested that the markers observed in the circulation were being produced in the tumor itself. In contrast, none of the 43 patients with benign disease or the six patients with nonfunctioning malignant tumors had elevated levels of hCG, hCG-alpha or hCG-beta. These data show that hCG and its subunits are prevalent and specific markers for islet-cell carcinoma, and suggest that ectopic secretion results from malignant derepression of the genome rather than overproduction by an aberrant "cell rest."

Adenoma, Islet Cell↗
PubMed1977

Insulin, proinsulin, glucagon and gastrin in pancreatic tumors and in plasma of patients with organic hyperinsulinism.

Insulin, proinsulin, glucagon and gastrin were determined in extracts of tumors of 27 patients with pancreatic islet cell neoplasia of pancreas, in one patient with nesidioblastosis, in extracts of uninvolved portions of the pancreas in 11 of the tumor patients and of 15 control pancreases. Mean insulin concentration in solitary adenomas and in adenomas of patients with adenomatosis was higher than in control pancreases; however, in all but 1 patient the insulin concentration in neoplastic islet tissue was lower than in islet tissue of control pancreas, assuming islet volume is 1% of pancreas. The percentage of proinsulin was elevated in 52% of tumors. Adenoma insulin content correlated with increments of plasma insulin after tolbutamide administration. Insulin and proinsulin concentrations in pancreas uninvolved by tumor were not suppressed. Fasting plasma glucagon was elevated in patients with islet cell adenomatosis and in patients with islet cell carcinoma some of whom had multiple endocrine adenomatosis. The mean concentration of glucagon in tumors was lower than in control pancreases. Elevated concentration of gastrin was found in some adenomas. The data indicate: 1) insulin-secreting islet cell tumors have decreased storage capacity for insulin, 2) elevated concentration of proinsulin in tumors may be due to decreased capacity to store insulin and in some to decreased conversion of proinsulin to insulin as well, 3) tolbutamide stimulates the exaggerated release of a relatively constant fraction of insulin stored in adenomas. 4) solitary adenomas may contain excess amounts of pancreatic hormones in addition to insulin, 5) elevated plasma glucagon in patients with organic hyperinsulinism may indicate malignancy, microadenomatosis or multiple endocrine adenoma syndrome, and 6) chronic hyperinsulinism and hypoglycemia due to adenoma do not suppress insulin and proinsulin content of uninvolved pancreas.

Adenoma↗