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Biomedical subjects

A Rubenstein

Publications and source records attributed to A Rubenstein.

52 records · Page 3Linked to original sources
PubMed1979

Somatostatinoma syndrome. Biochemical, morphologic and clinical features.

Diabetes mellitus, steatorrhea, cholelithiasis and a tumor distorting the duodenum prompted a work-up for somatostatinoma in a 52-year-old man. The responses of pancreatic B-cells but not of A-cells to nutrient stimuli were inhibited, and growth-hormone release was suppressed, suggesting somatostatin resistance in some target tissues. Plasma somatostatin-like immunoreactivity ranged from 9000 to 13,000 pg per milliliter (normal: 88+/-8, mean +/- S.E.M.) and was distributed in four molecular forms, including free somatostatin. The primary tumor contained 5 microgram of somatostatin-like immunoreactivity per milligram of wet tissue, distributed in three of the molecular forms noted in plasma. Plasma calcitonin was also elevated (4650 pg per milliliter; normal: less than 120). Immunocytochemical studies showed that cells of the primary tumor contained somatostatin and calcitonin but no other peptide hormones. Only somatostatin was present in the metastases. Somatostatin was localized electron microscopically in all secretory granules, irrespective of size and shape, whereas calcitonin was present only within a single subpopulation of small granules in the same cells.

C-Peptide↗
PubMed1979

Taste detection and preferences in diabetics and their relatives.

In order to determine whether a generalized defect in glucose recognition exists in diabetes, taste detection and preference were measured in adult onset diabetics (AOD), juvenile onset diabetics (JOD), and healthy first-degree relatives of diabetics (NR). Controls (C) were age and sex matched nondiabetics without first-degree diabetic relatives. The AOD and NR gorups showed significantly higher glucose thresholds than their controls. In contrast, glucose threshold in JOD was not different from C. The AOD group also demonstrated a higher sucrose threshold than C. This difference was not present for JOD or NR groups. No difference in salt detection was seen in any of the groups. Taste preference was assessed by two choice situations and ratings of test solutions of varying concentrations. No significant difference in glucose or sucrose preference were noted, but both the AOD and NR groups preferred lower salt concentrations than C. These findings indicate that thery may be a widespread impariment of cellular glucose recognition in AOD and their relatives, while JOD have a specific beta cell defect.

Adolescent↗
PubMed1977

Haemoglobin A1: An indicator of the metabolic control of diabetic patients.

The level of the minor glycosylated haemoglobins (HbA1) in ambulatory diabetic patients correlated closely with their physicians' ratings of the degree of control and their fasting plasma-glucose levels. In patients admitted to hospital for more detailed study, HbA1 correlated significantly with the mean fasting glucose, mean daily glucose, and highest daily glucose values. HbA1 measurement is a simple, rapid, and objective procedure to assess diabetic control and may serve both as a screening test for uncontrolled diabetes and as an indicator of the efficacy of various therapeutic regimens.

Adolescent↗
PubMed1976

Acute effect of ascorbic acid infusion on carbohydrate tolerance.

Large doses (1 to 2g/3 hr) of ascorbic acid were administered intravenously to normal weight and obese, nondiabetic subjects. Glucose tolerance and fasting plasma glucose levels were unaffected, despite a 3- to 8-fold rise in plasma concentrations of the vitamin. Infusion of ascorbic acid did not alter fasting serum insulin levels in normal subjects, but was associated with lower concentrations of hormone during an intravenous glucose tolerance test. Plasma glucose, serum insulin, growth hormone, and glucagon levels in obese subjects remained unchanged during the ascorbic acid infusion.

Ascorbic Acid↗
PubMed1975

Insulin and proinsulin release during calcium infusion in a patient with islet-cell tumor.

The infusion of calcium results in the release of gastrin, calcitonin, and serotonin from certain nonbeta islet cell tumors of the pancreas, medullary carcinomas of the thyroid, and carcinoid tumors, respectively. In this study, intravenous infusion of either calcium chloride or calcium aluconate in a patient with an islet-cell carcinoma resulted in a simultaneous rise in plasma immunoreactive insulin and proinsulin, and concurrent hypoglycemia. After resection of the tumor, calcium infusion caused no change in these parameters. Similarly, calcium infusion caused no change in plasma insulin or glucose in normal volunteers. The response of this tumor suggests that calcium infusion may be a useful provocative test to detect insulin-secreting neoplasia. A derangement of the stimulus-secretion coupling mechanism for insulin in the tumor cells may be responsible for their abnormal sensitivity to calcium ion.

Adenoma, Islet Cell↗
PubMed1975

C-peptide analysis in diagnosis of factitial hypoglycemia in an insulin-dependent diabetic.

Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower.

Adult↗
PubMedDate not supplied

Scrapie strain infection in vitro induces changes in neuronal cells.

PC12 cells, in the presence of nerve growth factor (NGF), support replication of the mouse-derived scrapie strains 139A and ME7, with the former yielding 100-1000-fold higher levels of infectivity. Infectivity remained cell-associated and cells did not show any gross morphological alterations, although changes were observed by electron microscopy in the form of an increased number of lipid droplets in 139A-infected cultures. Analysis of phospholipid metabolism in 139A infected cells indicated that scrapie replication did not change the inositol phosphate levels, but did stimulate phosphoinositide synthesis. Replication was not detected in PC12 cells infected with either the hamster-derived 263K or rat-derived 139R scrapie strains. Since scrapie-infected cultures did not exhibit cell death or any gross changes, any scrapie-induced effects would probably be manifested in nonvital cellular functions. When compared to controls, infection with the 139A scrapie strain resulted in decreased activity of the cholinergic pathway-related enzymes, as well as the GABA synthetic pathway; however, the adrenergic pathway was unaffected by scrapie infection. The effects of the 139A scrapie strain on the cholinergic system appeared to be dose-dependent and were first detected prior to the detection of scrapie agent replication in these cells. No neurotransmitter-related enzymatic changes were detected in 263K- or 139R-infected PC12 cells. The enzymatic changes observed in ME7-infected PC12 cells and in Chandler agent-infected mouse neuroblastoma cells suggest that the significant changes in neurotransmitter levels in cultures exhibiting low infectivity titers must involve factors other than, but not excluding, replication of the agent. The role of additional factors is also suggested in studies of protein kinase C activity in 139A- and 139R-infected PC12 cells. These studies emphasize the value of the PC12 cell model system in examining the scrapie strain-host cell interaction and, in addition, support the concept of variation among scrapie strains.

Acetylcholinesterase↗
PubMedDate not supplied

Response of rhesus serum high density lipoproteins to cycles of diet-induced hypercholesterolemia.

Two male rhesus monkeys underwent cyclical feeding of a hypercholesterolemic diet (2% cholesterol, 25% coconut oil) and a low-fat Purina monkey chow diet. During the latter diet, high density lipoprotein (HDL) exhibited two components with peak densities of d = 1.081 g/ml and 1.109 g/ml named HDLL and HDLH, respectively. During the initial hypercholesterolemic stage, except for apo A-II which remained unchanged, there was a transient rise in HDL (mainly HDLL) as well as in HDL cholesterol and apo A-I, all reaching maximal values after about 2 weeks from the onset of the diet. The two HDL species changed neither in size nor density as compared to their baseline counterparts, but had a comparatively higher content in cholesteryl ester and lesser amounts of triglycerides and phospholipids as compared to the normocholesterolemic animal. With the development of overt hypercholesterolemia (plasma cholesterol levels above 400 mg/dl), both HDL particles increased in density due to the loss of surface components (phospholipids and unesterified cholesterol) and core triglycerides with only minor changes in protein and cholesteryl ester contents. At this stage, the same two animals exhibited significant changes in the size and buoyant density of LDL. When returned to a normal Purina chow diet, the animals' serum cholesterol levels declined rapidly to normal levels; normalization of the HDL distribution also occurred but at a comparatively later time (26 weeks). Our studies indicate that the two HDL subsets characteristic of the normocholesterolemic rhesus monkey undergo significant changes in buoyant density as a function of the stage of hypercholesterolemia and that changes in concentration and size mainly affect the HDLL subspecies. At levels of plasma cholesterol below 400 mg/dl, this cholesterol increment is reflected by a significant increase in the number of the HDL subspecies without the overt participation of the low density lipoprotein classes characteristic of the advanced hyperlipidemic stage. Since we previously reported that greatly increased levels of cholesteryl esters enriched low density lipoproteins, beta-VLDL (very low density lipoprotein) and pre-beta-VLDL during overt diet-induced hypercholesterolemia, it is apparent that cholesterol is distributed differently among lipoprotein particles containing either apo A-I, apo B, or apo E depending on its concentration in plasma.

Animals↗
PubMedDate not supplied

Insulin-resistant diabetes with insulin receptor autoantibodies in a male patient without acanghosis nigricans.

A 51-yr-old, nonobese, male patient presented with hyperglycemia and a recent 40-pound weight loss. Severe insulin resistance was documented in studies in which high amounts of insulin were infused using the Biostator GCIIS. Diabetic control was finally achieved with subcutaneous injections of 470 U of insulin per day. Positive laboratory findings included a mild pancytopenia, elevated erythrocyte sedimentation rate, decreased C3 and properdin, and increased IgA. Antinuclear or other autoantibodies were not present. Insulin antibody levels were within the range usually present in insulin-treated diabetic patients. Acanthosis nigricans was not present. Incubation of the patient's serum with IM-9 lymphoblastoid cells revealed that an insulin receptor antibody was present in a serum dilution of 1:80. Insulin-resistant diabetes mediated by insulin receptor antibodies may present in patients with immunologic findings but without overt dermatologic stigmata.

Acanthosis Nigricans↗