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Biomedical subjects

M Lorenzi

Publications and source records attributed to M Lorenzi.

At least 109 records · Page 6Linked to original sources
PubMed1976

Somatostatin does not suppress plasma parathyroid hormone.

The effect of somatostatin on plasma parathyroid hormone (PTH) was studied in 6 subjects with normal parathyroid function and one patient with a parathyroid adenoma. In 5 subjects, including the one with the parathyroid adenoma, plasma PTH was measured by radioimmunoassay during a 4-hour infusion of somatostatin (500 mug/h). In 2 subjects, PTH responses to EDTA were compared with those observed during a simultaneous infusion of somatostatin and EDTA. In no instance was ther a discernible effect of the somatostatin infusion on plasma PTH. These results demonstrate that somatostatin does not suppress plasma PTH.

Adult↗
PubMed1976

Discordance of diabetic microangiopathy in identical twins.

In a pair of 19-year-old monozygotic twin girls, one developed insulin-dependent, ketosis-prone diabetes at the age of three and has required insulin for the past 16 years. Her identical twin has maintained normal oral and intravenous glucose tolerance with normal insulin release and glucagon suppression. An unequivocal hypertrophy of the muscle capillary basement membrane (1,800 +/- 148 A) was dound in the diabetic twin, while a normal thickness of 1,149 +/- 62 A was present in her nondiabetic sister. Follow-up of the present subjects and data from other discordant identical twins who have reached adulthood could determine whether muscle capillary basement membrane hypertrophy is an independent marker of genetic diabetes in adults. Discordance of diabetic microangiopathy in a pair of monozygotic twins has important implications regarding the influence of heredity and environment on diabetic microangiopathy.

Adult↗
PubMed1976

Studies on the mechanism of epinephrine-induced hyperglycemia in man. Evidence for participation of pancreatic glucagon secretion.

In man, epinephrine induces increases in plasma levels of glucagon, a lipolytic and hyperglycemic hormone. To determine glucagon's contribution to this hyperglycemia and lipolysis, the effects of inhibition of pancreatic alpha-cell responses to epinephrine were investigated with somatostatin and adrenergic receptor blockade. To avoid ambiguities that might result from concomitant changes in endogenous insulin secretion, these studies were performed in juvenile-type, insulin-deficient diabetic subjects. Compared with normal subjects, the diabetics had excessive glucagon responses to epinephrine, which had been infused to attain circulating levels within the range found in man in severe stress. Both somatostatin and propranolol completely prevented glucagon responses and diminished the glycemic response to epinephrine by 40 to 50 per cent. Free fatty acid responses to epinephrine were completely prevented by propranolol but unaffected with somatostatin. Phentolamine had no effect on glucose, free fatty acid, or glucagon responses to epinephrine. These studies demonstrate that epinephrine, via a beta-adrenergic receptor mechanism, causes excessive plasma glucagon elevation in human diabetes mellitus and indicate that this hyperglucagonemia participates in the hyperglycemic, but not the lipolytic, response to epinephrine. Catecholamine-induced hyperglucagonemia may thus provide an additional explantation for the deterioration in carbohydrate tolerance associated with stress.

Adult↗
PubMed1976

Effects of acute insulin withdrawal and administration on plasma glucagon responses to intravenous arginine in insulin-dependent diabetic subjects.

To assess further the role of insulin in the abnormal alpha-cell dysfunction found in human diabetes mellitus, the effects of acute insulin withdrawal and administration on plasma glucagon responses to intravenous arginine were studied in eight insulin-dependent diabetic subjects. Arginine infusions (30 gm. over 30 minutes) were performed during and at one and four hours after discontinuation of a 14-hour insulin infusion (1.5 U. per hour), which had rendered the subjects euglycemic, and on another occasion before and one and four hours into a five-hour infusion of insulin (1.5 U. per hour). During the last hour of the 14-hour infusion, glucagon responses to arginine (area under the curve, nanograms per milliliter per minute) were similar to those found in normal subjects (10.3 +/- 0.8 vs. 9.0 +/- 0.8, respectively). After discontinuation of the insulin infusions, glucagon responses increased progressively (p less than 0.01) to values (16.8 +/- 1.2) that exceeded those of normal subjects by four hours (p less than 0.01). These were similar to results found in the same subjects studied when their diabetes was in less than optimal control (14.9 +/- 1.3). Infusion of insulin under these conditions progressively decreased glucagon responses to arginine to values (9.6 +/- 0.8; p less than 0.01) that, at four hours, were similar to those of normal subjects and to values found at the end of the 14-hour infusion of insulin in the same diabetic individuals. These results demonstrate a rapid effect of insulin on glucagon responses to arginine and suggest that the abnormal responses seen in diabetes mellitus are the immediate result of insulin deficiency. Since abnormal glucagon responses to glucose in diabetes are not as readily corrected by insulin, the mechanisms underlying the abnormal responses to these two stimuli may differ.

Adolescent↗
PubMed1975

Abnormal pancreatic glucagon secretion and postprandial hyperglycemia in diabetes mellitus.

Plasma glucose and glucagon responses to standard meals containing carbohydrate, fat, and protein as in normal diets were studied in 12 subjects with insulin-dependent diabetes and 12 normal subjects. Diabetics had two to three times greater glucagon responses than did normal subjects. Fifteen units of insulin injection did not normalize these excessive glucagon responses, although postprandial hyperglycemia was reduced. Infusion of somatostatin at a dosage of 500 mug/hr prevented glucagon responses and diminished postprandial hyperglycemia by 60%. The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. Somatostatin and insulin, administered subcutaneously in the same syringe, also abolished postprandial hyperglycemia. These studies indicate that excessive glucagon secretion participates in the genesis of diabetic postprandial hyperglycemia. Somatostatin, an inhibitor of glucagon secretion, may thus prove useful as an adjunct to insulin in the treatment of diabetes mellitus.

Adult↗
PubMed1975

The effect of somatostatin on coagulation and platelet function in man.

Preliminary evidence has suggested that somatostatin might interfere with platelet function in the baboon. Because this agent is currently being administered experimentally to human beings, we studied its effect on coagulation and platelet function in man. In five subjects, a four-hour infusion of somatostatin (500 micrograms per hour) had no definite effect on platelet count, leukocyte count, hematocrit, platelet adhesiveness and aggregation, bleeding time, partial thromboplastin time, prothrombin time, and fibrinogen levels. A similar infusion for 18 hours in three subjects was likewise without effect. These studies indicate that somatostatin does not affect coagulation and platelet function in man and that its prolonged administration lacks ostensible toxicity.

Adenosine Diphosphate↗
PubMed1975

Prevention of human diabetic ketoacidosis by somatostatin. Evidence for an essential role of glucagon.

To evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we studied the effect of suppression of glucagon secretion by somatostatin on changes in plasma beta-hydroxybutyrate and glucose concentrations (as well as changes in their precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes. Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 hours after insulin was stopped. Plasma beta-hydroxybutyrate, glucose, free fatty acid, and glycerol levels were all markedly lower during suppression of glucagon secretion (p smaller than 0.001), whereas plasma alanine levels were higher (p smaller than 0.001). These studies indicate that insulin lack per se does not lead to fulminant diabetic ketoacidosis in man and that glucagon, by means of its gluconeogenic, ketogenic, and lipolytic actions, is a prerequisite to the development of this condition.

Adult↗
PubMed1975

Evidence for a physiologic role of pancreatic glucagon in human glucose homeostasis: studies with somatostatin.

To study the role of glucagon in human glucose homeostasis, experimental glucagon deficiency was produced by infusing somatostatin (i. v. 250 mug bolus, followed by infusion of 500 mug/hr) in six normal subjects and in two hypophysectomized patients-an insulin-dependent diabetic and a nondiabetic. In normal subjects, somatostatin lowered plasma glucagon from a mean (plus or minus SE) basal level of 85 plus or minus 15 to 33 plus or minus 10 pg/ml, p smaller than 0.001. Concurrently, plasma glucose fell from 90 plus or minus 2 to 73 plus or minus 3 mg/100 ml, p smaller than 0.001. Serum insulin and growth hormone fell slightly during somatostatin infusion, while plasma free fatty acids rose. In both hypophysectomized patients, somatostatin lowered plasma glucagon and glucose levels. In all subjects, after stopping somatostatin infusions, plasma glucagon and glucose returned promptly to control values, while serum growth hormone did not change. In additional in vitro studies, somatostatin (1 mug/ml) had no effect on muscle glucose uptake. Since it is known that somatostatin has no direct effect on hepatic glucose production, these results suggest that the fall in plasma glucose during somatostatin infusion resulted from inhibition of glucagon secretion, thus providing evidence that this hormone plays a physiologic role in the maintenance of fasting euglycemia in man.

Adult↗
PubMed1975

Plasma glucagon and alanine responses to acute insulin deficiency in man.

Plasma glucagon levels rose within 1 hr after withdrawal of insulin in 7 juvenile-type diabetics previously kept normoglycemic by prolonged intravenous infusions of insulin. These changes preceded subsequent elevations in plasma alanine levels. Individual rises in plasma glucagon were correlated with elevations in plasma glucose, beta-hydroxybutyrate, free fatty acid, and glycerol levels, suggesting that glucagon may play an important role in the development of diabetic ketoacidosis in man.

Adult↗
PubMed1975

Failure of somatostatin to inhibit tolbutamide-induced insulin secretion in patients with insulinomas: a possible diagnostic tool.

The effects of somatostatin on tolbutamide-stimulated insulin release were studied in 4 patients with insulin-producing tumors of the pancreas and in 6 normal subjects. In contrast to its effective inhibition of insulin release in normal subjects, somatostatin, without exception, failed to inhibit tolbutamide-induced insulin release in the patients with pancreatic beta-cell tumors. This differential effect of somatostatin may prove useful in the diagnosis of insulin-producing tumors of the pancreas.

Adenoma, Islet Cell↗
PubMed1975

Inhibition by somatostatin of ACTH secretion in Nelson's syndrome.

Somatostatin (GHIF), when administered as a 1-hr infusion (500 mug/hr) to 5 patients with Nelson's Syndrome;resulted in a sustained, progressive fall in plasma ACTH in each patient to 40% to 71% of basal values with a return toward initail levels after cessation of the infusion. The meanreduction in plasma ADTH was 48% (p less than 0.005). These finding suggest that GHIF receptors not fuctional or present in normal pituitary tissue are present in ACTH-producing pituitary tumors.

Adenoma↗
PubMed1975

Normalization of fasting hyperglucagonemia and excessive glucagon responses to intravenous arginine in human diabetes mellitus by prolonged infusion of insulin.

Infusion of insulin (1 U/hr) for 14 hr suppressed basal glucagon levels and normalized previously excessive glucagon responses to arginine in juvenile-onset, insulin-dependent diabetic subjects, indicating that abnormal pancreatic alpha-cell function in human juvenile-onset diabetes mellitus may be a consequence of insulin lack.

Adult↗
PubMedDate not supplied

Serum ferritin in colorectal cancer patients and its prognostic evaluation.

The aim of this study was to investigate the relationship between preoperative serum ferritin levels, clinico-pathological parameters and survival analysis of patients with colorectal cancer. Ninety-four patients (57 males) with a mean age of 65 years (39-87 years) underwent 63 curative and 31 palliative operations. Follow-up was at least 5 years. Patients were categorized with normal (30-215 ng/mL in men and 11-148 ng/mL in women), low, or high serum ferritin levels. Prognostic evaluation was undertaken with stratified survival analysis and Cox's regression model. Twenty-nine of the patients (30.9%) had raised ferritin levels and 14 (14.9%) had low values. Comparisons of the survival curves showed significant differences in stage C disease; specifically, patients with either low or high ferritin levels had a shorter survival than patients with normal levels. Patients who underwent palliative surgery and had high ferritin serum values also had a shorter survival. In multivariate analysis, the variables with a negative effect on survival were stage, serum ferritin levels and age. Our data suggest that patients with advanced colorectal cancer having normal preoperative serum ferritin levels may have a better prognosis, although the prognostic value related to this association requires further investigation.

Adult↗
PubMedDate not supplied

Hepatoid gastric carcinoma. A case report.

Alpha-fetoprotein (AFP) is normally produced by primary hepatic neoplasms and germ cell tumors. There have, however, been reports of its production in cases of gastrointestinal tract adenocarcinoma. Gastric hepatoid carcinomas constitute a clinicopathological entity of recent acquisition and have certain common characteristics, which include the presence of hepatoid foci and frequent liver metastases, even in cases of early gastric cancer, and increasing serum AFP levels. In this study the case of one patient who underwent gastric resection and presented clinical, humoral, histological and immunohistochemical characteristics typical of hepatoid gastric carcinoma is reported. More biological studies, as well as precise criteria for pathological definition and therapy, are still necessary for a better understanding of this pathology.

Adenocarcinoma↗