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Biomedical subjects

E Aguilar-Parada

Publications and source records attributed to E Aguilar-Parada.

17 recordsLinked to original sources
PubMed1985

Steroid secretion by a lipoid cell tumor causing virilization and its diagnosis with computerized tomography.

Presented is the case of a virilized woman with a lipoid cell tumor of the ovary localized by computerized tomography. The major secretory products of the tumor were testosterone and estradiol; the production of androgens was responsible for the clinical features and hindered the effects of estrogens. Elevated levels of estradiol indicated important ovarian aromatase activity as reflected by large ovarian-peripheral venous gradients.

Adult↗
PubMed1985

Functioning microvillous adenoma of the parathyroid gland containing nuclear pores and annulate lamellae.

The cytoplasmic membranes of chief cells in parathyroid adenomas from patients with primary hyperparathyroidism associated with either severe or mild hypercalcemia were examined in an attempt to correlate ultrastructural changes and biochemical findings. In the case involving the highest serum calcium level (17.5 mg/dl), the cytoplasmic membrane exhibited numerous long cytoplasmic processes (microvilli) that extended into wide intercellular spaces. In this respect this tumor, associated with severe hypercalcemia, was different from previously described parathyroid adenomas and from the adenomas of the present study that were associated with mild hypercalcemia (12.4 +/- 0.5 mg/dl); the active chief cells of the latter were characterized by a relatively straight plasmalemma with interdigitations and narrow intercellular spaces. Also of interest in the case involving severe hypercalcemia was the presence of numerous nuclear pores and annulate lamellae as well as an inconspicuous Golgi apparatus. These ultrastructural features would seem to indicate the existence of further morphologic parameters for the evaluation of chief cell activity.

Adenoma↗
PubMed1970

Studies of pancreatic alpha cell function in normal and diabetic subjects.

The development of a glucagon radioimmunoassay with a relatively high degree of specificity for pancreatic glucagon made possible studies of alpha cell function in healthy nondiabetic subjects and in patients with diabetes mellitus. In the former group mean fasting plasma glucagon averaged 108 mumug/ml (SEM +/-10). In 12 juvenile-type diabetics fasting glucagon averaged 110 (+/-9) and in 33 adult-type diabetics the average was 114 (+/-8). The diabetic averages did not differ significantly from the nondiabetic subjects; however, when hyperglycemia was induced by glucose infusion in the nondiabetic subjects so as to simulate the fasting hyperglycemia of the diabetics, mean glucagon fell to 57 mumug (+/-8), which was significantly below the diabetic mean. In 28 healthy subjects the infusion of arginine elicited a rise in glucagon of at least 100 mumug/ml with a peak level averaging 331 mumug/ml (+/-22) at 40 min. This response to arginine was diminished but not abolished during hyperglycemia induced by simultaneous glucose infusion. In everyone of 45 diabetic subjects tested the infusion of arginine elicited a rise in glucagon of at least 140 mumug/ml to levels significantly greater than in nondiabetics. The peak glucagon level in juvenile-type diabetics averaged 458 mumug/ml (SEM +/-36) and in adult-type diabetics averaged 452 mumug/ml (SEM +/-38). The glucagon response to arginine was unrelated to duration of diabetes, to body weight, type of diabetic treatment, or to other known factors. Marked hyperresponsiveness of glucagon to arginine infusion was observed in two patients with advanced Kimmelsteil-Wilson disease. Glucagon levels were markedly elevated in certain patients with severe diabetic ketoacidosis before treatment with insulin. The findings suggest that alpha cell function is inappropriately increased in diabetes mellitus and could play a significant role in the diabetic syndrome.

Adolescent↗
PubMed1969

The role of aminogenic glucagon secretion in blood glucose homeostasis.

Hyperaminoacidemia is a powerful stimulus of pancreatic glucagon secretion. These studies were designed to elucidate the role of aminogenic hyperglucagonemia in glucoregulation. Conscious dogs with previously implanted indwelling venous catheters were employed. The results support the view that a role of glucagon is to limit blood glucose decline during hyperaminoacidemia.First, a significant negative correlation between the area of glucagon increment during the 1st 20 min of a 10 amino acid infusion and the maximum fall in glucose concentration was observed. Second, when endogenous glucagon secretion was suppressed by means of a continuous glucose infusion, hyperaminoacidemia induced a maximal glucose decline which averaged 35 mg/100 ml, differing significantly from mean maximal fall of 3 mg/100 ml, which normally occurs in the presence of endogenous hyperglucagonemia. Third, when, during hyperglycemic suppression of endogenous glucagon secretion, 50 mmug of exogenous glucagon/min was infused via the mesenteric vein with the amino acids, the fall in glucose was reduced to an average of 5 mg/100 ml. Similarly when pancreozymin, administered during the combined infusion of glucose and amino acids, overcame glucose suppression of endogenous glucagon secretion, plasma glucose did not fall. Similar results were obtained when aminogenic hyperglucagonemia was prevented by other means. Hyperlipacidemia, induced by infusing a triglyceride emulsion and giving heparin injections, also suppressed aminogenic hyperglucagonemia in two of four experiments; in these two dogs glucose fell 15 and 11 mg/100 ml. In a final group of experiments, the canine pancreas was resected except for the uncinate process, which is virtually devoid of alpha-cells. In two dogs, in which this procedure resulted in zero portal venous glucagon levels, the administration of amino acids and/or pancreozymin resulted in a glucose decline of 14 and 16 mg/100 ml, despite the reduced beta-cell population resulting from the subtotal pancreotectomy. It thus appears that the secretion of pancreatic glucagon during hyperaminoacidemia in association with insulin secretion, serves to limit the decline of glucose concentration.

Amino Acids↗