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M Serrano Ríos

Publications and source records attributed to M Serrano Ríos.

At least 37 records · Page 2Linked to original sources

Pancreatic A and B cell hyperfunction in the Mendenhall syndrome.

A 16-year-old boy with persistent hyperglycaemia (approximately 16 mmol/l in the fasting state) and acanthosis nigricans had insulin resistance and received daily up to 2800 U of short-acting, soluble, highly purified porcine insulin. The number and affinity of insulin receptors were markedly decreased. No significant insulin binding to IgG could be detected. Immunoreactive insulin varied between 1344 and 2400 mU/l. Endogenous insulin secretion and proinsulin levels were grossly elevated in the fasting state (C-peptide 2.2-3.5 pmol/ml; proinsulin approximately 1 pmol/ml). After an oral glucose tolerance test and intravenous arginine infusion, B cell hypersecretion was confirmed. The molar ratio of C-peptide to immunoreactive insulin, normally approximately 7, was about 0.3, clearly indicating that most of the immunoreactive insulin was exogenous. The molar ratio of proinsulin to C-peptide, which is about 0.05 in fasting control subjects, was 0.23-0.45, clearly showing that too high a proportion of proinsulin was being secreted. This may indicate that the constant hyperstimulation of the B cell leads to reduced conversion of proinsulin to insulin. Immunoreactive glucagon levels were within normal limits fasting but were above normal after intravenous arginine infusion. Thus, in this case of diabetes with acanthosis nigricans, the severe insulin resistance, probably caused by a receptor defect, was associated with markedly increased B cell function.

Acanthosis Nigricans↗

[Primary double neoplasias (author's transl)].

Data of 22 patients with primary double tumors are reviewed, collected from a total of 39.000 clinical protocols of which 1.168 were malignant. All were histologically verified. Criteria were those established by Warren & Gates i.e. a) each tumor must present clear signs of malignancy, b) each tumor must be different from the other, c) all possibility that one tumor may be a metastasis of the other must be excluded. Twelve of the cases were male and 10 female, representing 1.88% of the total with malignancies. In 6 cases both tumors appeared simultaneously, while the time interval was between 1 and 43 years in the remaining 16. Hematologic neoplasias are predominant with 12/44, followed by digestive and urogenital ones with 8/44 in each sub-group. Association between double tumors is assessed and causal factors which may influence or favor the appearance of two or more neoplasias are discussed.

Adult↗

Nocturnal growth hormone surges in type 1 diabetes mellitus are both sleep- and glycemia-dependent: assessment under continuous sleep monitoring.

Our work has studied the relationship between nocturnal growth hormone (GH) surges, sleep and glycemia in seven conventionally treated type 1 diabetic patients under continuous sleep monitoring and the results were compared to those found in five age-matched healthy controls. On the experimental day, sleep was monitored from 24.00 to 07.00. Blood glucose levels and GH were assayed in both groups. As a group the diabetics had nocturnal GH responses higher than those in controls. However, the sleep-related GH release is not abnormally high in patients who maintain strict normoglycemia. Early-night hypoglycemia and/or rapidly decreasing blood glucose concentrations enhance sleep-related GH secretion in diabetics, whereas hypoglycemia not associated with slow-wave sleep (SWS) causes a moderate increase in GH. Late-onset nocturnal hypoglycemia is not potent enough to stimulate GH. It is proposed that in diabetics sleep-related GH production is probably not abnormally elevated within a wide range of stable glucose levels, but when these thresholds are crossed or when there is a rapid decrease in blood glucose, then GH secretion is inversely related to the changing blood glucose. Therefore, our study supports the conclusion that sleep-related GH secretion is finely modulated by the actual glycemic fluctuations in diabetic patients.

Adult↗

Acetylated low-density lipoproteins promote the release and metabolism of arachidonic acid by murine macrophages.

We studied the effect of acetyl-LDL on the synthesis of eicosanoids by primary cultures of mouse-resident peritoneal macrophages. A dosis of 150 micrograms of acetyl-LDL proteins promotes a maximal release of arachidonic acid metabolites into extracellular medium. This process is very rapid and reaches the maximal value about ten minutes after stimulation. The pattern of arachidonic acid metabolites released is different from that obtained when the cells are stimulated with a phagocytosable particle like zymosan or calcium ionophore A23187. The data show that the metabolism of arachidonic acid by cycloxigenase is diminished. In an unusual way the amounts of prostaglandin PGE2, 6-keto-prostaglandin PGF1 alpha and thromboxane TXB2 synthesized are similar.

Acetylation↗

[A model of extreme insulin resistance with carbohydrate intolerance in a patient with Werner's syndrome].

We present the study of a patient suffering insulin resistance with Werner's syndrome which had abnormal glucose tolerance determined by euglycemic fixing ("Clamp") using an artificial pancreas (Biostator GCIIS, Miles Martin) and the binding of insulin to its receptor in erythrocytes. The results obtained show a dose-response curve of insulin serum levels to dextrose infusion rate, shifted significantly to the right and bottom which indicates a diminished insulin sensitivity; similarly a moderate decrease in receptor is obtained with no decrease in their affinity and absence of abnormalities in contraregulatory hormones. These results are compatible with a postreceptor alteration.

Blood Glucose↗