RESUMO
To evaluate the glomerular filtration rate (GFR) response to a protein meal in patients with diabetes and to study the role of glucagon and growth hormone, we studied inulin clearance for three 30-minute periods before and 3 hours after an 80 g protein meal in seven healthy volunteers and 10 patients with diabetes. Patients with diabetes were chosen because their renal response to such a meal has been reported to be abnormal. All had an increase in GFR and plasma glucagon levels after the protein meal. The peak rise in GFR occurred from 1 to 2 1/2 hours after the meal (mean +/- SEM, delta 26 +/- 5 mL/min/m2, controls; delta 22 +/- 7 mL/min/m2, patients with diabetes), with the mean time to normal rise in GFR occurring at 2 hours after the meal. Similarly, plasma glucagon values peaked at different times in individual patients (delta 769 +/- 532 pg/mL, controls; delta 267 +/- 69 pg/mL, patients with diabetes), with the mean plasma glucagon rise occurring 1 hours after the meal. Premeal growth hormone levels tended to be higher in the patients with diabetes (7.6 +/- 1.4 vs 2.1 +/- 0.4 ng/mL), and did not change after the meal. To allow study of the contribution of the increased plasma glucagon to the rise in GFR, eight of these patients (five with diabetes) volunteered to undergo a second GFR response test with a simultaneous infusion of somatostatin. The glucagon response was significantly lowered at all time periods during the infusion (P less than 0.05); no significant change in growth hormone occurred. Without somatostatin in these eight patients, peak increase in postmeal GFR average 20.6 +/- 1.5 mL/min/m2; with the somatostatin, peak increase in GFR was 6.0 +/- 1.8 mL/min/m2 (P less than 0.01). Neither metabolic control nor degree of albuminuria was significantly different at the time of the two studies. Thus, as has been shown in animals, somatostatin infusion limits the rise in GFR after a protein meal in humans.
Assuntos
Diabetes Mellitus/fisiopatologia , Proteínas Alimentares/farmacologia , Glucagon/fisiologia , Rim/fisiopatologia , Somatostatina , Adolescente , Adulto , Glicemia/metabolismo , Taxa de Filtração Glomerular , Hormônio do Crescimento/fisiologia , Humanos , Fatores de TempoRESUMO
We studied the syndrome of acanthosis nigricans, obesity, insulin resistance, and hyperandrogenemia in 22 patients. Although isolated case reports in adolescents have appeared, this syndrome has not received full recognition as a pediatric entity. Our patients (17 girls, five boys) had a mean weight 5.7 SD above the mean for age, although mean height was only 0.5 SD above the mean for age. All patients had acanthosis nigricans. Their insulin resistance was significantly greater than that in a control group with comparable obesity. Fasting insulin concentration was 5.25 microU/ml in lean controls, 19.6 microU/ml in obese controls, and 49.8 microU/ml in study patients (P less than 0.002). Mean glucose disappearance rate during an insulin tolerance test was 6.7%/min in lean controls, 5.19%/min in obese controls, and 2.35%/min in study patients (P less than 0.02). After menarche, mean plasma testosterone concentration was 106 ng/dl, compared with less than 50 ng/dl in all lean and obese control patients. Data derived from our series of patients lead us to conclude that (1) this is a genetic syndrome, although the exact mode of inheritance is unclear; (2) the natural history of the syndrome invariably begins with the onset of obesity, followed by acanthosis nigricans that worsens with progressive weight gain; (3) acanthosis nigricans is thus a marker for hyperinsulinemia, which occurs before hyperandrogenemia; (4) hyperandrogenemia occurs only after menarche. Identification of this syndrome should permit monitoring for the development of hyperandrogenemia during puberty and determination of other affected family members.
Assuntos
Acantose Nigricans/genética , Resistência à Insulina , Obesidade/genética , Testosterona/sangue , Adolescente , Androstenodiona/sangue , Peso Corporal , Criança , Desidroepiandrosterona/sangue , Feminino , Hormônio Foliculoestimulante/sangue , Teste de Tolerância a Glucose , Humanos , Hiperinsulinismo/genética , Hormônio Luteinizante/sangue , Masculino , Menarca , Linhagem , SíndromeAssuntos
Carcinoma/tratamento farmacológico , Hipoparatireoidismo/induzido quimicamente , Hipotireoidismo/induzido quimicamente , Doenças do Recém-Nascido/induzido quimicamente , Radioisótopos do Iodo/efeitos adversos , Troca Materno-Fetal , Neoplasias da Glândula Tireoide/tratamento farmacológico , Feminino , Humanos , Hipocalcemia/etiologia , Hipotireoidismo/tratamento farmacológico , Lactente , Recém-Nascido , Radioisótopos do Iodo/uso terapêutico , Fenobarbital/uso terapêutico , Gravidez , Primeiro Trimestre da Gravidez , Tiroxina/uso terapêutico , Traqueia/cirurgia , Traqueotomia/efeitos adversosRESUMO
Four children with short stature who received irradiation to the head in conventional doses had clinical and laboratory evidence of hypothalamic-pituitary hormone deficiencies several years later. Growth hormone was deficient in all. One patient also had evidence of TSH, ACTH, and gonadotropin deficiency. Basal prolactin levels and prolactin response to synthetic TRF were normal in all patients tested. Treatment with human growth hormone significantly increased growth rate. We suggest that children should have the hypothalamic-pituitary area shielded from irradiation. Periodic measurements of hypothalamic-pituitary function should be performed in children who have had irradiation to the head, in order to detect and treat hormonal deficiencies before growth and development are seriously compromised.