No full-text available
To read the full-text of this research,
you can request a copy directly from the author.
¿Es la diabetes del adulto tipo-2 una variedad de la diabetes idiohipofisiaria?: Una proposición
... Sin embargo, existen lineamientos generales que deben tenerse presente. La alteración genética presente en algunas de estas mujeres no puede ser modificada, sin embargo, se puede prevenir la expresión de esta alteración genética con un estilo de vida saludable, lo cual requiere modificar ciertos hábitos, con conductas tales como: 1) Controlar situaciones de estrés: es sabido que las situaciones de tensión aguda intensa provocan alteraciones en el metabolismo de carbohidratos, lo cual puede ocasionar graves problemas en las pacientes que padecen diabetes (97) y SOP. 2) Adecuada alimentación: una dieta baja en carbohidratos es fundamental para estas pacientes. Además, se debe tener especial atención en considerar las oscilaciones naturales de las hormonas energéticas durante el día, pues estos ritmos determinan en qué momento del día los alimentos se incorporarán sintomatología bastante heterogénea y con una etiología que no ha sido completamente determinada. ...
The diabetogenic activity of growth hormone (GH) was studied through the production of an insulin antagonist in the plasma of normal rat. This antagonist, called alpha2-inhibitor, has an inhibitory activity on the glucose uptake by isolated testis, epididymal fat and hemidiaphragm of normal rat, is GH-dependent and has been identified with a fraction of plasma alpha2-glycoproteins.
The functional dependence of alpha2-inhibitor from GH was studied in two conditions: a) post-stress hypersecretion of GH; and, b) post-administration of rat GH, without stress. The results showed the production of the alpha2-inhibitor in both conditions, 3 hours post-stress or GH administration. Since the normal intact Sprague-Dawley male rat has no plasma alpha2-inhibitor, it is concluded that it was induced by the stress.
In the 80% pancreatectomized rat, the systemic stress produced, together with the increment of plasma alpha2-inhibitor, a transient state of diabetes mellitus that lasted 4 hours and attained the peak 2 hours post-stress.
Serum growth hormone, free fatty acids and blood glucose have been measured half-hourly for twenty-four hours in seven male patients with juvenile diabetes. Three of the patients had newly diagnosed diabetes and the four other patients had had diabetes for six to nine years. In five of the patients the studies were made during good as well as poor control.
The serum growth hormone level was high and fluctuating in the newly diagnosed diabetics as well as in the diabetics with diabetes of some years duration when compared with the growth hormone level of nondiabetics. The three newly diagnosed diabetics had significantly lower diurnal serum growth hormone concentration during good control compared with poor control. In the two patients with diabetes for some years the diurnal serum growth hormone concentration was unaltered in one and higher in the other in good compared with poor control.
To evaluate the importance of the raised levels of growth hormone that characterize poor diabetic control, we gave growth hormone for 21 to 45 hours in the form of hourly 100-micrograms pulses to 14 diabetics being treated by insulin pump. Insulin-pump settings and meals were kept constant. Mean 24-hour levels of growth hormone (+/- S.E.M.) rose from 8 +/- 1 to 16 +/- 2 ng per milliliter--values identical to those observed in 12 other patients with poorly controlled diabetes (17 +/- 3 ng per milliliter). Plasma glucose concentrations doubled within 8 to 10 hours and remained elevated until growth hormone was discontinued (fasting glucose level rose from 86 +/- 11 to 204 +/- 17 mg per deciliter at 18 hours and to 240 +/- 20 mg per deciliter at 42 hours). The hyperglycemia was due mainly to a marked stimulation of hepatic glucose production that occurred without changes in levels of free insulin or glucagon. Levels of circulating free fatty acids, ketones, and branched-chain amino acids were also increased. The moderate elevations in growth hormone levels that occur in poorly controlled diabetes can themselves reproduce the whole spectrum of abnormal metabolic fuel concentrations that are associated with poor diabetic control, despite optimized insulin treatment. Thus, hypersecretion of growth hormone may be the cause as much as the consequence of poor diabetic control.
The exact mechanisms by which growth hormone (GH) damages the kidney inducing diabetic nephropathy has not yet been elucidated. Recently, it has been shown that transferrin has the same diabetogenic effects of GH, being its mediator. Transferrin was studied using immunohistochemistry and immunoelectron microscopy in cases of early diabetic nephropathy, and in controls. Transferrin was only found in diabetic cases in podocytes and Bowman's capsule cells, but also in the tubular cells of both diabetic and non-diabetic controls. Immuno-electron microscopy for the presence of transferrin showed positive signals in the cytoplasm of diabetic podocytes, but not in pedicels. This selective deposition was associated with signs of organelle and cytoskeleton damage. On the basis of previous evidence and present glomerular findings, these results suggest an indirect diabetogenic effect on the kidney by GH mediated through transferrin.
Adrenal and liver participation in the rats poststress diabetic response
- Kawada Vargas L
- Me
Papel del hígado en la hiperglucemia del lóbulo anterior de la hipófisis en el sapo
- Campos Ca
- Curutchet Jl
al final; idiohipofisaria, de idio, especial. Esta última caracterizada por: disminución tolerancia a la glucosa, hiperglucemia, glucosuria, a veces cetonuria, resistencia insulínica y reversible al suspender tratamiento con HCr Action diabetogéne de l extrait antero hypophysaire
- Houssay Ba
- Metahipofisaria
- Ba De Meta Houssay
- C Rietti