Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0011854 (
type 1 diabetes
)
20,749
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In a previous paper we have demonstrated that growth hormone (GH) responses to
growth hormone releasing hormone
(
GHRH
) are higher in premenopausal normal women than in age matched healthy men. As in
type I diabetes mellitus
various disturbances of GH secretion have been reported, the aim of our study was to assess the effect of sex on basal and
GHRH
stimulated GH secretion in
type I diabetes mellitus
. In 21 female and 23 male type I diabetic patients and 28 female and 30 male control subjects GH levels were measured before and after stimulation with
GHRH
(1 microgram/kg body weight i.v.) by radioimmunoassay. GH responses to
GHRH
were significantly higher in female than in male control subjects (p less than 0.02), whereas the GH levels following
GHRH
stimulation were similar in female and male type I diabetic patients. GH responses to
GHRH
were significantly higher in the male type I diabetic patients than in the male control subjects (p less than 0.001); in the female type I diabetic patients and the female control subjects, however, GH responses to
GHRH
were not statistically different. The absence of an effect of sex on
GHRH
stimulated GH responses in
type I diabetes mellitus
provides further evidence of an abnormal GH secretion in this disorder.
...
PMID:Enhanced growth hormone responses to growth hormone releasing hormone in male type I diabetic patients. 179 41
Increased circulating growth hormone (GH) levels and aberrant response to different stimuli characterize both
type 1 diabetes
mellitus and chronic uremia and are associated with severe retinal, kidney and heart complications. Combined kidney and pancreas transplantation is a therapy that restores the endogenous, closed-loop, insulin secretion in diabetes and cure uremia. To evaluate if combined transplantation can restore a normal secretion and response of GH to
growth hormone releasing hormone
(GH-RH), we studied four groups of subjects: (1) seven type 1 diabetic patients with end-stage renal failure who had received pancreas and kidney transplantation (KPTx); (2) six diabetic uremic subjects, candidates for combined transplantation (IDDUP); (3) nine patients with chronic uveitis on immunosuppressive therapy comparable to pancreas recipients, six of whom treated only with prednisone (UVEST), while three (4) were treated with both prednisone and cyclosporin (UVESTCY). All subjects underwent a GH-RH test (50 microg intravenously, i.v., at 13:00 h). Serum insulin levels were significantly higher in IDDUP compared to UVEST (P=0.05) both at baseline and post GH-RH stimulus, while were similar to KPTx (P=0.2) and UVESTCY (P=0.7). In contrast, plasma free fatty acids were similar in all groups. In IDDUP baseline plasma glycerol was higher than in KPTx (P=0.04) and UVEST (P=0.02) and similar to UVESTCY (P=0.36); glycerol concentration did not change after GH-RH (P=0.08). Before and after GH-RH, serum GH levels tended to be higher in IDDUP (P=0.5) and KPTx (P=0.2) compared to UVEST and UVESTCY. Our results indicate that: 1) kidney-pancreas transplantation does not normalize the GH response to GH-RH; 2) GH abnormalities are not due either to the chronic immunosuppressive therapy or to the insulin effect on GH release; 3) GH abnormalities are probably secondary to functional and/or organic complications of the hypothalamus and/or pituitary as a sequela of diabetes mellitus.
...
PMID:Persistence of anomalies in the growth hormone-releasing hormone-stimulated growth hormone response in diabetic-uremic patients after combined kidney-pancreas transplantation. 1083 Feb 43
Type I diabetes mellitus
(T1D) is due to a loss of immune tolerance to islet antigen and thus, there is intense interest in developing therapies that can re-establish it. Tolerance is maintained by complex mechanisms that include inhibitory molecules and several types of regulatory T cells (Tr). A major historical question is whether gene therapy can be employed to generate Tr cells. This review shows that gene transfer of immunoregulatory molecules can prevent T1D and other autoimmune diseases. In our studies, non-viral gene transfer is enhanced by in vivo electroporation (EP). This technique can be used to perform DNA vaccination against islet cell antigens and when combined with appropriate immune ligands results in the generation of Tr cells and protection against T1D. In vivo EP can also be applied for non-immune therapy of diabetes. It can be used to deliver protein drugs such as glucagon-like peptide 1 (GLP-1), leptin or transforming growth factor beta (TGF-beta). These act in T1D or type II diabetes (T2D) by restoring glucose homeostasis, promoting islet cell survival and growth or improving wound healing and other complications. Furthermore, we show that in large animals EP can deliver peptide hormones, such as
growth hormone releasing hormone
(
GHRH
). We conclude that the non-viral gene therapy and EP represent a safe and efficacious approach with clinical potential.
...
PMID:Plasmid-based gene therapy of diabetes mellitus. 1721 47
Growth hormone (GH) response to dexamethasone (DEX) in 10 poorly controlled insulin dependent diabetic patients (
IDDM
) without clinical evidence of diabetic complications and in 10 healthy controls, was studied. GH responses to DEX were compared with pituitary GH response to
growth hormone releasing hormone
(
GHRH
). Fasting GH values were not significantly higher in
IDDM
in comparison with the controls. The peak GH responses to
GHRH
and DEX were similar in the controls and
IDDM
patients (23.8 +/- 6.49 vs 38.87 +/- 7.26, p > 0.05 in
GHRH
test and 13.71 +/- 3.59 vs 17.33 +/- 5 23, p > 0.05 in DEX test). No significant difference between area under curve during
GHRH
(1386. +/- 490.69 vs 1966.89 +/- 561.46, p > 0.05) and during DEX test (1085.8 +/- 239 856 vs 501.87 +/- 847.16, p > 0 05) in the controls and
IDDM
patients, were established There was no significant correlation between basal and peak GH values and AUC during both tests, and HbA1C and duration of diabetes It is concluded that GH response to
GHRH
was normal and that our patients had preserved the integrity of the hypothalamo-pituitary axis, thanks to the suggested mechanism of dexamethasone action via somatostatin.
...
PMID:[Effects of dexamethasone on growth hormone response in insulin dependent diabetes mellitus]. 1797 66