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Pivot Concepts:
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Target Concepts:
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Query: UMLS:C0011849 (
diabetes
)
277,896
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Endocrine pancreas
transplantation could provide an ideal solution to the problem posed by IDDM. Although preliminary clinical success achieved over the past few years has been considerably higher with whole pancreatic transplant than with isolated islet grafts, both approaches remain experimental. Islet grafts might gain, over time, increasing credibility and might eventually provide an easier alternative in terms of grafting procedures and patient management, as compared with the more "traumatizing" whole-pancreas transplantation, but only if the pending technical problems are fully surmounted. Combined pancreas/kidney (either simultaneous pancreas/kidney [SPK] or pancreas after kidney [PAK]) transplantation, under general immunosuppression, in IDDM patients also suffering from end-stage renal disease (ESRD) is a procedure that may be worth pursuing in selected cases. However, there are still quite serious reservations about the scaled-up applicability of pancreas transplant alone (PTA) in patients with "brittle" IDDM; major restrictions are not only the necessity of pharmacological immunosuppression, but also the lower functional performance of PTA, especially as compared with SPK grafting. In terms of islets, as problems of human islet yield and purity are gradually being overcome, the problem of islet graft-directed immune destruction hampers the success of ongoing clinical trials in IDDM patients. The invariable requirement of general immunosuppression affects pancreatic as much as islet grafts, although a number of alternative, yet experimental, immunoprotection strategies in progress might suit islets better than they would whole organs. Another issue concerns the relative inadequacy of cadaveric donor organ availability, the requirements of which are more stringent for islets because of the persistent variability of islet cell yield per organ. Tremendous experimental efforts are in progress to create xenogeneic porcine/bovine islets and, perhaps over a longer period of time, human/nonhuman engineered insulin-producing cells suitable for graft within special immunoisolation barrier membranes.
Diabetes
Care 1997 May
PMID:Perspectives in pancreatic and islet cell transplantation for the therapy of IDDM. 913 62
Endocrine pancreas
plasticity may be defined as the ability of the organ to adapt the beta-cell mass to the variations in insulin demand. For example, during late pregnancy and obesity, the increase of the beta-cell mass, in association with beta-cell hyperactivity, contributes to insulin oversecretion in response to insulin resistance. There is increasing evidence that the ability of the beta-cell mass to expand in adult mammals is much higher than previously thought. During pregnancy, placental hormones, especially placental lactogens, are mainly responsible for the changes in beta-cell mass. The factors involved in beta-cell growth in obesity are far from clear, although increased free fatty acids seem to be the main candidate. Many data suggest that the impairment of insulin secretion in type 2 diabetes is partly related to reduction of beta-cell mass, at least relative to prevailing insulin demand. This defect may originate from genetic predisposition, but the situation is likely worsened by environmental factors such as hyperglycemia (glucotoxicity) and hyperlipidemia (lipotoxicity). Better understanding of beta-cell growth and regeneration mechanisms may allow new strategies in the treatment of type 2 diabetes based on early limitation of beta-cell damage and/or restoration of a functional beta-cell mass.
Diabetes
2001 Feb
PMID:Endocrine pancreas plasticity under physiological and pathological conditions. 1127 94
Endocrine pancreas
producing insulin, glucagon, somatostatin and pancreatic polypeptide is under the influence of different types of regulation; among them the regulatory role of enteropancreatic axis plays an important role. Incretin effect of glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) is significantly involved in the insulin secretion which is modulated by many other hormones.
Diabetes mellitus
, similarly to disturbances of other hormones, can cause impaired regulation of insulin and other pancreatic hormones.
...
PMID:[Pancreatic hormones and hormonal regulation of insulin secretion]. 1699 14