Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin was discovered in 1921 and soon became widely available in high-income countries. However, many people currently in need of this life-saving medicine are unable to access it. This is a global phenomenon, impacting not only populations of low- and middle-income countries but low-income populations in the U.S. In the U.S., the rate of diabetic ketoacidosis remains high in certain subpopulations, the cost of insulin being the main precipitating factor. On a global level the main cause of mortality for a child with type 1 diabetes is a lack of access to insulin, and in sub-Saharan Africa the life expectancy of a child with type 1 diabetes can be as low as 1 year. One lens for considering the issue of access to health and medicines is to consider society as a three-legged stool. In this paradigm, the role of the public sector is to provide "protections" to the population it serves; the private sector is made up of "responsible businesses" that supply many of the goods and services people need; and the plural sector comprises communities and not-for-profits providing the "social affiliations" that are needed. For HIV/AIDS, each of these "legs" played a role in improving access. Civil society raised awareness of the issue and advocated for access to treatment. Governments provided funding and responses both nationally and globally. Finally, the private sector played its role, under pressure from civil society and governments, in lowering the price of medicines and developing programs to expand access. Here, we use this framework to describe the shortcomings in access to insulin from a U.S. and global perspective.
 ...
PMID:Why Are We Failing to Address the Issue of Access to Insulin? A National and Global Perspective. 2990 80

Autoimmune destruction of pancreatic beta cells is the characteristic feature of type 1 diabetes mellitus. Consequently, both short- and intermediate-acting insulin analogs are under development to compensate for the lack of endogenous insulin gene expression. Basal insulin is continuously released at low levels in response to hepatic glucose output, while post-prandial insulin is secreted in response to hyperglycemia following a meal. As an alternative to multiple daily injections of insulin, glucose-regulated insulin gene expression by gene therapy is under development to better endure postprandial glucose excursions. Controlled transcription and translation of proinsulin, presence of glucose-sensing machinery, prohormone convertase expression, and a regulated secretory pathway are the key features unique to pancreatic beta cells. To take advantage of these hallmarks, we generated a new lentiviral vector (LentiINS) with an insulin promoter driving expression of the proinsulin encoding cDNA to sustain pancreatic beta-cell-specific insulin gene expression. Intraperitoneal delivery of HIV-based LentiINS resulted in the lowering of fasting plasma glucose, improved glucose tolerance and prevented weight loss in streptozoticin (STZ)-induced diabetic Wistar rats. However, the combinatorial use of LentiINS and anti-inflammatory lentiviral vector (LentiVIP) gene therapy was required to increase serum insulin to a level sufficient to suppress non-fasting plasma glucose and diabetes-related inflammation.
 ...
PMID:Lentivirus Mediated Pancreatic Beta-Cell-Specific Insulin Gene Therapy for STZ-Induced Diabetes. 3313 Mar 11


<< Previous 1 2 3 4