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Beta Cell ERKonomics. Functions of ERK1/2 in Pancreatic Beta Cells

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Air date: Wednesday, May 30, 2012, 3:00:00 PM
Time displayed is Eastern Time, Washington DC Local
Views: Total views: 213, (55 Live, 158 On-demand)
Category: Wednesday Afternoon Lectures
Runtime: 01:01:50
Description: Diabetes mellitus is a huge health burden due to decreased quality of life and the escalating cost of treatment. Obesity, insulin resistance and metabolic abnormalities in liver, adipose, and muscle are important factors in disease. Most of the gene loci recently found associated with type 2 diabetes, however, encode proteins that enable insulin production from pancreatic beta cells. Nutrients and hormones regulate not only insulin secretion, but also the capacity of b cells to continue to produce insulin. During the onset of diabetes, pancreatic beta cells become unable to produce sufficient insulin to maintain blood glucose within the normal range. Among important nutrient-sensing pathways are the mitogen-activated protein kinases, ERK1/2. These protein kinases are essential for nutrient-stimulated insulin gene transcription, and also contribute to reduced nutrient-induced insulin gene transcription following long term hyperglycemia and hyperglycemia combined with proinflammatory cytokines. The core ERK1/2 cascade kinases are associated with the insulin gene and we are examining how they act on the insulin gene promoter. We are also examining molecular mechanisms of action of small molecules that enhance b-cell function. These molecules stimulate insulin production by b cells, improve oral glucose tolerance of mice, and restore insulin production by human islets in long term culture. We have identified a number of changes that take place in b cells treated with these drugs, including epigenetic alterations, and changes in concentrations of key transcription factors. These small molecules may offer promise for future diabetic therapies.

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NLM Title: Beta cell ERKonomics : functions of ERK1/2 in pancreatic beta cells [electronic resource] / Melanie H. Cobb.
Series: ERKonomics in [beta] cells
Author: Cobb, Melanie H.
National Institutes of Health (U.S.)
Publisher:
Other Title(s): ERKonomics in [beta] cells
Abstract: (CIT): Diabetes mellitus is a huge health burden due to decreased quality of life and the escalating cost of treatment. Obesity, insulin resistance and metabolic abnormalities in liver, adipose, and muscle are important factors in disease. Most of the gene loci recently found associated with type 2 diabetes, however, encode proteins that enable insulin production from pancreatic beta cells. Nutrients and hormones regulate not only insulin secretion, but also the capacity of b cells to continue to produce insulin. During the onset of diabetes, pancreatic beta cells become unable to produce sufficient insulin to maintain blood glucose within the normal range. Among important nutrient-sensing pathways are the mitogen-activated protein kinases, ERK1/2. These protein kinases are essential for nutrient-stimulated insulin gene transcription, and also contribute to reduced nutrient-induced insulin gene transcription following long term hyperglycemia and hyperglycemia combined with proinflammatory cytokines. The core ERK1/2 cascade kinases are associated with the insulin gene and we are examining how they act on the insulin gene promoter. We are also examining molecular mechanisms of action of small molecules that enhance b-cell function. These molecules stimulate insulin production by b cells, improve oral glucose tolerance of mice, and restore insulin production by human islets in long term culture. We have identified a number of changes that take place in b cells treated with these drugs, including epigenetic alterations, and changes in concentrations of key transcription factors. These small molecules may offer promise for future diabetic therapies.
Subjects: Insulin-Secreting Cells--enzymology
Mitogen-Activated Protein Kinases--metabolism
Publication Types: Lectures
Webcasts
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Caption Text: Download Caption File
NLM Classification: QU 141
NLM ID: 101587410
CIT Live ID: 10526
Permanent link: http://videocast.nih.gov/launch.asp?17289

 

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