Re: Researchers Clarify Mechanisms For Beta-Cell Formation

[Guest guest]

Very interesting!

Researchers Clarify Mechanisms For Beta-Cell

Formation

>

>

> 20-Sep-2004

> Researchers Clarify Mechanisms For Beta-Cell Formation

> September 2004 - A new study by researchers at Joslin Diabetes

> Center sheds light on the key mechanisms by which new

> pancreatic

> beta cells normally form in response to insulin resistance.

> These

> findings may some day help researchers devise ways of staving

> off

> full-blown diabetes.

> Insulin resistance is a condition in which the body needs

> increasing

> amounts of insulin to function properly, including keeping

> blood

> glucose levels in the normal range. It is a major contributor

> to

> type 2 diabetes, obesity and the metabolic syndrome, which

> affect

> nearly one-quarter of the American population.

> For years, the body compensates for insulin resistance in order

> to

> delay the onset of clinical type 2 diabetes: The pancreas

> secretes

> more insulin and, in fact, more insulin-producing beta cells

> form

> within the pancreas. This formation of new beta cells is the

> focus

> of intensive research: Which cells give rise to these new beta

> cells

> and how? (Some researchers, for example, theorize that the new

> cells

> are derived from immature ductal cells--the cells that line the

> ducts of the pancreas.) And what signals this replication of

> beta

> cells to occur?

> To study these questions, Rohit N. Kulkarni, M.D., Ph.D.,

> Jonathon

> N. Winnay, and C. Kahn, M.D., of Joslin Diabetes Center

> in

> Boston; Ulupi S. Jhala Ph.D., of The Whittier Institute of the

> University of California in La Jolla, Calif.; Stan Krajewski

> Ph.D.,

> at the Burnham Institute in La Jolla; and Marc Montminy M.D.,

> Ph.D.,

> at The Salk Institute for Biological Studies in San Diego,

> Calif.,

> studied this compensatory growth in two different genetically

> engineered animal models of insulin resistance called IR/IRS-1

> mice

> and LIRKO mice. Dr. Kahn is the K. Iacocca Professor of

> Medicine at Harvard Medical School.

> The results of immunohistochemical staining suggest that these

> new

> beta cells are not derived from duct cells. Rather, the

> beta-cell

> growth in insulin-resistant states occurs by

> " epithelial-to-mesenchymal transition, " a mechanism in which

> cells

> take on a more primitive form and begin replicating. It is

> possible

> that the response originates from potential beta-cell stem

> cells, a

> more primitive cell that has yet to differentiate into a beta

> cell.

> They also showed that insufficiency of a protein called PDX-1,

> which

> is critical for the development of pancreatic islets that

> contain

> beta cells, limited the growth response in insulin-resistant

> states--suggesting that PDX-1 likely plays an important role in

> regulating this growth.

> The results were published in the September 2004 issue of The

> Journal of Clinical Investigation. The research was funded by

> the

> National Institutes of Health, the Juvenile Diabetes Research

> Foundation Center for Islet Transplantation at Harvard Medical

> School, the Beta Cell Biology Consortium and the Larry Hillblom

> Foundation.

> " Our paper clearly demonstrates a potential mechanism for

> beta-cell

> growth during insulin resistance, which in turn, occurs as a

> normal

> protective response to delay the onset of type 2 diabetes in

> obese

> and other susceptible individuals, " says Dr. Kulkarni, an

> Investigator in the Cellular and Molecular Physiology Section

> at

> Joslin, Assistant Professor of Medicine of Harvard Medical

> School,

> and the lead and corresponding author of the study. " Using two

> different animal models of insulin resistance, we have

> identified

> the key players that are involved in this crucial compensatory

> response. Dissecting the pathways that regulate the process of

> epithelial-to-mesenchymal transition will have therapeutic

> implications for both type 1 and type 2 diabetes. For example,

> modulating one or more proteins involved in this critical

> transition

> process may allow us to enhance the ability of beta cells to

> replicate in the body or to formulate methods to expand the

> formation of new cells as a source for transplantation in type

> 1

> diabetes. "

> There are two major types of diabetes. An estimated 800,000

> Americans have type 1 diabetes, in which the pancreas is unable

> to

> produce insulin. People with type 1 diabetes must take daily

> insulin

> injections to survive. An estimated 18 million Americans have

> type 2

> diabetes, in which the pancreas doesn't produce enough insulin

> and/or the body is unable to use insulin properly (insulin

> resistance). Poorly controlled diabetes can lead to a host of

> complications, including heart attacks, strokes, blindness,

> kidney

> failure, blood vessel damage and nerve damage.

> Source: Joslin Diabetes Center

> Printer-Friendly Version

>

>

>

>

>

>

> Don't miss out on important news! Would you like to

> receive

> important diabetes and health related news like this via

> email? Join tens of thousands of other satisfied readers,

> subscribe to The Diabetic News using the form below:

>

> Your Email Address:

>

> More Free Subscriptions Available »

>

>

>

>

>

>

>

>

> Copyright © CAPCO Marketing. All Rights Reserved.

>

>

> friends are quiet angels who lift us to our feet, when our wings have

> forgotten how to fly

>

>

>

>

>

>

>

[Guest guest]

Very interesting!

Researchers Clarify Mechanisms For Beta-Cell

Formation

>

>

> 20-Sep-2004

> Researchers Clarify Mechanisms For Beta-Cell Formation

> September 2004 - A new study by researchers at Joslin Diabetes

> Center sheds light on the key mechanisms by which new

> pancreatic

> beta cells normally form in response to insulin resistance.

> These

> findings may some day help researchers devise ways of staving

> off

> full-blown diabetes.

> Insulin resistance is a condition in which the body needs

> increasing

> amounts of insulin to function properly, including keeping

> blood

> glucose levels in the normal range. It is a major contributor

> to

> type 2 diabetes, obesity and the metabolic syndrome, which

> affect

> nearly one-quarter of the American population.

> For years, the body compensates for insulin resistance in order

> to

> delay the onset of clinical type 2 diabetes: The pancreas

> secretes

> more insulin and, in fact, more insulin-producing beta cells

> form

> within the pancreas. This formation of new beta cells is the

> focus

> of intensive research: Which cells give rise to these new beta

> cells

> and how? (Some researchers, for example, theorize that the new

> cells

> are derived from immature ductal cells--the cells that line the

> ducts of the pancreas.) And what signals this replication of

> beta

> cells to occur?

> To study these questions, Rohit N. Kulkarni, M.D., Ph.D.,

> Jonathon

> N. Winnay, and C. Kahn, M.D., of Joslin Diabetes Center

> in

> Boston; Ulupi S. Jhala Ph.D., of The Whittier Institute of the

> University of California in La Jolla, Calif.; Stan Krajewski

> Ph.D.,

> at the Burnham Institute in La Jolla; and Marc Montminy M.D.,

> Ph.D.,

> at The Salk Institute for Biological Studies in San Diego,

> Calif.,

> studied this compensatory growth in two different genetically

> engineered animal models of insulin resistance called IR/IRS-1

> mice

> and LIRKO mice. Dr. Kahn is the K. Iacocca Professor of

> Medicine at Harvard Medical School.

> The results of immunohistochemical staining suggest that these

> new

> beta cells are not derived from duct cells. Rather, the

> beta-cell

> growth in insulin-resistant states occurs by

> " epithelial-to-mesenchymal transition, " a mechanism in which

> cells

> take on a more primitive form and begin replicating. It is

> possible

> that the response originates from potential beta-cell stem

> cells, a

> more primitive cell that has yet to differentiate into a beta

> cell.

> They also showed that insufficiency of a protein called PDX-1,

> which

> is critical for the development of pancreatic islets that

> contain

> beta cells, limited the growth response in insulin-resistant

> states--suggesting that PDX-1 likely plays an important role in

> regulating this growth.

> The results were published in the September 2004 issue of The

> Journal of Clinical Investigation. The research was funded by

> the

> National Institutes of Health, the Juvenile Diabetes Research

> Foundation Center for Islet Transplantation at Harvard Medical

> School, the Beta Cell Biology Consortium and the Larry Hillblom

> Foundation.

> " Our paper clearly demonstrates a potential mechanism for

> beta-cell

> growth during insulin resistance, which in turn, occurs as a

> normal

> protective response to delay the onset of type 2 diabetes in

> obese

> and other susceptible individuals, " says Dr. Kulkarni, an

> Investigator in the Cellular and Molecular Physiology Section

> at

> Joslin, Assistant Professor of Medicine of Harvard Medical

> School,

> and the lead and corresponding author of the study. " Using two

> different animal models of insulin resistance, we have

> identified

> the key players that are involved in this crucial compensatory

> response. Dissecting the pathways that regulate the process of

> epithelial-to-mesenchymal transition will have therapeutic

> implications for both type 1 and type 2 diabetes. For example,

> modulating one or more proteins involved in this critical

> transition

> process may allow us to enhance the ability of beta cells to

> replicate in the body or to formulate methods to expand the

> formation of new cells as a source for transplantation in type

> 1

> diabetes. "

> There are two major types of diabetes. An estimated 800,000

> Americans have type 1 diabetes, in which the pancreas is unable

> to

> produce insulin. People with type 1 diabetes must take daily

> insulin

> injections to survive. An estimated 18 million Americans have

> type 2

> diabetes, in which the pancreas doesn't produce enough insulin

> and/or the body is unable to use insulin properly (insulin

> resistance). Poorly controlled diabetes can lead to a host of

> complications, including heart attacks, strokes, blindness,

> kidney

> failure, blood vessel damage and nerve damage.

> Source: Joslin Diabetes Center

> Printer-Friendly Version

>

>

>

>

>

>

> Don't miss out on important news! Would you like to

> receive

> important diabetes and health related news like this via

> email? Join tens of thousands of other satisfied readers,

> subscribe to The Diabetic News using the form below:

>

> Your Email Address:

>

> More Free Subscriptions Available »

>

>

>

>

>

>

>

>

> Copyright © CAPCO Marketing. All Rights Reserved.

>

>

> friends are quiet angels who lift us to our feet, when our wings have

> forgotten how to fly

>

>

>

>

>

>

>

[Guest guest]

Very interesting!

Researchers Clarify Mechanisms For Beta-Cell

Formation

>

>

> 20-Sep-2004

> Researchers Clarify Mechanisms For Beta-Cell Formation

> September 2004 - A new study by researchers at Joslin Diabetes

> Center sheds light on the key mechanisms by which new

> pancreatic

> beta cells normally form in response to insulin resistance.

> These

> findings may some day help researchers devise ways of staving

> off

> full-blown diabetes.

> Insulin resistance is a condition in which the body needs

> increasing

> amounts of insulin to function properly, including keeping

> blood

> glucose levels in the normal range. It is a major contributor

> to

> type 2 diabetes, obesity and the metabolic syndrome, which

> affect

> nearly one-quarter of the American population.

> For years, the body compensates for insulin resistance in order

> to

> delay the onset of clinical type 2 diabetes: The pancreas

> secretes

> more insulin and, in fact, more insulin-producing beta cells

> form

> within the pancreas. This formation of new beta cells is the

> focus

> of intensive research: Which cells give rise to these new beta

> cells

> and how? (Some researchers, for example, theorize that the new

> cells

> are derived from immature ductal cells--the cells that line the

> ducts of the pancreas.) And what signals this replication of

> beta

> cells to occur?

> To study these questions, Rohit N. Kulkarni, M.D., Ph.D.,

> Jonathon

> N. Winnay, and C. Kahn, M.D., of Joslin Diabetes Center

> in

> Boston; Ulupi S. Jhala Ph.D., of The Whittier Institute of the

> University of California in La Jolla, Calif.; Stan Krajewski

> Ph.D.,

> at the Burnham Institute in La Jolla; and Marc Montminy M.D.,

> Ph.D.,

> at The Salk Institute for Biological Studies in San Diego,

> Calif.,

> studied this compensatory growth in two different genetically

> engineered animal models of insulin resistance called IR/IRS-1

> mice

> and LIRKO mice. Dr. Kahn is the K. Iacocca Professor of

> Medicine at Harvard Medical School.

> The results of immunohistochemical staining suggest that these

> new

> beta cells are not derived from duct cells. Rather, the

> beta-cell

> growth in insulin-resistant states occurs by

> " epithelial-to-mesenchymal transition, " a mechanism in which

> cells

> take on a more primitive form and begin replicating. It is

> possible

> that the response originates from potential beta-cell stem

> cells, a

> more primitive cell that has yet to differentiate into a beta

> cell.

> They also showed that insufficiency of a protein called PDX-1,

> which

> is critical for the development of pancreatic islets that

> contain

> beta cells, limited the growth response in insulin-resistant

> states--suggesting that PDX-1 likely plays an important role in

> regulating this growth.

> The results were published in the September 2004 issue of The

> Journal of Clinical Investigation. The research was funded by

> the

> National Institutes of Health, the Juvenile Diabetes Research

> Foundation Center for Islet Transplantation at Harvard Medical

> School, the Beta Cell Biology Consortium and the Larry Hillblom

> Foundation.

> " Our paper clearly demonstrates a potential mechanism for

> beta-cell

> growth during insulin resistance, which in turn, occurs as a

> normal

> protective response to delay the onset of type 2 diabetes in

> obese

> and other susceptible individuals, " says Dr. Kulkarni, an

> Investigator in the Cellular and Molecular Physiology Section

> at

> Joslin, Assistant Professor of Medicine of Harvard Medical

> School,

> and the lead and corresponding author of the study. " Using two

> different animal models of insulin resistance, we have

> identified

> the key players that are involved in this crucial compensatory

> response. Dissecting the pathways that regulate the process of

> epithelial-to-mesenchymal transition will have therapeutic

> implications for both type 1 and type 2 diabetes. For example,

> modulating one or more proteins involved in this critical

> transition

> process may allow us to enhance the ability of beta cells to

> replicate in the body or to formulate methods to expand the

> formation of new cells as a source for transplantation in type

> 1

> diabetes. "

> There are two major types of diabetes. An estimated 800,000

> Americans have type 1 diabetes, in which the pancreas is unable

> to

> produce insulin. People with type 1 diabetes must take daily

> insulin

> injections to survive. An estimated 18 million Americans have

> type 2

> diabetes, in which the pancreas doesn't produce enough insulin

> and/or the body is unable to use insulin properly (insulin

> resistance). Poorly controlled diabetes can lead to a host of

> complications, including heart attacks, strokes, blindness,

> kidney

> failure, blood vessel damage and nerve damage.

> Source: Joslin Diabetes Center

> Printer-Friendly Version

>

>

>

>

>

>

> Don't miss out on important news! Would you like to

> receive

> important diabetes and health related news like this via

> email? Join tens of thousands of other satisfied readers,

> subscribe to The Diabetic News using the form below:

>

> Your Email Address:

>

> More Free Subscriptions Available »

>

>

>

>

>

>

>

>

> Copyright © CAPCO Marketing. All Rights Reserved.

>

>

> friends are quiet angels who lift us to our feet, when our wings have

> forgotten how to fly

>

>

>

>

>

>

>

[Guest guest]

thanks for the information!

Regards,

Researchers Clarify Mechanisms For Beta-Cell

Formation

>

>

> 20-Sep-2004

> Researchers Clarify Mechanisms For Beta-Cell Formation

> September 2004 - A new study by researchers at Joslin Diabetes

> Center sheds light on the key mechanisms by which new

pancreatic

> beta cells normally form in response to insulin resistance.

> These

> findings may some day help researchers devise ways of staving

> off

> full-blown diabetes.

> Insulin resistance is a condition in which the body needs

> increasing

> amounts of insulin to function properly, including keeping

blood

> glucose levels in the normal range. It is a major contributor

to

> type 2 diabetes, obesity and the metabolic syndrome, which

> affect

> nearly one-quarter of the American population.

> For years, the body compensates for insulin resistance in

order

> to

> delay the onset of clinical type 2 diabetes: The pancreas

> secretes

> more insulin and, in fact, more insulin-producing beta cells

> form

> within the pancreas. This formation of new beta cells is the

> focus

> of intensive research: Which cells give rise to these new beta

> cells

> and how? (Some researchers, for example, theorize that the new

> cells

> are derived from immature ductal cells--the cells that line

the

> ducts of the pancreas.) And what signals this replication of

> beta

> cells to occur?

> To study these questions, Rohit N. Kulkarni, M.D., Ph.D.,

> Jonathon

> N. Winnay, and C. Kahn, M.D., of Joslin Diabetes Center

> in

> Boston; Ulupi S. Jhala Ph.D., of The Whittier Institute of the

> University of California in La Jolla, Calif.; Stan Krajewski

> Ph.D.,

> at the Burnham Institute in La Jolla; and Marc Montminy M.D.,

> Ph.D.,

> at The Salk Institute for Biological Studies in San Diego,

> Calif.,

> studied this compensatory growth in two different genetically

> engineered animal models of insulin resistance called IR/IRS-1

> mice

> and LIRKO mice. Dr. Kahn is the K. Iacocca Professor of

> Medicine at Harvard Medical School.

> The results of immunohistochemical staining suggest that these

> new

> beta cells are not derived from duct cells. Rather, the

> beta-cell

> growth in insulin-resistant states occurs by

> " epithelial-to-mesenchymal transition, " a mechanism in which

> cells

> take on a more primitive form and begin replicating. It is

> possible

> that the response originates from potential beta-cell stem

> cells, a

> more primitive cell that has yet to differentiate into a beta

> cell.

> They also showed that insufficiency of a protein called PDX-1,

> which

> is critical for the development of pancreatic islets that

> contain

> beta cells, limited the growth response in insulin-resistant

> states--suggesting that PDX-1 likely plays an important role

in

> regulating this growth.

> The results were published in the September 2004 issue of The

> Journal of Clinical Investigation. The research was funded by

> the

> National Institutes of Health, the Juvenile Diabetes Research

> Foundation Center for Islet Transplantation at Harvard Medical

> School, the Beta Cell Biology Consortium and the Larry

Hillblom

> Foundation.

> " Our paper clearly demonstrates a potential mechanism for

> beta-cell

> growth during insulin resistance, which in turn, occurs as a

> normal

> protective response to delay the onset of type 2 diabetes in

> obese

> and other susceptible individuals, " says Dr. Kulkarni, an

> Investigator in the Cellular and Molecular Physiology Section

at

> Joslin, Assistant Professor of Medicine of Harvard Medical

> School,

> and the lead and corresponding author of the study. " Using two

> different animal models of insulin resistance, we have

> identified

> the key players that are involved in this crucial compensatory

> response. Dissecting the pathways that regulate the process of

> epithelial-to-mesenchymal transition will have therapeutic

> implications for both type 1 and type 2 diabetes. For example,

> modulating one or more proteins involved in this critical

> transition

> process may allow us to enhance the ability of beta cells to

> replicate in the body or to formulate methods to expand the

> formation of new cells as a source for transplantation in type

1

> diabetes. "

> There are two major types of diabetes. An estimated 800,000

> Americans have type 1 diabetes, in which the pancreas is

unable

> to

> produce insulin. People with type 1 diabetes must take daily

> insulin

> injections to survive. An estimated 18 million Americans have

> type 2

> diabetes, in which the pancreas doesn't produce enough insulin

> and/or the body is unable to use insulin properly (insulin

> resistance). Poorly controlled diabetes can lead to a host of

> complications, including heart attacks, strokes, blindness,

> kidney

> failure, blood vessel damage and nerve damage.

> Source: Joslin Diabetes Center

> Printer-Friendly Version

>

>

>

>

>

>

> Don't miss out on important news! Would you like to

> receive

> important diabetes and health related news like this via

> email? Join tens of thousands of other satisfied

readers,

> subscribe to The Diabetic News using the form below:

>

> Your Email Address:

>

> More Free Subscriptions Available »

>

>

>

>

>

>

>

>

> Copyright © CAPCO Marketing. All Rights Reserved.

>

>

> friends are quiet angels who lift us to our feet, when our wings have

> forgotten how to fly

>

>

>

>

>

>

>