Life-extending protein keeps blood sugar in check

[Guest guest]

FYI..

http://tinyurl.com/48x2u

And a press release from " Cell Metabolism " :

Life-extending protein keeps blood sugar in check

A protein that extends lifespan in yeast, worms, and flies keeps

blood sugar under control in mice, reports a new study in the August

Cell Metabolism. The findings suggest therapeutic interventions for

the prevention and treatment of metabolic disorders, such as type 2

diabetes, which frequently arise with age, the researchers said.

The team found that mice with an excess of the protein Sirt1 in

cells of the pancreas have improved glucose tolerance and enhanced

insulin secretion in response to glucose. Glucose is the principal

circulating sugar in the blood and the major energy source of the

body.

" Mice with an increased amount of Sirt1 show a better response to

high blood glucose levels that regularly occur after eating sweets,

such as cookies or cakes, " said Shin-ichiro Imai of Washington

University School of Medicine. " The mice respond fast to high

glucose by raising insulin levels, clearing the blood of the

circulating sugar. "

" Under normal feeding conditions, when glucose levels are lower, the

mice with elevated Sirt1 appear normal, " Imai added. " This is good

news, suggesting that therapies designed to manipulate the amount of

Sirt1 might improve insulin response in those with type 2 diabetes

without causing other problems. "

Pancreatic b cells have a highly coordinated mechanism that senses

rises in blood glucose and converts that information into signals

that increase the secretion of insulin, Imai explained. Insulin

produced by the pancreas allows cells to take up glucose from the

bloodstream and burn it for energy. A failure to make or respond to

insulin in people with diabetes causes blood sugar levels to rise.

The researchers found that Sirt1 is present in pancreas cells that

secrete insulin hormone. Mice genetically modified to have an excess

of Sirt1 in b cells of the pancreas had improved glucose tolerance

and enhanced insulin secretion in response to glucose.

The altered mice maintained their improved b cell function with age,

they reported. Further analyses found that Sirt1 regulates genes

involved in insulin secretion by b cells.

" Together, these results establish that an increase dosage of Sirt1

has beneficial effects on mammalian physiology, " Imai said. " Our

findings also provide new insight into the physiological and

molecular functions of Sirt1 in glucose metabolism and suggest

therapeutic interventions for the prevention and treatment of

diabetes and other age-associated metabolic disorders. "

The researchers include A. Moynihan, A. Grimm, Marie

M. Plueger, Ernesto Bernal-Mizrachi, Ford, Corentin Cras-

Méneur, M. Alan Permutt, and Shin-ichiro Imai of the Washington

University School of Medicine in St. Louis, Missouri. This work was

supported by grants from NIA; NIDDK through the Washington

University Diabetes Research Training Center; the National Center

for Research Resources; and the Washington University Center for

Aging (to S.-i.I.), the Lucille P. Markey Special Emphasis Pathway

in Human Pathology (to K.A.M.), and the Glenn/AFAR Scholarship for

Research in the Biology of Aging (to K.A.M. and A.A.G.).

Moynihan et al.: " Increased Dosage of Mammalian Sir2 in Pancreatic ß

Cells Enhances Glucose-Stimulated Insulin Secretion in Mice "

Publishing in Cell Metabolism, Vol. 2, August 2005, pages 105-117.

DOI 10.1016/j.cmet.2005.07.001 http://www.cellmetabolism.org

Mike

[Guest guest]

Hi All,

For the whole Medline abstract only available paper:

Cell Metab. 2005 Aug;2(2):105-17. Related Articles, Links

Increased dosage of mammalian Sir2 in pancreatic beta cells enhances

glucose-stimulated insulin secretion in mice.

Moynihan KA, Grimm AA, Plueger MM, Bernal-Mizrachi E, Ford E, Cras-Meneur C,

Permutt

MA, Imai S.

Sir2 NAD-dependent deacetylases connect transcription, metabolism, and aging.

Increasing the dosage or activity of Sir2 extends life span in yeast, worms, and

flies and promotes fat mobilization and glucose production in mammalian cells.

Here

we show that increased dosage of Sirt1, the mammalian Sir2 ortholog, in

pancreatic

beta cells improves glucose tolerance and enhances insulin secretion in response

to

glucose in beta cell-specific Sirt1-overexpressing (BESTO) transgenic mice. This

phenotype is maintained as BESTO mice age. Pancreatic perfusion experiments

further

demonstrate that Sirt1 enhances insulin secretion in response to glucose and

KCl.

Microarray analyses of beta cell lines reveal that Sirt1 regulates genes

involved in

insulin secretion, including uncoupling protein 2 (Ucp2). Isolated BESTO islets

also

have reduced Ucp2, increased ATP production, and enhanced insulin secretion

during

glucose and KCl stimulation. These findings establish the importance of Sirt1 in

beta cell function in vivo and suggest therapeutic interventions for type 2

diabetes.

PMID: 16098828

--- mikesheldrick <mike@...> wrote:

> FYI..

>

> http://tinyurl.com/48x2u

>

> And a press release from " Cell Metabolism " :

>

> Life-extending protein keeps blood sugar in check

>

> A protein that extends lifespan in yeast, worms, and flies keeps

> blood sugar under control in mice, reports a new study in the August

> Cell Metabolism. The findings suggest therapeutic interventions for

> the prevention and treatment of metabolic disorders, such as type 2

> diabetes, which frequently arise with age, the researchers said.

>

> The team found that mice with an excess of the protein Sirt1 in

> cells of the pancreas have improved glucose tolerance and enhanced

> insulin secretion in response to glucose. Glucose is the principal

> circulating sugar in the blood and the major energy source of the

> body.

>

> " Mice with an increased amount of Sirt1 show a better response to

> high blood glucose levels that regularly occur after eating sweets,

> such as cookies or cakes, " said Shin-ichiro Imai of Washington

> University School of Medicine. " The mice respond fast to high

> glucose by raising insulin levels, clearing the blood of the

> circulating sugar. "

>

> " Under normal feeding conditions, when glucose levels are lower, the

> mice with elevated Sirt1 appear normal, " Imai added. " This is good

> news, suggesting that therapies designed to manipulate the amount of

> Sirt1 might improve insulin response in those with type 2 diabetes

> without causing other problems. "

>

> Pancreatic b cells have a highly coordinated mechanism that senses

> rises in blood glucose and converts that information into signals

> that increase the secretion of insulin, Imai explained. Insulin

> produced by the pancreas allows cells to take up glucose from the

> bloodstream and burn it for energy. A failure to make or respond to

> insulin in people with diabetes causes blood sugar levels to rise.

>

> The researchers found that Sirt1 is present in pancreas cells that

> secrete insulin hormone. Mice genetically modified to have an excess

> of Sirt1 in b cells of the pancreas had improved glucose tolerance

> and enhanced insulin secretion in response to glucose.

>

> The altered mice maintained their improved b cell function with age,

> they reported. Further analyses found that Sirt1 regulates genes

> involved in insulin secretion by b cells.

>

> " Together, these results establish that an increase dosage of Sirt1

> has beneficial effects on mammalian physiology, " Imai said. " Our

> findings also provide new insight into the physiological and

> molecular functions of Sirt1 in glucose metabolism and suggest

> therapeutic interventions for the prevention and treatment of

> diabetes and other age-associated metabolic disorders. "

>

> The researchers include A. Moynihan, A. Grimm, Marie

> M. Plueger, Ernesto Bernal-Mizrachi, Ford, Corentin Cras-

> Méneur, M. Alan Permutt, and Shin-ichiro Imai of the Washington

> University School of Medicine in St. Louis, Missouri. This work was

> supported by grants from NIA; NIDDK through the Washington

> University Diabetes Research Training Center; the National Center

> for Research Resources; and the Washington University Center for

> Aging (to S.-i.I.), the Lucille P. Markey Special Emphasis Pathway

> in Human Pathology (to K.A.M.), and the Glenn/AFAR Scholarship for

> Research in the Biology of Aging (to K.A.M. and A.A.G.).

>

> Moynihan et al.: " Increased Dosage of Mammalian Sir2 in Pancreatic ß

> Cells Enhances Glucose-Stimulated Insulin Secretion in Mice "

> Publishing in Cell Metabolism, Vol. 2, August 2005, pages 105-117.

> DOI 10.1016/j.cmet.2005.07.001 http://www.cellmetabolism.org

>

> Mike

>

>

>

>

Al Pater, PhD; email: old542000@...

____________________________________________________

Start your day with - make it your home page

http://www./r/hs

[Guest guest]

Hi All,

For the whole Medline abstract only available paper:

Cell Metab. 2005 Aug;2(2):105-17. Related Articles, Links

Increased dosage of mammalian Sir2 in pancreatic beta cells enhances

glucose-stimulated insulin secretion in mice.

Moynihan KA, Grimm AA, Plueger MM, Bernal-Mizrachi E, Ford E, Cras-Meneur C,

Permutt

MA, Imai S.

Sir2 NAD-dependent deacetylases connect transcription, metabolism, and aging.

Increasing the dosage or activity of Sir2 extends life span in yeast, worms, and

flies and promotes fat mobilization and glucose production in mammalian cells.

Here

we show that increased dosage of Sirt1, the mammalian Sir2 ortholog, in

pancreatic

beta cells improves glucose tolerance and enhances insulin secretion in response

to

glucose in beta cell-specific Sirt1-overexpressing (BESTO) transgenic mice. This

phenotype is maintained as BESTO mice age. Pancreatic perfusion experiments

further

demonstrate that Sirt1 enhances insulin secretion in response to glucose and

KCl.

Microarray analyses of beta cell lines reveal that Sirt1 regulates genes

involved in

insulin secretion, including uncoupling protein 2 (Ucp2). Isolated BESTO islets

also

have reduced Ucp2, increased ATP production, and enhanced insulin secretion

during

glucose and KCl stimulation. These findings establish the importance of Sirt1 in

beta cell function in vivo and suggest therapeutic interventions for type 2

diabetes.

PMID: 16098828

--- mikesheldrick <mike@...> wrote:

> FYI..

>

> http://tinyurl.com/48x2u

>

> And a press release from " Cell Metabolism " :

>

> Life-extending protein keeps blood sugar in check

>

> A protein that extends lifespan in yeast, worms, and flies keeps

> blood sugar under control in mice, reports a new study in the August

> Cell Metabolism. The findings suggest therapeutic interventions for

> the prevention and treatment of metabolic disorders, such as type 2

> diabetes, which frequently arise with age, the researchers said.

>

> The team found that mice with an excess of the protein Sirt1 in

> cells of the pancreas have improved glucose tolerance and enhanced

> insulin secretion in response to glucose. Glucose is the principal

> circulating sugar in the blood and the major energy source of the

> body.

>

> " Mice with an increased amount of Sirt1 show a better response to

> high blood glucose levels that regularly occur after eating sweets,

> such as cookies or cakes, " said Shin-ichiro Imai of Washington

> University School of Medicine. " The mice respond fast to high

> glucose by raising insulin levels, clearing the blood of the

> circulating sugar. "

>

> " Under normal feeding conditions, when glucose levels are lower, the

> mice with elevated Sirt1 appear normal, " Imai added. " This is good

> news, suggesting that therapies designed to manipulate the amount of

> Sirt1 might improve insulin response in those with type 2 diabetes

> without causing other problems. "

>

> Pancreatic b cells have a highly coordinated mechanism that senses

> rises in blood glucose and converts that information into signals

> that increase the secretion of insulin, Imai explained. Insulin

> produced by the pancreas allows cells to take up glucose from the

> bloodstream and burn it for energy. A failure to make or respond to

> insulin in people with diabetes causes blood sugar levels to rise.

>

> The researchers found that Sirt1 is present in pancreas cells that

> secrete insulin hormone. Mice genetically modified to have an excess

> of Sirt1 in b cells of the pancreas had improved glucose tolerance

> and enhanced insulin secretion in response to glucose.

>

> The altered mice maintained their improved b cell function with age,

> they reported. Further analyses found that Sirt1 regulates genes

> involved in insulin secretion by b cells.

>

> " Together, these results establish that an increase dosage of Sirt1

> has beneficial effects on mammalian physiology, " Imai said. " Our

> findings also provide new insight into the physiological and

> molecular functions of Sirt1 in glucose metabolism and suggest

> therapeutic interventions for the prevention and treatment of

> diabetes and other age-associated metabolic disorders. "

>

> The researchers include A. Moynihan, A. Grimm, Marie

> M. Plueger, Ernesto Bernal-Mizrachi, Ford, Corentin Cras-

> Méneur, M. Alan Permutt, and Shin-ichiro Imai of the Washington

> University School of Medicine in St. Louis, Missouri. This work was

> supported by grants from NIA; NIDDK through the Washington

> University Diabetes Research Training Center; the National Center

> for Research Resources; and the Washington University Center for

> Aging (to S.-i.I.), the Lucille P. Markey Special Emphasis Pathway

> in Human Pathology (to K.A.M.), and the Glenn/AFAR Scholarship for

> Research in the Biology of Aging (to K.A.M. and A.A.G.).

>

> Moynihan et al.: " Increased Dosage of Mammalian Sir2 in Pancreatic ß

> Cells Enhances Glucose-Stimulated Insulin Secretion in Mice "

> Publishing in Cell Metabolism, Vol. 2, August 2005, pages 105-117.

> DOI 10.1016/j.cmet.2005.07.001 http://www.cellmetabolism.org

>

> Mike

>

>

>

>

Al Pater, PhD; email: old542000@...

____________________________________________________

Start your day with - make it your home page

http://www./r/hs