Kerstin Bellmann - Academia.edu (original) (raw)

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Papers by Kerstin Bellmann

Research paper thumbnail of The mechanism whereby heat shock induces apoptosis depends on the innate sensitivity of cells to stress

Cell Stress and …, 2010

The cellular response to heat shock (HS) is a paradigm for many human diseases collectively known... more The cellular response to heat shock (HS) is a paradigm for many human diseases collectively known as “protein conformation diseases” in which the accumulation of misfolded proteins induces cell death. Here, we analyzed how cells having a different apoptotic threshold die ...

Research paper thumbnail of Chronic rapamycin treatment causes glucose intolerance and hyperlipidemia by upregulating hepatic gluconeogenesis and impairing lipid deposition in adipose …

Diabetes, 2010

OBJECTIVE The mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) pathway is a critical s... more OBJECTIVE The mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) pathway is a critical signaling component in the development of obesity-linked insulin resistance and operates a nutrient-sensing negative feedback loop toward the phosphatidylinositol 3-...

Research paper thumbnail of Obese Mice Lacking Inducible Nitric Oxide Synthase Are Sensitized to the Metabolic Actions of Peroxisome Proliferator-Activated Receptor-  Agonism

Diabetes, 2008

OBJECTIVE-Synthetic ligands for peroxisome proliferatoractivated receptor-␥ (PPAR-␥) improve insu... more OBJECTIVE-Synthetic ligands for peroxisome proliferatoractivated receptor-␥ (PPAR-␥) improve insulin sensitivity in obesity, but it is still unclear whether inflammatory signals modulate their metabolic actions. In this study, we tested whether targeted disruption of inducible nitric oxide (NO) synthase (iNOS), a key inflammatory mediator in obesity, modulates the metabolic effects of rosiglitazone in obese mice.

Research paper thumbnail of The mechanism whereby heat shock induces apoptosis depends on the innate sensitivity of cells to stress

Cell Stress and …, 2010

The cellular response to heat shock (HS) is a paradigm for many human diseases collectively known... more The cellular response to heat shock (HS) is a paradigm for many human diseases collectively known as “protein conformation diseases” in which the accumulation of misfolded proteins induces cell death. Here, we analyzed how cells having a different apoptotic threshold die ...

Research paper thumbnail of Chronic rapamycin treatment causes glucose intolerance and hyperlipidemia by upregulating hepatic gluconeogenesis and impairing lipid deposition in adipose …

Diabetes, 2010

OBJECTIVE The mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) pathway is a critical s... more OBJECTIVE The mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) pathway is a critical signaling component in the development of obesity-linked insulin resistance and operates a nutrient-sensing negative feedback loop toward the phosphatidylinositol 3-...

Research paper thumbnail of Obese Mice Lacking Inducible Nitric Oxide Synthase Are Sensitized to the Metabolic Actions of Peroxisome Proliferator-Activated Receptor-  Agonism

Diabetes, 2008

OBJECTIVE-Synthetic ligands for peroxisome proliferatoractivated receptor-␥ (PPAR-␥) improve insu... more OBJECTIVE-Synthetic ligands for peroxisome proliferatoractivated receptor-␥ (PPAR-␥) improve insulin sensitivity in obesity, but it is still unclear whether inflammatory signals modulate their metabolic actions. In this study, we tested whether targeted disruption of inducible nitric oxide (NO) synthase (iNOS), a key inflammatory mediator in obesity, modulates the metabolic effects of rosiglitazone in obese mice.

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