Diabesity/Bibliography: Difference between revisions
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==Primary Research Papers== | ==Primary Research Papers== | ||
1) Umut Özcan, et al. (2004) Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes. ''Science'' '''306''', 457-461. | 1) Umut Özcan, et al. (2004) Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes. ''Science'' '''306''', 457-461.<br /> | ||
Through the use of cell culture and mouse models, this article shows that obesity causes stress in cells' endoplasmic reticulum. This leads to suppression of insulin receptor signalling via the hyper-activation of c-Jun N-terminal kinase (JNK) along with serine phosphorylation of insulin receptor substrate–1 (IRS-1). Mice which lack X- box–binding protein–1 (XBP-1), a transcription factor that modulates ER stress response, develop insulin resistance. The article argues that ER stress is an important feature of peripheral insulin resistance and type 2 diabetes at multiple levels. It is hypothesised that pharmacologic alteration of this pathway may offer chances of treating obesity. | Through the use of cell culture and mouse models, this article shows that obesity causes stress in cells' endoplasmic reticulum. This leads to suppression of insulin receptor signalling via the hyper-activation of c-Jun N-terminal kinase (JNK) along with serine phosphorylation of insulin receptor substrate–1 (IRS-1). Mice which lack X- box–binding protein–1 (XBP-1), a transcription factor that modulates ER stress response, develop insulin resistance. The article argues that ER stress is an important feature of peripheral insulin resistance and type 2 diabetes at multiple levels. It is hypothesised that pharmacologic alteration of this pathway may offer chances of treating obesity. | ||
2) Giovanni Solinas, et al. (2007) JNK1 in Hematopoietically Derived Cells Contributes to Diet-Induced Inflammation and Insulin Resistance without Affecting Obesity. ''Cell Metabolism'' '''6''', 386–397. | 2) Giovanni Solinas, et al. (2007) JNK1 in Hematopoietically Derived Cells Contributes to Diet-Induced Inflammation and Insulin Resistance without Affecting Obesity. ''Cell Metabolism'' '''6''', 386–397.<br /> | ||
Obesity-induced insulin resistance is a major factor in the subsequent diagnosis of type 2 diabetes. Jun kinases (JNKs) are key negative regulators of insulin sensitivity in obese persons. Activation of JNKs (mainly JNK1) in insulin target cells causes the phosphorylation of insulin receptor substrates (IRSs) at serine and threonine residues that inhibit insulin signaling. JNK1 activation is also required for accumulation of visceral fat. Here we used reciprocal adoptive transfer experiments to determine whether JNK1 in myeloid cells, such as macrophages, also contributes to insulin resistance and central adiposity. Our results show that deletion of Jnk1 in the nonhematopoietic compartment protects mice from high-fat diet (HFD)-induced insulin resistance, in part through decreased adiposity. Conversely, removing JNK1 from hematopoietic cells has no effect on adiposity but causes protection against insulin resistance induced by a high fat diet, by decreasing obesity-induced inflammation. | Obesity-induced insulin resistance is a major factor in the subsequent diagnosis of type 2 diabetes. Jun kinases (JNKs) are key negative regulators of insulin sensitivity in obese persons. Activation of JNKs (mainly JNK1) in insulin target cells causes the phosphorylation of insulin receptor substrates (IRSs) at serine and threonine residues that inhibit insulin signaling. JNK1 activation is also required for accumulation of visceral fat. Here we used reciprocal adoptive transfer experiments to determine whether JNK1 in myeloid cells, such as macrophages, also contributes to insulin resistance and central adiposity. Our results show that deletion of Jnk1 in the nonhematopoietic compartment protects mice from high-fat diet (HFD)-induced insulin resistance, in part through decreased adiposity. Conversely, removing JNK1 from hematopoietic cells has no effect on adiposity but causes protection against insulin resistance induced by a high fat diet, by decreasing obesity-induced inflammation. | ||
Revision as of 05:43, 14 October 2009
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Review Articles
- Magni P. et al. (2009) Feeding behavior in mammals including humans. Ann.N.Y.Acad.Sci. 1163:221-232. PMID 19456343
JOHN PARK BIBLIOGRAPHY (WILL SORT THIS OUT SOON)
1) Speakman J. et al. (2008) Thrifty vs Drifty Gene Theory of Obesity Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the 'drifty gene' hypothesis. International Journal of Obesity (2008) 32, 1611–1617 The discussion of thrifty genes and drifty genes, on obesity and diabetes. Suggestion made that the case for Thrifty genes may not be correct, but rather a different hypothesis is proposed
2. Cameron, N et al. (2006) Childhood Obesity Contemporary Issues, p154, CRC press, Taylor and Francis Group. Discusses how obesity relates very closely to Diabetes. Relates genetic and environmental factors and summarises the thrifty gene hypothesis .
3. Marchand L, (2002) The Pima Indians: Pathfinders for health, Obesity and Diabetes, Online resource: http://diabetes.niddk.nih.gov/DM/pubs/pima/obesity/obesity.htm NIDDK research conducted on the Pima Indians for the past 30 years has helped scientists prove that obesity is a major risk factor in the development of diabetes. One-half of adult Pima Indians have diabetes and 95% of those with diabetes are overweight. Scientists use the "thrifty gene" theory proposed in 1962 by geneticist James Neel to help explain why many Pima Indians are overweight
4. Neel JV (1962). "Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?". Am. J. Hum. Genet. 14: 353–62. PMID 13937884.
The original paper that proposes the Thrifty genotype.
Again evidence that suggests the Thrifty genotype in Type 2 diabetes. And obesity Joffe, Barry; Paul Zimmet (1998-08-17). "The thrifty genotype in type 2 diabetes". Endocrine 9 (2): 139–141. doi:10.1385/ENDO:9:2:139.
Primary Research Papers
1) Umut Özcan, et al. (2004) Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes. Science 306, 457-461.
Through the use of cell culture and mouse models, this article shows that obesity causes stress in cells' endoplasmic reticulum. This leads to suppression of insulin receptor signalling via the hyper-activation of c-Jun N-terminal kinase (JNK) along with serine phosphorylation of insulin receptor substrate–1 (IRS-1). Mice which lack X- box–binding protein–1 (XBP-1), a transcription factor that modulates ER stress response, develop insulin resistance. The article argues that ER stress is an important feature of peripheral insulin resistance and type 2 diabetes at multiple levels. It is hypothesised that pharmacologic alteration of this pathway may offer chances of treating obesity.
2) Giovanni Solinas, et al. (2007) JNK1 in Hematopoietically Derived Cells Contributes to Diet-Induced Inflammation and Insulin Resistance without Affecting Obesity. Cell Metabolism 6, 386–397.
Obesity-induced insulin resistance is a major factor in the subsequent diagnosis of type 2 diabetes. Jun kinases (JNKs) are key negative regulators of insulin sensitivity in obese persons. Activation of JNKs (mainly JNK1) in insulin target cells causes the phosphorylation of insulin receptor substrates (IRSs) at serine and threonine residues that inhibit insulin signaling. JNK1 activation is also required for accumulation of visceral fat. Here we used reciprocal adoptive transfer experiments to determine whether JNK1 in myeloid cells, such as macrophages, also contributes to insulin resistance and central adiposity. Our results show that deletion of Jnk1 in the nonhematopoietic compartment protects mice from high-fat diet (HFD)-induced insulin resistance, in part through decreased adiposity. Conversely, removing JNK1 from hematopoietic cells has no effect on adiposity but causes protection against insulin resistance induced by a high fat diet, by decreasing obesity-induced inflammation.