Diabesity/Bibliography: Difference between revisions
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Endoplasmic reticulum stress causing hyper-activation of Jun kinases (JNKs), which leads to phosphorylation of insulin receptor substrates (IRSs), inhibiting insulin signalling | Endoplasmic reticulum stress causing hyper-activation of Jun kinases (JNKs), which leads to phosphorylation of insulin receptor substrates (IRSs), inhibiting insulin signalling: <br /> | ||
Umut Özcan, et al. (2004) Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes. ''Science'' '''306''', 457-461.<br /> | Umut Özcan, et al. (2004) Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes. ''Science'' '''306''', 457-461.<br /> | ||
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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 /> | 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 /> | ||
Dysfunction of the pancreatic β-cells<br /> | Dysfunction of the pancreatic β-cells, which do not produce or secrete enough insulin to compensate for insulin resistance:<br /> | ||
Hiroshi Karasawaa, Seiko Nagata-Gotoa, Kiyosumi Takaishia and Yoshihiro Kumagae. (2009) A novel model of type 2 diabetes mellitus based on obesity induced by high-fat diet in BDF1 mice. ''Metabolism Clinical and Experimental'' '''58''', 296–303.<br /> | Hiroshi Karasawaa, Seiko Nagata-Gotoa, Kiyosumi Takaishia and Yoshihiro Kumagae. (2009) A novel model of type 2 diabetes mellitus based on obesity induced by high-fat diet in BDF1 mice. ''Metabolism Clinical and Experimental'' '''58''', 296–303.<br /> | ||
The Hormone Resistin, secreted by adipocytes, which causes resistance to insulin:<br /> | |||
Claire M. Steppan, et al. (2001) The hormone resistin links obesity to diabetes. ''Nature'' '''409''', 307-312.<br /> | |||
[[User:Nicholas Devlin|Nicholas Devlin]] 12:04, 14 October 2009 (UTC) | |||
Revision as of 06:04, 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
Causes of type 2 diabetes in obese subjects
Endoplasmic reticulum stress causing hyper-activation of Jun kinases (JNKs), which leads to phosphorylation of insulin receptor substrates (IRSs), inhibiting insulin signalling:
Umut Özcan, et al. (2004) Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes. Science 306, 457-461.
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.
Dysfunction of the pancreatic β-cells, which do not produce or secrete enough insulin to compensate for insulin resistance:
Hiroshi Karasawaa, Seiko Nagata-Gotoa, Kiyosumi Takaishia and Yoshihiro Kumagae. (2009) A novel model of type 2 diabetes mellitus based on obesity induced by high-fat diet in BDF1 mice. Metabolism Clinical and Experimental 58, 296–303.
The Hormone Resistin, secreted by adipocytes, which causes resistance to insulin:
Claire M. Steppan, et al. (2001) The hormone resistin links obesity to diabetes. Nature 409, 307-312.
Nicholas Devlin 12:04, 14 October 2009 (UTC)