Diabesity: Difference between revisions

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imported>Luke Kennedy Burke
imported>Luke Kennedy Burke
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<ref>"Part 2," Appetite and obesity. 2006. Retrieved July 21, 2009 from [http://www.appetiteandobesity.org/part2.html http://www.appetiteandobesity.org/part2.html]</ref>
<ref>"Part 2," Appetite and obesity. 2006. Retrieved July 21, 2009 from [http://www.appetiteandobesity.org/part2.html http://www.appetiteandobesity.org/part2.html]</ref>


==The immunology of obesity==
==The immunology of obesity== by Luke Kennedy Burke
 
Type 2 diabetes has long been thought of as primarily a metabolic disease. A series of recent studies have challenged this dogma and implicated an unlikely candidate system in the promotion of disease onset - the immune system. Mild inflammation of fat tissue in obese patients reportedly acts through immune-cell processes to impair insulin signalling in adipocytes. This work therefore provides a novel way of understanding the link between obesity and type 2 diabetes.
Type 2 diabetes has long been thought of as primarily a metabolic disease. A series of recent studies have challenged this dogma and implicated an unlikely candidate system in the promotion of disease onset - the immune system. Mild inflammation of fat tissue in obese patients reportedly acts through immune-cell processes to impair insulin signalling in adipocytes. This work therefore provides a novel way of understanding the link between obesity and type 2 diabetes.



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A brief overview of your interest group (be sure to put its name in bold in the first sentence) and the scope of the article goes here.[1]

The following list of sections should serve as a loose guideline for developing the body of your article. The works cited in references 2-5 are all fake; their purpose is to serve as a formatting model for your own citations.


Title of Part 1

Title of Subpart 1

In here you could write about various informations linked to various references for example from journals. [2] [3]


Title of Subpart 2

You can also insert diagram.


Title of Part 2

You can also cite published work accessible online. [4]

==The immunology of obesity== by Luke Kennedy Burke

Type 2 diabetes has long been thought of as primarily a metabolic disease. A series of recent studies have challenged this dogma and implicated an unlikely candidate system in the promotion of disease onset - the immune system. Mild inflammation of fat tissue in obese patients reportedly acts through immune-cell processes to impair insulin signalling in adipocytes. This work therefore provides a novel way of understanding the link between obesity and type 2 diabetes.

Key References

Normalization of obesity-associated insulin resistance through immunotherapy http://www.nature.com/nm/journal/v15/n8/full/nm.2001.html

Genetic deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice http://www.nature.com/nm/journal/v15/n8/full/nm.1994.html

Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters http://www.nature.com/nm/journal/v15/n8/full/nm.2002.html

CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity http://www.nature.com/nm/journal/v15/n8/full/nm.1964.html

The protein kinase IKKepsilon regulates energy balance in obese mice http://www.cell.com/retrieve/pii/S0092867409007934

T-ing up inflammation in fat http://www.nature.com/nm/journal/v15/n8/full/nm0809-846.html

References

  1. See the "Writing an Encyclopedia Article" handout for more details.
  2. First Author and Second Author, "The perfect reference for Subpart 1," Fake Journal of Neuroendocrinology 36:2 (2015) pp. 36-52.
  3. First Author and Second Author, "Another perfect reference for Subpart 1," Fake Journal of Neuroendocrinology 25:2 (2009) pp. 62-99.
  4. "Part 2," Appetite and obesity. 2006. Retrieved July 21, 2009 from http://www.appetiteandobesity.org/part2.html