Genetics of obesity: Difference between revisions
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Obesity is the condition of excessive fat accummulation typically defined as a BMI of 30 or more. It presents as a major risk factor for premature mortality and is attributable to a number of chronic diseases: cardiovascular, metabolic and cancerous (1). With the onset of the obesity epidemic, an increasing number of institutions are researching into the causes of this current trend. While the environmental influences (including the ease of access to high energy palatable foods and sedentary lifestyle) cannot be neglected, there is much focus on genomics to explain inter-individual variation in susceptibility to adiposity (2). | Obesity is the condition of excessive fat accummulation typically defined as a BMI of 30 or more. It presents as a major risk factor for premature mortality and is attributable to a number of chronic diseases: cardiovascular, metabolic and cancerous (1). With the onset of the obesity epidemic, an increasing number of institutions are researching into the causes of this current trend. While the environmental influences (including the ease of access to high energy palatable foods and sedentary lifestyle) cannot be neglected, there is much focus on genomics to explain inter-individual variation in susceptibility to adiposity (2). | ||
{{Image|leptin_pathway.png|right| | {{Image|leptin_pathway.png|right|550px|}} | ||
Although several genes have been identified, they are limited to monogenic causes. Many of these are mutations of proteins in the “leptin pathway” which has an important role in energy balance. Each of those represented in the diagram has been shown to cause obesity, most often through twin studies. | Although several genes have been identified, they are limited to monogenic causes. Many of these are mutations of proteins in the “leptin pathway” which has an important role in energy balance. Each of those represented in the diagram has been shown to cause obesity, most often through twin studies. |
Revision as of 06:05, 19 October 2010
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Begin your article with a brief overview of the scope of the article on interest group. Include the article name Genetics of Obesity in the first sentence.[1]
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Overview
Obesity is the condition of excessive fat accummulation typically defined as a BMI of 30 or more. It presents as a major risk factor for premature mortality and is attributable to a number of chronic diseases: cardiovascular, metabolic and cancerous (1). With the onset of the obesity epidemic, an increasing number of institutions are researching into the causes of this current trend. While the environmental influences (including the ease of access to high energy palatable foods and sedentary lifestyle) cannot be neglected, there is much focus on genomics to explain inter-individual variation in susceptibility to adiposity (2).
Although several genes have been identified, they are limited to monogenic causes. Many of these are mutations of proteins in the “leptin pathway” which has an important role in energy balance. Each of those represented in the diagram has been shown to cause obesity, most often through twin studies.
In the case of all (except for MC4R) the quantity of mutations remains insignificant in the average population. However these findings do suggest there can be more common multifactorial influences on susceptibility to adiposity which are likely to be involved in similar pathways (7).
Population genetics
Thrifty gene hypothesis
The thrifty gene hypothesis was first put forward by Neel in 1962[2] It states that, in history, a genotype that stores energy more efficiently in times of food abundance would have been advantageous to our ancestors to survive times of food shortage. It is widely accepted that this genotype has been naturally selected through years of food shortage but in modern day society has become a source health problems. These days food is almost always easily available so those showing the thrifty phenotype are in constant food storage mode preparing their bodies for a period of food shortage that never comes. This is suggested to be causing the widespread prevalence of obesity and type 2 diabetes in the developed world.
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[5]
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How to write the same reference twice:
Reference: Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431 PMID 17072591
First time: <ref name=Berridge07>Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. ''Psychopharmacology'' 191:391–431 PMID 17072591 </ref>
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This will appear like this the first time [6] and like this the second time [6]
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References
- ↑ See the "Writing an Encyclopedia Article" handout for more details.
- ↑ Neel JV. Diabetes mellitus: a 'thrifty' genotype rendered detrimental by 'progress'? Am J Hum Genetics 1962;4:352-3.
- ↑ Person A et al. (2010) The perfect reference for subpart 1 J Neuroendocrinol 36:36-52
- ↑ Author A, Author B (2009) Another perfect reference J Neuroendocrinol 25:262-9
- ↑ Johnstone LE et al. (2006)Neuronal activation in the hypothalamus and brainstem during feeding in rats Cell Metab 2006 4:313-21. PMID 17011504
- ↑ 6.0 6.1 Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431 PMID 17072591