Analyzing a Peer-Reviewed Research
• Read the article evaluating its strengths and weaknesses in terms of scholarly writing, bias, opinion, quality of evidence, and appropriateness to its target audience.
• Then, write the body of your paper that includes the following:
? A 1-paragraph introduction to your paper
o Article Summary
? A 1-paragraph summary of the article you have selected
? An analysis of the strengths and weaknesses of the article, including an assessment of the writing in terms of bias, opinion, quality of evidence, and appropriateness to its target audience (Be sure your analysis is written in a scholarly manner and appropriate voice.)
? A 1-paragraph summary of your paper
• In addition, create the following to be included with your paper:
o Title page
? Include your reference using correct APA formatting
o Appendix that includes the information from the Grammarly report (copy and paste the results) I’d take of this part
Submit your paper (title page, 2 pages of content, reference page, and appendix) as described above.
Genetics of obesity
Martínez-Hernández, Alfredo; Enríquez, Luís; Moreno-Moreno, María Jesús; Martí, Amelia. Public Health Nutrition 10. 10A (Oct 2007): 1138-44.
The aim was to review and update advances in genetics of obesity.
Analysis and interpretation of recent investigations about regulating the energy balance as well as about gene-nutrient interactions and current nutrigenomic research methods.
Background and main statements
Obesity results from a long-term positive energy balance. However, its rising prevalence in developed and developing societies must reflect lifestyle changes, since genetic susceptibility remains stable over many generations. Like most complex diseases, obesity derives from a failure of adequate homoeostasis within the physiological system controlling body weight. The identification of genes that are involved in syndromic, monogenic and polygenic obesity has seriously improved our knowledge of body weight regulation. This disorder may arise from a deregulation at the genetic level (e.g. gene transcription or altered protein function) or environmental exposure (e.g. diet, physical activity, etc.).
In practice, obesity involves the interaction between genetic and environmental factors.
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While it is clear that environmental factors play a significant role in the development of obesity, research work over the last decades has clearly documented a genetic contribution to obesity-related phenotypes as well. Obesity and its related traits represent the archetype of a common complex phenotype. The configuration of multiple genes can range from polygenic (i.e. many genes with a relatively small contribution) to oligogenic (i.e. few genes with large measurable effects often expressed on a residual polygenic background) 1 . Indeed, it is this oligogenic architecture that justified all current efforts to map genes for complex phenotypes.
Prior to the mid-1990s, most of the work on genetics of human obesity had been limited to demonstrating that variation in a wide range of obesity-related phenotypes could be attributable to varying degrees to the effects of genes2 . Quantitative genetics analyses (twins, siblings and family studies) have shown significant heritability, individual’s chances of being obese are increased when having obese relatives, with estimates of heritability generally ranging from 30% to 70%. Different sets of monozygotic twins overfed showed differences in the degree to which excess calories were stores of fat, but the tendency towards increased adiposity within each set of twins were very similar, indicating that genetic factors play a major role in the individual susceptibility to gain weight in a specific environment 3-5 .
From the late 1980s through the early 1990s, segregation analysis was utilised in an effort to dissect further the genetic component underlying human obesity by attempting to detect the effects of anonymous major genes on obesity-related phenotypes. A number of these studies have reported consistent evidence of an anonymous major gene effect accounting for as much as 40% of the variation in body mass index (BMI) or fat mass in a variety of populations 2 .
By the early to mid-1990s, researchers began to focus on the goal of identifying the specific genes involved. Initially, such efforts to identify specific genes influencing complex traits such as those associated to obesity relied on the use of a priori selected candidates genes. Such candidates genes are selected on the basis of their perceived role or function in biochemical pathways relevant to the specific phenotype of interest (e.g. the structural gene for a circulating protein). The conservation of hypothalamic pathways in rodents and humans has certainly aided in choosing suitable candidates genes. All the spontaneously occurring obesity mutations in mice either have been found to harbour functionally relevant mutations in humans too or have led to the identification of a system/pathway in which other genes were found to be mutated. The tools recently developed allow easy determination of most gene polymorphisms from a blood sample, especially single-nucleotide polymorphism (SNP). This advancement opens a new era where research work devoted to study the interaction among diets, metabolic variables, disease risk factors and gene polymorphism can be carried out. According to the last available version of the Gene Obesity Map (2004) there are more than 600 genes, markers and chromosomal regions involved in body weight regulation and obesity development 6 .
Genetics of body weight regulation
Body weight regulation and stability depends upon an axis with three interrelated components: food intake, energy expenditure and adipogenesis, although there are still many unknown features concerning fuel homoeostasis and energy balance. There are 358 studies on obese humans reporting positive associations with 113 candidate genes. Among them, 18 genes are supported by at least five positive studies 6 (Fig. 1). Here we will summarise a number of mutations in genes encoding factors regulating food/energy intake and factors implicated in energy expenditure and adiposity.Fig. 1
Genetics of obesity
Genes encoding factors regulating food/energy intake
It was generally accepted that hypothalamic and brain stem centres are involved in the regulation of food intake and energy balance but information on the relevant regulatory factors and their genes was scarce before the last decade1 . Insulin remained the only candidate for the key role in body weight regulation for a long time. The discovery of leptin is one of the most exciting findings of the last decade. This cytokine-like peptide mainly expressed by adipocytes is now believed to be a key regulator of fat metabolism and energy intake. Leptin is the product of human homologue of mouse ‘obese’ gene, whose homozygous mutation caused hereditary obesity in mice (monogenic).
The mechanisms participating in the effects of leptin and other peptides on food intake and body weight regulation are now becoming clearer. Certain areas of the hypothalamus are rich in specific receptors binding regulatory peptides and triggering central regulatory mechanisms. Factors acting at the central nervous system level include neuropeptide Y (NPY), corticotropin-releasing hormone, proopiomelanocortin, [alpha]-melanocyte-stimulating hormone, agouti-related protein, melanin-concentrating hormone, cocaine- and amphetamine-regulated transcript and other molecules. Interaction between them involving complex neuronal mechanisms eventually influence the behaviour and provide important links with neuroendocrine regulation of other vital functions of the organism 2 .
Studies in humans have failed to find leptin or any other mutant gene to be the unique ‘obesity gene’. Conversely, multifactorial patterns involving ac