Millions of Americans are diagnosed with type 2 diabetes; a disorder linked to insulin resistance and elevated levels of glucose in the bloodstream. The risk factors tied to this disorder deal with weight surplus, or obesity and inactivity in an individual's lifestyle, in that the fat storage cells in the body ultimately become unresponsive to insulin, a hormone that is secreted by the pancreas. Insulin is a key factor in regulating the levels of blood sugar in the bloodstream, and thus the failure to respond to insulin can lead to adverse effects in which the blood vessels can be destroyed due to the increased levels of glucose and fatty acids that are present. The underlying principle that is linked to this problem is the failure of certain fat and muscle cells to respond to insulin in order to absorb the glucose that is produced. Thus, the pancreas pumps more insulin due to the body's response failure, until the cells of the pancreas that take part in this process are ultimately damaged (Sapolsky, 2004). Due to the adverse impact on an individual's health, further investigations and studies are critical to allow medical professionals to recognize and be fully aware of the moderating factors that can contribute to type 2 diabetes.
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A number of physiological studies have been completed examining the genetic and environmental factors that play a role in diabetes. To further investigate genetic influences involved in diabetic individuals, Seo, Park, Kim, Lee, and Hong (2010), conducted a study investigating the differences in gene expression tied to metabolic processes that regulate glucose and lipid levels. Prior to data collection, Seo et al. (2010) hypothesized a significant difference in the way the recessive genes are expressed for the diabetic and non-diabetic groups in reference to the genes that control the metabolic pathways of glucose and lipid synthesis. Consistent with this hypothesized result, data figure 3A looks at the key recessive genes linked to lipid production that include, 3-hyroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR), Sterol regulatory element-binding protein 1 (SREBP1), acetyl-CoA carboxylase 1 (ACC1), stearoyl-CoA desaturase 1 (SCD1), and glycerol-3-phosphate acyltransferase ( GPAT). Additionally, 3B further investigates lipid transport by analysis of lipoprotein lipase (LPL), uncoupling proteins 2 (UCP2), and hepatic lipase (HL). These recessive genes are depicted on the x-axis of the figures and are measured in terms of mRNA expression, to reveal the differences that reside between diabetic and non-diabetic groups.
Changes in the metabolic pathway associated with lipid metabolism is the primary focus of figure 3A and 3B, thus the relevant questions and factors addressed not only deal with recessive genes of lipid synthesis but also the role of the transport genes that carry fatty acids to the liver. The main question at hand that Seo et al. (2010) sought to address were the differences that appear in terms of how the recessive genes are expressed when comparing the diabetic conditions to a non-diabetic equal. Understanding these differences, in turn can help to pinpoint the factors that can lead to the onset of diabetes by focusing on the recessive genes that showed significant differences among both groups. The role of obesity was also questioned in terms of fat storage cells that reside in the body that can ultimate lead to insulin resistance, in addition to the what role cholesterol and triglycerides play in bringing about diabetic symptoms. Essentially, what the study sought to address, the questions proposed and the hypothesized results focus on the targeted genes that deal with hyperglycemia and hyperlipidemia, in which the data retrieved from the experiment can aid in detecting to what degree these genes play a role in type 2 diabetes. Essentially, the primary data figure 3A and 3B for analysis demonstrate the differences that involve factors leading to hyperlipidemia, or an increase of lipids in the bloodstream.
Building on these questions and factors, Seo et al. (2010), formulated an experiment that used an animal representation of the disorder in which male rats were studied and analyzed throughout the course of 35 weeks. The Otsuka Lon-Evans Tokushoma Fatty (OLETF) rats served as the experimental group and exemplified the primary characteristics of type 2 diabetes. The OLETF rats were compared to a non-diabetic control group, on basis of gene expression. The animals were sacrificed in order to obtain liver samples for further analysis of cholesterol and triglycerides. The data collected are based on the differences of these two groups, and are presented in figure 3A and 3B.
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Statistical analysis was conducted to determine any significant differences. The mean values in the figure that were collected for each recessive gene were considered significant if the resulting p values were 0.05 or less. The genes that were analyzed and noted in figure 3A are associated with hyperlipidemia, and include HMGCR, SREBP1, ACC1, SCD1 and GPAT. According to Seo et al. (2010), after the analysis of the data a significant difference was found for SCD1 and HMGCR, where "expression of the SCD1 gene was 4.7 times higher in OLETF than LETO rats; HMGCR was 25.5 times higher in OLETF rats" (p. 102). Additionally, UCP2, LPL and HL genes were observed, revealing a significant difference between both groups for the HL gene in that it was expressed at a greater extent for the OLETF rats. Error bars are present in figure 3A and 3B in order to visually compare both groups and determine if the differences are significant. According to Seo et al., the overall findings of the experiment depicted in the figure show an increase in lipid production and transport for the diabetic rats.
The information that is supplied by the resulting data of figure 3A and 3B indicate that OLETF rats not only exhibit high glucose levels but show an increase in lipid synthesis as well; therefore considerable attention has been paid to the association of diabetes and obesity. The HMGCR gene is notably expressed in the OLETF group as indicated in the data figure 3A; since this gene is a "rate-controlling enzyme" that contributes to the synthesis of cholesterol, as is expected, the diabetic group showed an increase in cholesterol levels as well (p. 102). SCD1 plays a role in the regulation of unsaturated fatty acids, therefore, an increased mRNA expression of this gene, as is noted in the figure 3A, indicates high levels of triglycerides and cholesterol in the body. In examining the role of the recessive gene, hepatic lipase, its significant increase in the diabetic group plays a role in "lipoprotein uptake which would lower the high concentration of plasma lipid in OLETF rats" (p.102). All significant differences observed between the experimental and control group revealed a pattern of lipid production and transport increase that was apparent in the diabetic rats. Therefore, in addressing adverse physiological health states of this disorder, it is important to recognize the pathway connecting these recessive genes related to lipid increase and diabetes.
With further analysis of blood samples to test glucose levels, Seo et al., found that glucose processes in diabetic rats "were regulated to restore homeostasis", in that the recessive genes that are linked to glucose production are altered in order to decrease the levels of sugar in the bloodstream (p. 102). Thus, the key component in the onset of type 2 diabetes can be linked to the lipid recessive genes which can ultimately bring on or intensity the conditions and symptoms related to diabetes when the gene is highly expressed. In formulating therapeutic solutions, targeting these lipid recessive genes can aid in the advancement of treatments for diabetic individuals.