Telomere length loss due to smoking and metabolic traits
Telomere Length Loss Due To Smoking and Metabolic Traits
The telomere is an intrinsic part of the chromatid that helps it to absorb fusion and sustain integrity and stability. Evidently, the telomere contains numerous nucleotides at the end of chromosomes preventing it from deterioration with neighboring tissues. Analysis assert that when the telomere shortens, they die accruing danger to the chromosomes (Blackburn & Epel, 2012). Therefore, their role in body tissues is crucial an indication that they must be considered to ensure the well-being of an individual. In a more critical review, the telomere protects genetic data making it easy for the cells to oxidize. Information indicates that the maintenance of the telomere requires complex factors such as the telomere enzyme that contains protein TERT and RNA telomerase.
Influence of the telomere size by metabolic traits and smoking
In the first perception, the shortening of the telomere associates impaired secretion and resistance of insulin. Research indicates that the b-cells in the body senses the plasma glucose level and secrete insulin to engage metabolism. Critically, the hormone upholds metabolism in the entire body enhancing glucose uptake within the skeletal muscles and the adipose body tissues. Investigation elucidates that the impaired secretion accrues the deficiency of telomerase enzyme absorbing glucose metabolism (Blackburn & Epel 2012). Evidently, the enzyme plays a critical role in chromosomal end extension increasing the nucleotides. Such an aspect contributes to the extension of the telomeres; thus, providing a suitable platform for DNA replication. The aspect rather accelerates the shortening of the telomeres since replication cannot be prevented. Therefore, since the impaired insulin accrues telomerase enzyme deficiency the nucleotides cannot increase. Such an aspect will withhold chromatid integrity. Evidently, the aspect of insulin impairment can be improved through the introduction of several treatment approaches. In the first place, the use of thiazolidinediones and pioglitazone which targets insulin resistance. Evidence indicates that the systems are effective despite the fact that they retain peptides extending cardiac load. Fortunately, GITT proves to be the best approach in stimulating insulin secretion spurring telomere extension.
The research will determine the manner in which smoking and metabolic traits spur telomere shortening in different samples at distinct periods (Huzen et al., 2014). It will analyze the effect in terms of size to the telomere accrued by smoking and ineffectiveness of the metabolic activities.
The sampling involved participants with material observations accrued to individuals with short telomere. For instance, individuals they claimed bone marrow failure that was imperatively realized in children. Such a symptom associates the fact that the victim lacks adequate platelets to enhance adequate blood clotting. Secondly, the victims of the condition had pulmonary fibrins where the lung accrues scarring and do not engage functionality to completion. Further, most of them had exposure to liver diseases where lipids are not broken down to completion. It is a condition where an individual has high exposure to chronic diseases. Further, an individual with minimized telomere has skin abnormalities where the skin’s pigment is inadequate. Further, they lacked adequate spots and patches in the skin.
The research involved a sampling hypothetical approach where conclusions were drawn according to the findings from the majority of the participants. The study will hypothetically determine the shortness of telomere among individuals in the sample and the rate in which it keeps on changing. Secondly, it will assert the number of individuals associated with smoking in the sample.
Critically, the experimental task invited a quantitative polymerase approach to determine telomere size among the participants. It is a concept where a participant should consider several samples associated with the respective observations and carry out the test. The research will involve several demographics to ascertain which group is highly influenced by the defect. It is evident that the children can only engage it as a result of metabolic traits while the adults engage it through smoking, aging and metabolic traits. Therefore, the researcher engaged two samples of 50 children, 50 youth, and 50 adults (Hartmann, Boehner, Groenen & Kalb, 2010). Secondly, the participant compared the findings to draw a clear conclusion regarding the existence of short telomere. It is vital to consider the outcomes of the samples to enhance objectivity when drawing the conclusion.
The finding indicated that the telomere is normally influenced by the variables at the interval of 0.001(Huzen et al., 2014). The findings asserted that the telomere length loss associated dependent variables such as smoking. Evidently, it is the dependent variable because its contribution to telomere shortening depends on the amount of smoke consumed by the patients. In contrast, the metabolic traits from the independent variable in the sense that their influence is constant to the telomere.
The results retrieved from the tests had average attrition of 0.66 telomere length units from the distinct demographics. The information was identical in the different samples showing that it was reliable. In a more critical review, the experiment was done on a different occasion where the telomere length changed by 0.001.
Critically, the sampling size was viable where every sample involved 50 respondents, and 37 of them contributed positively to the experiment contributing to the conclusion. Such an aspect allowed a confidential ground to draw the conclusion. Evidently, it is important to consider the observations when determining the respective samples so that one can engage an objective test.
The study plays an intrinsic role to the world through the provision of knowledge regarding the effects of smoking and metabolic aspects to chromosomes in the body. It is a perception where it narrows down to assert the steps with which the smoking components combines with oxygen enhancing stress. Further, the study asserts respective metabolic aspects in the body which spur telomere shortening. Such an aspect is realized in cases where impaired insulin secretion and resistance is realized leading to inadequate glucose uptake that accelerate telomere shortening. It is essential to an individual where one can understand the kind of environment which favor the body tissues; thus, keep it safe (Hartmann, Boehner, Groenen & Kalb, 2010).
Huzen, J., Wong, L. S. M., Veldhuisen, D. J., Samani, N. J., Zwinderman, A. H., Codd, V., … & Harst, P. (2014). Telomere length loss due to smoking and metabolic traits. Journal of Internal Medicine, 275(2), 155-163.
Hartmann, N., Boehner, M., Groenen, F., & Kalb, R. (2010). Telomere length of patients with major depression is shortened but independent from therapy and severity of the disease. Depression and Anxiety, 27(12), 1111-1116.
Blackburn, E. H., & Epel, E. S. (2012). Telomeres and adversity: Too toxic to ignore. Nature, 490(7419), 169-171.
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