The biological basis of energy homeostasis
In humans, homeostasis is regulated by a complex and effective biological system. The system works concisely, regardless of the limits and challenges that affect energy inputs (Johnson, 2009). These systems are responsible for the regulation of the processes of up-taking, storing and spending energy in the body. Humans control their energy homeostasis through a complex method regulated at the organ, cellular as well as molecular levels. Therefore, it is important to understand the genetic and biological basis of energy homeostasis, which is important in providing an opportunity to develop treatments of metabolic syndromes such as obesity.
In normal conditions, mammals regulate blood glucose concentration in their bodies through two major factors- insulin and glucagon hormones (Cummings & Overduin, 2010). Insulin is a metabolic hormone involved in transporting glucose into body cells. However, when the glucose level inside the body cells is high, the cells receive signals instructing them to convert it into glycogen. The aim is to prevent the soluble glucose from interfering with metabolism. In this way, the hormone prevents the development of hyperglycemia. On the other hand, glucagon hormone is produced by the alpha cells of the pancreas. This metabolic hormone acts to produce an effect opposite to the function of insulin. It makes body cells break down glycogen to form glucose by gluconeogenesis process. It protects the body from developing hypoglycemia.
Deficiency of this hormones leads to diabetes. In this way, the cells cannot convert glucose into insoluble glycogen, resulting into hyperglycemia.
Recent and current research on metabolic syndrome
Over the years, a number of studies have attempted to define the cause of obesity, diabetes and other syndromes in human energy homeostasis.
Hill (2009) developed a research study that attempted to understand and address obesity epidemic. The aim was to investigate the cause of the rapid and sudden increase in the prevalence of obesity, which occurred between late 1980s and 2005. The study used a quantitative approach to examine the trends and causes of the problem in various populations. According to this study, a number of etiologies are responsible for the phenomenon, including biological, environmental and behavioral factors.
In a study, Okosun, Liao, Rotimi, Prewitt and Cooper (2009) aimed at evaluating the relationship between abdominal adiposity with accumulation of multiple metabolic syndromes among white, Hispanic and black communities in the US. The study used an analytical approach, focusing on a quantitative methodology. The results indicate that waist circumference (adiposity) is a marker for multiple metabolic syndromes all ethnic groups in the US.
A current study by Kelly, Rayner, Mijovic & Barnett (2013) aims at finding the number of molecular markers and genetic mutations associated with metabolic syndrome. Using an empirical research and a review of current and recent studies, the paper shows that more than 600 genetic markers and a number of chromosomal regions are linked to or associated with obesity. However, no single gene mutation has been found or linked with the development of the condition.
Value and application of research findings
The recent and current research studies have shown that lifestyle, environmental and genetic factors are responsible for the increasing rates of metabolic syndromes. In addition, the studies indicate the importance of using multiple dimensions to address the problem, which is one of the leading public health problems in the modern world.
References
Cummings , D. E., & Overduin, J. (2010). Gastrointestinal regulation of food intake. Journal of Clinical Investigation, 117(3), 13-23.
Hill, J. O. (2009). Understanding and addressing the epidemic of obesity: An energy balance perspective. Endocrine Reviews, 27(7), 750-761.
Johnson, M. D. (2009). Human Biology: Concepts and Current Issues. San Francisco, CA: Benjamin-Cummings Publishing Company.
Okosun, I. S., Liao, Y., Rotimi, C. N., Prewitt, T. E., & Cooper, R. S. (2009). Abdominal adiposity and clustering of multiple metabolic syndrome in White, Black and Hispanic Americans. Annals of epidemiology, 10(5), 263-270.
Kelly, M. A., Rayner, M. L., Mijovic, C. H., & Barnett, A. H. (2013). Molecular aspects of type 1 diabetes. Molecular Pathology, 56(1), 1-2.