Introduction
Metabolic syndrome (MetSynd) is a pre-diabetes condition that predisposes individuals to type 2 diabetes mellitus (type 2 DM) and coronary heart disease. Fonseca (2005) lists its major medical characteristics as the increased waistline, increased triglyceride levels, high blood pressure, elevated blood sugar levels, and reduced cholesterol (high-density lipoprotein) levels. The main risk factors associated with MetSynd include elevated blood sugar levels, high blood pressure, morbid obesity, insulin resistance, and low high-density lipid (LDL) levels (Fonseca, 2005).
One of the leading causes of MetSynd is insulin resistance. Usually, elevated blood sugar level triggers the secretion of insulin from the pancreas, which helps in the metabolism of excess blood sugar and lipids. Insulin resistance is caused by inadequate insulin in the blood. Thus, insulin resistance, if uncontrolled, leads to type 2 DM. Research shows that, over time, the MetSynd lipoproteins (LDLs) become oxidized and interact with the endothelial cells of blood vessels (Fonseca, 2005). This attracts macrophages (immune cells) that cause inflammations and plaques in the blood vessels. Thus, the MetSynd diagnosed in the 45-year-old patient caused the type 2 DM condition and the decline in vascular integrity of the patient’s blood vessels.
Type 2 Diabetes and Metabolic Syndrome
One of the crucial events in the pathophysiology of metabolic syndrome and type 2 diabetes mellitus (DM) is the damage to cellular mitochondria (Nicolson, 2007). The mitochondria are the sites for cellular energy production. Studies associate the mitochondrial damage in metabolic syndrome with the development of type 2 DM, insulin resistance, and fatigue in patients (Nicolson, 2007). Mitochondrial damage also causes insulin resistance. Thus, mitochondrial damage causes organ (pancreatic) dysfunction, which leads to insulin resistance.
The pancreatic dysfunction is caused by conformational changes in the mitochondrial structure and lipid (LDL) oxidation, which interfere with the energy production process (Houston & Egan, 2005). MetSynd also increases the synthesis of the Reactive Oxygen Species (ROS), a compound, which, when at high levels, causes vascular dysfunction (Houston & Egan, 2005). In normal mitochondria, the production of ROS is regulated by enzymes and antioxidants found in the cells. The writer of this paper will tell the patient that his condition (MetSynd) affected the secretion of insulin from the pancreas resulting in insulin resistance. Over time, this condition caused gradual damage to the mitochondria, which affected insulin secretion from the pancreas. This led to the development of type 2 diabetes. The writer will also tell this patient that his condition (MetSynd) caused an over-secretion of ROS in the cells, which damaged cell (pancreatic cell) organelles including the mitochondria resulting in mitochondrial dysfunction. This affected insulin secretion and, over time, led to type 2 diabetes mellitus (DM).
Moreover, high levels of lipids in insulin-resistant or obese people damage the cellular mitochondria. This implies that, even before the patient was diagnosed with metabolic syndrome, the accumulation of oxidized lipids (HDLs) caused gradual harm to the mitochondria in the pancreas.
Metabolic Syndrome and Pathophysiologic Changes
Among the pathophysiologic changes in the structure of blood vessels associated with MetSynd are a rise in the levels of inflammatory proteins and an abnormal lipoprotein level in the blood. These factors increase the risk of atherosclerosis in patients diagnosed with MetSynd. Another pathophysiologic change is the elevated ROS level. In the blood vessels, the ROS molecules help conserve the vascular integrity of the vessels. However, in MetSynd patients, the ROS molecules occur in higher amounts. This causes gradual harm to blood vessels. According to Fonseca (2005), the accumulation of LDLs in MetSynd patients causes pathophysiologic changes to blood vessels resulting in atherosclerosis (hardening of arteries). In the 45-year-old patient, the oxidation of his cellular lipoproteins led to the production of macrophages, which, over time, caused lesions in the patient’s blood vessels.
The interaction between oxidized lipoproteins and the endothelial cells causes lesions. The macrophages adhere to these lesions and produce ROS, which causes atherosclerotic plaques. Over time, the plaques accumulate in the blood vessels forming small blood clots, which, if located in the coronary vessels cause heart complications such as myocardial infarction. Thus, due to his condition (MetSynd), the vascular integrity of the patient’s blood vessels will continue to decline with age.
Conclusion
Metabolic Syndrome (MetSynd) is a chronic condition that predisposes individuals to type 2 diabetes and atherosclerosis. This condition is caused by interference in lipid and blood glucose metabolism. High blood pressure, increased LDL level, hyperglycemia, and ROS compounds cause MetSynd and type 2 DM. In this paper, the MetSynd diagnosis in the patient predisposed him to type 2 DM. MetSynd, which is associated with mitochondrial dysfunction, affected the secretion of hormones (insulin) from the patient’s glandular organs such as the pancreas. This led to insulin resistance that caused Type 2 diabetes. Also, his MetSynd condition, over time, led to the accumulation of ROS molecules, which caused a gradual loss of the integrity of blood vessels.
References
Fonseca, V. (2005). The metabolic syndrome, hyperlipidemia and insulin resistance. Clinical Cornerstone, 7(4), 61-72.
Houston, M., & Egan, B. (2005). The Metabolic Syndrome. Pathophysiology, diagnosis, clinical aspects, prevention and nonpharmacologic treatment: emphasis on lifestyle modifications, nutrition, nutritional 2 of 3 supplements, vitamins, minerals, antioxidants, weight management and exercise. Journal of American Nutraceutical Association, 8(2), 63-83.
Nicolson, G. (2007). Metabolic syndrome and mitochondrial function: molecular replacement and antioxidant supplements to prevent membrane oxidation and restore mitochondrial function. Journal of Cellular Biochemistry, 100(2), 352-369.