الفهرس 
METABOLIC SYNDROME
Evidence for a neuroendocrine alteration of the HPA axis in abdominal obesity:Only 14 pages are availabe for public view
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Abstract
T
he prevalence of metabolic syndrome manifestations is rapidly increasing worldwide, and is becoming an important health problem. Actually, metabolic syndrome includes a combination of clinical complications such as obesity (central adiposity), insulin resistance, glucose intolerance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. All these alterations predispose individuals to type 2 diabetes and cardiovascular disease inducing earlier mortality rates among people.
Metabolic syndrome identifies clinical symptoms and lab results, including abdominal obesity, insulin resistance, hyperglycemia, hyperlipidemia, and hypertension, that lead to an increased risk of cardiovascular disease (CVD). Obesity typically results in insulin and leptin resistance and a shift from expansion of subcutaneous fat to deposition of abdominal and ectopic fat. These conditions cause metabolic dysregulation.
Prevalence of metabolic syndrome varies markedly from country to country. This seems to be caused by two factors:
1) Variations of lifestyle (especially, diet, smoking and level of physical exercise) between countries.
2) Variations in ethnicity. In all settings and all population, the prevalence of metabolic syndrome increase with age.
The aim of this study is to evaluate role of HPA (Hypothalamic Pituitary Adrenal axis) activity in relation to obesity in metabolic syndrome patients by using the overnight 1 mg dexamethasone suppression test.
The study included two groups:
Group A: This group included 60 patients diagnosed as metabolic syndrome with at least 3 of 5 criteria of metabolic syndrome according to the most updated definition, and were further classified into:
1- Overweight (BMI ≥ 25) or obese metabolic syndrome patients (BMI ≥ 30).
2- Non- obese metabolic syndrome patients (BMI < 25).
Group B: This group included a control group of 30 participants (healthy non metabolic syndrome patients) and were further classified into two groups:
1- Overweight (BMI ≥ 25) or obese (BMI ≥ 30).
2- Non obese healthy (BMI < 25).
All patients were subjected to: Full history taking with full clinical evaluation, laboratory tests including FBS, 2hPP, HOMA-IR, lipid profile, renal and liver functions, calculation of BMI with measurement of waist circumference and the overnight dexamethasone suppression test.
Metabolic syndrome patients (group A (both obese (group I) and non -obese groups (group II)) showed high levels of serum cortisol compared to group B (healthy control) with significant response to suppression to overnight dexamethasone suppression test. However, there was no statistical significant difference between subgroups of group A (group I and group II) in response to suppression which therefore, indicates that in our study, serum cortisol is irrelevant as a cause of obesity in Obese metabolic syndrome patients rather than non -obese metabolic syndrome patients.
In conclusion, there was no statistical significant difference in the current study between serum cortisol after 1 mg over night dexamethasone suppression test between Obese metabolic syndrome patients and non - obese metabolic syndrome patients which implicates minor role for cortisol in Obesity of metabolic syndrome patients.