| Abstract/Notes |
Insulin Resistance Syndrome(IRS) is known as metabolic syndrome, syndrome X, glucose intolerance, prediabetes, and type III diabetes. IRS is the long-term detrimental result of elevated insulin (hyperinsulinemia) and serum glucose levels (hyperglycemia). Initially insulin insensitivity develops in skeletal muscle and adipose tissue, where insulin receptor sensitivity is compromised, and eventually insulin's ability to inhibit triglyceride synthesis is compromised. IRS usually does not have any definitive symptoms. According to the American Diabetes Association the risk factors to developing IRS are: having a genetic family member with diabetes, being overweight with abdominal obesity, being over forty-five years of age, being physically inactive, and being a woman with a history of gestational diabetes. Diagnosis of IRS is made when at least three of the following pathognomonic features are recognized: elevated waist circumference (40 inches or more in males and 35 inches or more in females), elevated triglycerides (150 mg/dL or more), reduced HDL-C (less than 40 mg/dL), elevated blood pressure (systolic 130 or more and diastolic 85 or more mmHg), and elevated fasting glucose (100 mg/dL or more) (1). People with IRS have a five times higher risk of developing diabetes and are twice as likely of developing cardiovascular disease.2 Insulin resistance like obesity and diabetes are conditions that involve systemic inflammation. Other laboratory markers often associated with obesity and IRS include elevation of C-reactive protein, uric acid, oxidized LDL, liver function tests, glycosylated hemoglobin, triglycerides, and glucose. Insulin receptor insensitivity appears to be related to autophosphorylation of the cell's insulin receptor and the subsequent phosphorylation of the insulin receptor substrate. This insensitivity seems to be related to the high concentration of adipose hormones leptin and resistin, and cytokines such as tumor necrosis factor. Simultaneously adipocytes decrease synthesis of adiponectin to further decrease receptor response. This series of responses result in increased levels of insulin, which through stimulation of the autonomic nervous system causes sodium retention and increased blood pressure. This abstract is reproduced with the permission of the publisher; full text is available by subscription.
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