Insulin Resistance

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In recent years, essential hypertension, in conjunction with several other physiological parameters (glucose intolerance, upper-body obesity, elevated triglycerides), has been shown to be related to insulin resistance. The combination of these variables has been called the insulin resistance syndrome or Syndrome X (Reaven, 1988). Insulin resistance is commonly cited as a causal agent for Type II diabetes. In contrast to Type I diabetes, which is characterized by the body's lack of insulin production, normal or even enhanced amounts of insulin are typically available in Type II diabetes; the insulin receptors, however, are insensitive to insulin. It is generally thought that insulin resistance represents an adaptive bodily response to prevent additional weight gain that accompanies unhealthy lifestyles and dietary practices. Under conditions of extreme insulin resistance, an overabundance of sugars and lipids remains in the bloodstream rather than being absorbed into body tissue. According to this theory, the same underlying process is responsible for onset of both essential hypertension and Type II diabetes.

Insulin resistance (impaired insulin sensitivity) has been shown to be associated with several pathological processes of blood pressure regulation, including increased sodium and fluid retention, vascular hypertrophy, and increased sympathetic nervous system activity (Hjer-mann, 1992; O'Hare, 1988), variables already hypothesized to be involved in explaining the stress—hypertension link. Regarding the relation between insulin resistance and the sympathetic nervous system, the fight-flight response involves increased glucose utilization by the brain; consequently, it has been hypothesized that peripheral insulin resistance increases in an adaptive maneuver to preserve glucose for use by the brain (Julius, 1995). Importantly, for purposes of the current discussion, both elevated SBP and DBP are associated with hyperinsu-linemia (Denker and Pollock, 1992). Additionally, impaired insulin sensitivity has been detected among normotensive offspring of hypertensive patients, suggesting that insulin dysfunction precedes the development of hypertension (Endre et al., 1994). As with the high-renin and volume dependent types of hypertension, not all hypertensive patients exhibit hyperinsulinemia or increased insulin resistance. Reaven (2003) estimates that only about half of patients diagnosed with hypertension exhibit insulin-related dysfunctions. In sum, although it is clear that hyperinsulinemia is related to the onset of some cases of hypertension, it is unknown through which mechanism (fluid retention, vascular hypertrophy, and enhanced nervous system activity) it exerts its effect on blood pressure regulation.

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