Identification and Management of Metabolic Syndrome: The Role of the APN

Douglas H. Sutton, EdD, MSN; Deborah A. Raines, PhD


Topics in Advanced Practice Nursing eJournal. 2007;7(2) 

In This Article


The clinical significance of elevated plasma glucose, particularly in the obese person, may be indicative of insulin resistance. In insulin resistance, tissue has a diminished ability to respond to the action of insulin. In a person with normal metabolism, insulin is released from the beta cells of the islets of Langerhans in the pancreas. The presence of insulin signals insulin-sensitive tissues, including muscle, adipose tissue, and liver cells, to absorb glucose and maintain the circulating blood glucose at a normal level. In an insulin-resistant person, the release of insulin does not trigger the expected insulin response of absorption by muscle, adipose tissue, and liver cells; therefore, the circulating blood glucose levels rise.

To compensate for increased serum glucose levels, the pancreas secretes more insulin. This compensatory mechanism, referred to as hyperinsulinemia, tries to maintain normal glucose levels. Eventually, the beta cells of the pancreas are unable to overcome insulin resistance through hypersecretion of insulin, which results in an elevated serum glucose level. Insulin resistance in fat cells results in hydrolysis of stored triglycerides, which elevates free fatty acids in the blood plasma. Insulin resistance in muscle reduces glucose uptake, whereas insulin resistance in the liver reduces glucose storage, with both effects serving to elevate circulating blood glucose.

Approximately 50% of patients with hypertension have also been found to be insulin-resistant.[15] Exactly how insulin resistance influences BP remains unclear, however. In many previously normotensive individuals, elevated serum glucose levels seem to precede the development of essential hypertension.[16,17,18] In addition to developing essential hypertension and glucose intolerance, these insulin-resistant patients tend to also develop elevated plasma triglyceride levels and low HDL-C. All of these findings are consistent with the diagnosis of metabolic syndrome.

Cytokines and obesity. Metabolic syndrome has also been associated with a state of chronic, low-grade inflammation.[19,20] Inflammatory cytokines provoke insulin resistance in both adipose tissue and muscle.[20,21] Cytokines are nonantibody proteins secreted by inflammatory leukocytes considered to be key modulators of inflammation.[22] In the obese individual, adipose tissue produces excess cytokines and is believed to exacerbate this syndrome.

Specifically, elevated insulin and glucose concentrations are associated with hypertrophied subcutaneous fat cells or adipocytes. Adipocytes can secrete signaling messengers called adipokines and act as an endocrine cell affecting other tissue and physiologic functions. The presence of adipokine triggers the release of[21]:

  • Cytokines;

  • Resistin;

  • Adiponectin;

  • Leptin;

  • Tumor necrosis factor (TNF); and

  • Plasminogen activator inhibitor (PAI)-1.

These peptide hormones have been implicated in insulin sensitivity and energy homeostasis, thereby exacerbating metabolic syndrome.

Prothrombotic factors: proinflammatory state. A growing body of research now implicates high circulating levels of prothrombotic factors and the presence of a proinflammatory state as being indicative of an even higher risk for acute cardiovascular syndromes.[23,24,25,26,27] The use of the high-sensitivity C-reactive protein (hsCRP) serum test, as a marker of low-grade vascular inflammation, is among the most promising recent risk assessment developments for both atherosclerotic CVD and metabolic syndrome.

Currently, the AHA recommends the use of hsCRP as an adjunct to traditional risk factor screening in individuals at intermediate risk, as identified by Framingham scoring, that is, those whose 10-year risk for coronary heart disease is in the range of 10% to 20%.[26] The AHA endorsed the test as the only inflammatory biomarker currently available with "adequate standardization" and "predictive value" to substantiate use in the outpatient clinical setting.[26]

On the basis of prior studies, levels of hsCRP < 1, 1-3, and > 3 mg/L have been defined as lower, moderate, and higher cardiovascular risk groupings, respectively.[27] Given the relatively low cost of this test, clinicians might consider this at the same time as lipid screening.

The AHA/NHLBI scientific statement lists several risk factors for the development of metabolic syndrome. Many of these are outlined in Table 1 as well as their clinical relevance.[2]


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