Endocrine Abstracts

Objective: The metabolic syndrome (MS) is characterized by a marked sympathetic activation. Whether this adrenergic overdrive is mainly dependent on the obese state or it can be detected also in absence of obesity is unknown, however.

Design and Methods: In 25 male patients (age 41.4±yrs., mean±S.E.M.) with MS (ATP III criteria) and in 12 age-matched healthy male controls, we measured body mass index (BMI), waist circumference (WC), beat-to-beat arterial blood pressure (Finapres), heart rate (EKG), HOMA index and efferent post-ganglionic muscle sympathetic nerve traffic (microneurography, MSNA). Measurements were performed at rest and during arterial baroreceptor stimulation and deactivation via vasoactive drug infusion.

Results: Patients with MS were classified as obese (MSO, n=16, BMI 33.7±0.7 kg/m² and WC 109.2±1.3 cm) and lean (MSL, n=9, BMI 26.2±0.7 kg/m² and WC 96.3±0.7 cm). HOMA index was significantly greater in MSO than in MSL (5.1±0.3 vs. 3.9±0.3, P<0.05), while all the other variables of the MS were similarly altered in the 2 groups. Both MSO and MSL displayed MSNA values greater than C (62.4±1.5 and 52.8±1.7 vs 39.7±1.2 bs/100 hb, P<0.05). Compared to C, both the bradicardic and the tachycardic responses to vasoactive drugs were impaired in MSL (−24.4±4 and −29.5±6%, P<0.05), a further impairment being detected in MSO (−40.6±7 and −46.2±8%, P<0.05). This was the case also for sympathoinhibitory and sympathoexcitatory responses to baroreceptor manipulation (MSL −26.6±5 and −39.4±7%, MSO −39.8±8 and −51.1±6%, P<0.05 for all).

Conclusions: These data provide evidence that the sympathetic activation and the baroreflex impairment characterizing the MS are independent on the presence of obesity. They also show that the obese state exerts potentiating effects on the sympathetic alterations seen in the MS, presumably because of the greater autonomic (baroreflex impairment) and metabolic (insulin resistance) alterations seen when the obese state and the MS are combined together.