Relation of obesity and diet to sympathetic nervous system activity.

Abstract

The hypothesis that dietary intake and obesity stimulate the sympathetic nervous system was investigated in a cross-sectional study of 572 men aged 43-85 years from the Normative Aging Study. Habitus was represented by body mass index, as a measure of overall adiposity, and by the ratio of abdomen-to-hip circumference (abdomen/hip ratio), as a measure of centripetal fat distribution. Sympathetic activity was assessed by measurement of 24-hour urinary norepinephrine excretion. Increased body mass index and total caloric intake were independently associated with increased 24-hour urinary norepinephrine excretion (p=0.0001 andp=0.0055, respectively). In addition, mean urinary norepinephrine excretion was higher in subjects classified as either hyperglycemic (serum fasting glucose 2:113 mg/dl) and hyperinsulinemic (serum fasting insulin >19 /tIU/ml) (p=0.0023) or in subjects classified as either hyperglycemic or hyperinsulinemic (/>=0.0063) than the mean urinary norepinephrine excretion in normal subjects. These relations were demonstrated to be independent of age, smoking status, and physical activity. Our results are consistent with the hypothesis that insulin mediates sympathetic stimulation in response to dietary intake and increases sympathetic nervous system activity in the obese. (Hypertension 1991;17:669-677)

Sympathetic Overdrive and Cardiovascular Risk in the Metabolic Syndrome

“…The obese state, even when unaccompanied by a blood pressure elevation, displays signs of adrenergic activation, such as increased resting heart rate values and elevated plasma norepinephrine values (16). This has been confirmed by the results of the Normative Aging Study, which in a large number of subjects has shown a close direct relationship between 24-h urinary figures of norepinephrine metabolites and body mass index values (17). This has also been confirmed by the evidence that an augmented sympathetic neural discharge to skeletal muscle as well as an increased spillover rate of norepinephrine from sympathetic nerve endings, particularly at the level of the kidney, takes place in obese normotensive subjects (18,19).…”

Undernutrition during suckling in rats elevates plasma adiponectin and its receptor in skeletal muscle regardless of diet composition: a protective effect?

“…Several central and peripheral abnormalities can contribute to the development of hypertension in obesity including endothelial dysfunction, activation of the rennin-angiotensin system and sympathetic nervous system (SNS). 45 In humans, SNS activity is increased with obesity, 46,47 and high-caloric intake in rats can increase SNS activity, increasing norepinephrine turnover in peripheral tissues and elevating blood pressure. 48 Elevated leptin may contribute to increased SNS activity as leptin acts in the ventromedial and dorsomedial hypothalamus to increase renal sympathetic activity and blood pressure.…”

Obesity and the Insulin Resistance Syndrome

“…In distinctiorr to NE, epinephrine decreased with increasing body weight and increasing upper body fat distribution (26,27). As shown in Fig.…”

“…3), the rate of appearance of tritiated NE in the circulation (23,26,27), and implanted microelectrodes (28) was increased in the obese. There was, moreover, a relationship between insulin and glucose levels and SNS activity (26); those individuals in the upper decile for fasting plasma glucose and/or insulin level excreted more NE over a 24 hour period than those in the lower deciles for these variables. See text for details.…”