Feast or Famine: The Sympathetic Nervous System Response to Nutrient Intake

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Abstract
1. The use of tritiated norepinephrine (NE) to measure the turnover rate of NE in sympathetically innervated organs was pioneered in the laboratory of Julius Axelrod. This technique provides an organ specific assessment of sympathetic activity, integrated over a 24 h period, in free living laboratory animals. As such it has proved useful in estimating changes in sympathetic outflow in different physiologic and patho-physiologic states. 2. Studies employing NE turnover techniques in laboratory rodents have demonstrated conclusively that fasting suppresses and overfeeding stimulates the sympathetic nervous system (SNS). These changes in sympathetic activity also occur in humans. 3. Diet-induced changes in SNS activity are regulated by insulin-mediated glucose uptake and metabolism in central neurons sensitive to insulin and located anatomically in the ventro-medial hypothalamus. The regulation is imposed by descending inhibition of tonically active sympathetic brainstem centers. 4. Diet-induced changes in SNS activity mediate changes in energy production known as dietary thermogenesis. The capacity for dietary thermogenesis serves as a potential buffer against weight gain. 5. Insulin stimulated SNS activity contributes to obesity-related hypertension. The insulin resistance of obesity, and consequent hyperinsulinemia, drives sympathetically mediated thermogenesis, restoring energy balance at the expense of SNS over activity. The association of obesity and hypertension, therefore, may be the unintended consequence of mechanisms recruited in the obese to limit further weight gain.