Several studies support the idea that a low RMR is associated with weight gain. A low metabolic rate has been shown to precede body weight gain in infants, children, and in adult Pima Indians and Caucasians. Based on the assumption that formerly obese, weightreduced subjects exhibit the metabolic characteristics that predisposed them to obesity, several studies have compared metabolic rates in formerly obese subjects to those of weight-matched controls who have never been obese.
A meta-analysis of 12 such studies corroborates the prospective data by demonstrating a 3–5% lower mean RMR in the formerly obese subjects. Moreover, these data indicate that a low RMR is more frequent among formerly obese subjects than among never-obese control subjects. Studies of the contribution of the sympathoadrenal activity to this trait have yielded conflicting results, probably because comparisons of lean and obese subjects provide only very limited information about the role of the SNS in the aetiology of obesity. Furthermore, they do not discern between the causes and the consequences of weight gain.
How ever, longitudinal studies both in Pima Indians and in Caucasians have shown a relationship between low urinary norepinephrine excretion and weight gain, and a relationship between low urinary epinephrine excretion and the development of central obesity.
These results strongly suggest that a low SNS activity is also a risk factor for weight gain in humans. SNS activity increases in response to weight gain, thereby attenuating the original impairment.
A meta-analysis of 12 such studies corroborates the prospective data by demonstrating a 3–5% lower mean RMR in the formerly obese subjects. Moreover, these data indicate that a low RMR is more frequent among formerly obese subjects than among never-obese control subjects. Studies of the contribution of the sympathoadrenal activity to this trait have yielded conflicting results, probably because comparisons of lean and obese subjects provide only very limited information about the role of the SNS in the aetiology of obesity. Furthermore, they do not discern between the causes and the consequences of weight gain.
How ever, longitudinal studies both in Pima Indians and in Caucasians have shown a relationship between low urinary norepinephrine excretion and weight gain, and a relationship between low urinary epinephrine excretion and the development of central obesity.
These results strongly suggest that a low SNS activity is also a risk factor for weight gain in humans. SNS activity increases in response to weight gain, thereby attenuating the original impairment.
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