Abstract
Sustaining weight loss by caloric restriction invokes metabolic (decreased energy expenditure), autonomic (decreased sympathetic and increased parasympathetic nervous system tone), neuroendocrine (decreased thyroid hormones and leptin), and behavioral (increased hunger) changes that conspire to favor the regain of lost weight [1]. The similarities between this “weight-reduced phenotype” and states of congenital leptin deficiency, and the remediation of these states in response to leptin repletion, suggest that the metabolic opposition to sustained weight loss is integrated in part via leptin signaling pathways [1]. A key question is whether the neural circuitry of the hypothalamus and other brain regions that mediate these responses can be influenced by specific aspects of diet. In this issue of Molecular Metabolism, McNay and Speakman [2] suggest that the macronutrient content of the diet affects both the anatomy and function of this circuitry.
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