Maternal Stress, Neuropeptide Y System and the Offspring’s Vulnerability to Obesity and Metabolic Syndrome

Maternal Stress, Neuropeptide Y System and the Offspring’s Vulnerability to Obesity and Metabolic Syndrome

A recent report in the FASEB Journal indicates that Neuropeptide Y (NPY) system is a potential mediator of programming for the offspring’s vulnerability to obesity and metabolic syndrome induced by maternal low-protein diet (LPD).

According to CDC more than one-third of U.S. adults (35.7%) are obese. As stated by Ogden C. et al., 17.1% of U.S. children are now obese, and overall, up to 2/3 of children and adolescents in the United States are overweight or obese (JAMA, 2006,  295, 1549). According to Wikipedia and Forbes, United Kingdom has the most overweight population in Europe, with 22% of Britons now obese.

Obesity is a multifactorial condition. Among the ‘environmental’ factors, psychological stress may play an important role, even though this factor is often overlooked among the long list of causes related to excess weight gain. Traditionally, stress is linked to obesity through hypothalamic effects on food intake or peripherally, through catecholamine-mediated beta-adrenergic effects, or glucocorticoid and parasympathetic activity. The role of these factors in chronic stress, however, remains uncertain.

On the other hand, the adrenergic co-transmitter NPY is released primarily in conditions of prolonged activation of the sympathetic nerves, observed during chronic stress, and recent research has implicated NPY in the pathogenesis of obesity. NPY is a major component of the stress response, and often synergizes with the actions of the major stress hormones such as glucocorticoids and catecholamines.

A recent study indicates that chronic stress in mice, combined with high-fat diet (HFD), results in up-regulation of NPY and NPY2 (Y2R) receptor expression in visceral adipose tissue (VAT), where the activation of the VAT NPY-Y2R systems leads to abdominal obesity and metabolic-like syndrome (Kuo, L. et al., 2007, Nat. Med. 13, 803). Interestingly, previous research in humans and animals also indicates that maternal stress, psychosocially or metabolically, increases the risk of obesity and diabetes in the progeny.

In the FASEB study, Ruijun Han and colleagues from the Department of Integrative Biology and Physiology, Stress Physiology Center, University of Minnesota, Minneapolis, Minnesota, investigated whether the NPY system also plays a role in the programming of obesity induced by maternal LPD.

The study demonstrates that female offspring of mice fed low-protein diet (LPD) during pregnancy and lactation had lower birth weight but grew faster on HFD and developed abdominal adiposity and glucose intolerance compared to control females. This impaired metabolic phenotype was associated with elevated circulating NPY levels and up-regulation of NPY-Y2R adipogenic pathway in the visceral fat.

The authors propose that the peripheral NPY system is a mediator and a marker for adult obesity and metabolic dysfunction induced by maternal stress.

SOURCE: FASEB J. 2012, 26:3528. doi: 10.1096/fj.12-203943. Epub 2012 Apr 25.

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