MONDAY, Oct. 29 (HealthDay News) -- Prevention of the allostatic overload that auto-perpetuates obesity requires early genetic intervention, according to an experimental study published online Oct. 24 in the Journal of Clinical Investigation.
Noting that in many obese patients, after an initial period of weight loss, continued weight loss ceases and weight rebounds, Viviana F. Bumaschny, M.D., from the Consejo Nacional de Investigaciones Científicas y Técnicas in Buenos Aires, Argentina, and colleagues challenged the hypothesis that chronic weight gain induces an allostatic regulatory state that defends a supranormal adipose mass. A reversible genetic mouse model of early-onset hyperphagia and severe obesity was generated by selectively blocking expression of the proopiomelanocortin gene (Pomc) in hypothalamic neurons.
The researchers found that, in these obesity-programmed mice, eutopic reactivation of central POMC transmission at different stages of obesity progression normalized or reduced food intake. Rescue of hypothalamic Pomc lessened associated comorbidities such as hyperglycemia, hyperinsulinemia, and hepatic steatosis, and restored normal locomotor activity. As the level of obesity at the time of Pomc induction increased, the effectiveness of treatment to normalize body weight and adiposity decreased progressively.
"In conclusion, our findings show that obesity is a self-perpetuating condition and reinforce the importance of early consultation and weight management in children to prevent obesity, especially when taking into account that the probability of adult obesity exceeds 50 percent in people who were overweight at 6 years of age," the authors write.
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