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Abstract:
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Perinatal stress may cause metabolic and hormonal disruptions during adulthood. The aim of this study was to
evaluate the effects of early postnatal nociceptive stimulation (NS) on body weight and other metabolic parameters
during adulthood and to determine whether CB1 endocannabinoid receptors (CB1Rs) may be involved in these effects.
Male mice were subjected to NS during lactation with a daily subcutaneous injection of saline solution. Subsequently,
both control and NS-mice were treated from day 40 to 130, with an oral dose (1 μg/g body weight) of SR141716A,
a specific CB1R antagonist/inverse agonist. Mice body weight and food intake was periodically evaluated. Adult
animals were then killed to evaluate epididymal fat pads and metabolic parameters. NS did not influence food intake
in adult animals, but caused significant increases in body weight, epididymal fat pads, and circulating levels of leptin,
corticosterone, and triglycerides (TGs). Chronic treatment with SR141716A normalized these parameters, with the
exception of corticosterone levels. This treatment also reduced plasma levels of glucose, insulin, and total cholesterol
in both adult control and NS-mice. In addition, fatty acid (FA) amide hydrolase (FAAH) activity (the enzyme able to
hydrolyze endocannabinoids) from liver and epididymal fat of adult NS-mice was decreased by 40–50% in comparison
to activities found in same tissues of control mice. Results suggest that overactive liver and epididymal fat CB1R due
to early NS may be involved in late metabolic alterations, which are sensitive to chronic treatment with SR141716A. |