Dannylo Wesley Nóbrega de Sousa - Uninove

glucose-fed rats was associated with a reduction of plasma monounsaturated fatty acids
(contributing to insulin resistance) 23 , indicating that kinin B1 receptor may be involved in
the signaling of obesity.
Obesity is a chronic mild inflammation disease linked to augmented levels of pro-
inflammatory cytokines in the circulation and peripheral tissues 24 . Adipose tissue actively
secrets a variety of adipocytokines (leptin, resistin, adiponectin, IL-1β and TNF-α) 25 that
contributes to the inflammatory process, and also are involved in appetite and satiety
signals, energy balance and energy expenditure. Dysregulation of adipose tissue-derived
IL-1β and TNF-α results in impaired insulin signaling and lipid metabolism 26 .
As kinin B1 receptor is induced and up-regulated following tissue injury, its contribution to
inflammatory states has been shown, initially mediating neutrophil migration and
infiltration of macrophages 14 . Kinin B1receptor activation on these cells causes the release
of cytokines 27 . Kinin B1 receptor antagonist reversed the infiltration of macrophages in
inflammatory tissue 28 . Macrophages represent an important source of pro-inflammatory
cytokines known to propagate and amplify the inflammatory process in adipose tissue 29 .
In addition, functional deficiency of the kinin B1 receptor can protect mice from obesity
through a mechanism that may involve leptin signaling 30 . Thus, a possible therapeutic use
of kinin B1 receptors antagonist in Cushing’s syndrome is strengthened with the results
from our study.
Conclusion
Our data suggest that chronic hypercortisolism, as seen in Cushing's syndrome is related to
the higher amount of kinin B1 receptors mRNA in VAT, the fat deposit responsible for
obesity-related complications and increased mortality. Gene expression of kinin B2
receptor remained unchanged. Based on these preliminary results, we intend now to
compare the group of patients with Cushing's syndrome with obese and nonobese subjects.
The extraction of biological material of these new groups has already been performed and
the mRNA expression analysis is being developed in our laboratory. In addition, we are not
sparing efforts to increase the number of patients with Cushing's syndrome, which will
allow a more accurate analysis of kinin B1 and B2 receptors expression in human adipose
deposits.
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