This study provides the largest, so far, hypothesis-generating evidence for a putative positive risk/benefit ratio for treatment of obese patients with type 2 diabetes mellitus with the DJBL as an alternative treatment option for this patient population.

In diet‐induced obese rats, leptin‐mediated natural killer (NK) cell activation has been demonstrated to be impaired by abrogated intracellular JAK2‐STAT3 signaling. The contribution of the obese microenvironment to this NK cell dysfunction and its reversibility remains elusive. In this study, the functions of NK cells from diet‐induced obese rats after adoptive transfer into lean littermates were investigated using in vivo and in vitro approaches. Endogenous NK cells of normal‐weight and diet‐induced obese F344 rats were depleted in vivo. Then, NK cells from either normal‐weight or obese donors were transferred. The numbers of peripheral blood NK cells were analyzed by fluorescence‐activated cell sorting (FACS) and the distribution pattern of NK cells in lung and spleen by immunohistochemistry. Ob‐R expression was evaluated by immunohistology and activation of intracellular target proteins of Ob‐R by immunoblotting. The numbers of NK cells in blood and lung were significantly higher in obese animals compared to lean ones after transfer of NK cells from obese F344 rats. This was correlated with increased postreceptor signaling (JAK‐2p, PKBpT308, ERK‐2p) without altered Ob‐R expression in those NK cells transferred to lean (ob→nw) vs. obese (ob→ob) animals. These results show for the first time that the altered phenotype of NK cells from obese rats can be normalized by generation of a physiological (metabolic) environment of lean rats.

According to our data, suicidality seems to be a substantial problem in primary care patients with somatoform disorders. Dysfunctional illness perceptions may play a vital role in the understanding and management of active suicidal ideation in these patients, in addition to more established factors.