In this manuscript, the authors described that expression of deltaFosB was increased in the thoracic IML, in the TH cells of the RVLM and AP and in the CRH cells in the PVN in Zucker diabetic fatty rats, and that delataFosB expression was decreased in the POMC cells of the ARC. The authors concluded that increased activation of the IML is likely driven by RVLM activated by inputs from the PVN, NTS and AP. However, no evidences suggesting causal relationships between activities in PVN, ARC, NTS and IML were shown. It is not certain whether activated cells in the PVN or NTS really projected to the IML. Mechanisms underlying increased cardiac sympathetic nerve activity in type 2 diabetes mellitus are very interesting topics.
Although the data are interesting, cautious interpretation concerning increased deltaFosB expression is necessary. Relationship between increased activity and cardiac autonomic neuropathy is also not clear.
Following points should be considered carefully.

1 line 309: Were heart rate and blood pressure measured? Bradycardia and hypertension were found in this study? Was really blood pressure increased in these animals to induce decreased heart rate? Is there any evidence suggesting increased cardiac output?
 line320-322: CRH in the peripheral blood may be originated mainly not from the median eminence. Previous data of low CRH concentrations in the plasma do not necessarily suggest that activated CRH cells in the present study are pre-sympathetic.