ABSTRACT
Major depressive disorder (MDD) increases the risk of type 2 diabetes (T2D) by 60% in untreated patients, and hypercortisolism is common in MDD as well as in some patients with T2D. Patients with MDD, despite hypercortisolism, show inappropriately normal levels of corticotropin-releasing hormone (CRH) and plasma adrenocorticotropin (ACTH) in the cerebrospinal fluid, which might implicate impaired negative feedback. Also, a positive feedback loop of the CRH-norepinephrine (NE)-CRH system may be involved in the hypercortisolism of MDD and T2D. Dysfunctional CRH receptor 1 (CRHR1) and CRH receptor 2 (CRHR2), both of which are involved in glucose regulation, may explain hypercortisolism in MDD and T2D, at least in a subgroup of patients. CRHR1 increases glucose-stimulated insulin secretion. Dysfunctional CRHR1 variants can cause hypercortisolism, leading to serotonin dysfunction and depression, which can contribute to hyperglycemia, insulin resistance, and increased visceral fat, all of which are characteristics of T2D. CRHR2 is implicated in glucose homeostasis through the regulation of insulin secretion and gastrointestinal functions, and it stimulates insulin sensitivity at the muscular level. A few studies show a correlation of the CRHR2 gene with depressive disorders. Based on our own research, we have found a linkage and association (i.e., linkage disequilibrium [LD]) of the genes CRHR1 and CRHR2 with MDD and T2D in families with T2D. The correlation of CRHR1 and CRHR2 with MDD appears stronger than that with T2D, and per our hypothesis, MDD may precede the onset of T2D. According to the findings of our analysis, CRHR1 and CRHR2 variants could modify the response to prolonged chronic stress and contribute to high levels of cortisol, increasing the risk of developing MDD, T2D, and the comorbidity MDD-T2D. We report here the potential links of the CRH system, NE, and their roles in MDD and T2D.
ABSTRACT
An integrated sensor for the measurement and monitoring of position and inclination, characterized by low cost, small size and low weight, has been designed, realized and calibrated at the Geomatics Lab of the University of Calabria. The design of the prototype, devoted to the monitoring of landslides and structures, was aiming at realizing a fully automated monitoring instrument, able to send the data acquired periodically or upon request by a control center through a bidirectional transmission protocol. The sensor can be released with different accuracy and range of measurement, by choosing bubble vials with different characteristics. The instrument is provided with a computer, which can be programmed so as to independently perform the processing of the data collected by a single sensor or a by a sensor network, and to transmit, consequently, alert signals if the thresholds determined by the monitoring center are exceeded. The bidirectional transmission also allows the users to vary the set of the monitoring parameters (time of acquisition, duration of satellite acquisitions, thresholds for the observed data). In the paper, hardware and software of the sensor are described, along with the calibration, the results of laboratory tests and of the first in field acquisitions.
ABSTRACT
Changes in total and segmental body composition were studied in 101 obese women before and 2, 6, 12, and 24 months after biliopancreatic diversion (BPD) and data 24 months after surgery were matched to 53 control subjects. The patients were studied by anthropometry, indirect calorimetry, and double-emission x-ray absorptiometry (DXA). The combination of calorimetry and body composition analysis allowed estimation of visceral and muscle lean mass. We observed a significant (analysis of variance [ANOVA]: P <.05) progressive reduction of fat and lean body mass (LBM) following BPD, with stabilization of both parameters between 12 and 24 months at levels not different from controls. Fat loss was significant in the arms, legs, and trunk segments. After 24 months, there was no significant difference in segmental fat mass between post-BPD patients and controls. Calorimetric data seem to confirm lean body mass (LBM) reduction. Visceral lean mass (kg) was significantly reduced from 8.1 +/- 2.2 in obese subjects to 6.5 +/- 1.8 in post-BPD patients at 24 months (P <.05); the control value was 7.2 +/- 1.8. Muscular lean mass (kg) was also significantly reduced, from 50.2 +/- 5.8 to 39.8 +/- 5.7 in the same subjects (P <.05), with a control value of 42.5 +/- 5.9. The decrease in muscle and visceral LBM reached control values without significant differences. Viscera/muscle ratio in pre-BPD patients was preserved in post-BPD patients at 24 months, but it was reduced during weight loss. Body composition studies showed a logarithmic relationship between fat and lean mass and a physiological contribution of lean mass to weight loss in the BPD patients. In conclusion, weight loss after BPD was achieved with an appropriate decline of LBM and with all parameters reaching, at stable weight, values similar to weight-matched controls.
