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Depression is a psychiatric disorder that negatively affects how a person feels, thinks, and acts. Several studies have reported a positive association between vitamin D (VD) deficiency and depression. Therefore, we aimed to examine the effects of intraperitoneal injection of VD3, fluoxetine (antidepressant), and a combination of VD3 + fluoxetine on a rat model of chronic unpredictable mild stress (CUMS). A total of 40 male Wistar rats (224-296 g) were divided into five groups ( n = 8 each) as follows: (1) the control group, (2) the CUMS group, (3) the CUMS group that received vitamin D (10 μg/kg), (4) the CUMS group that received fluoxetine (5 mg/kg), and (5) the CUMS group that received both vitamin D (10 μg/kg) and fluoxetine (5 mg/kg). The CUMS model was produced by exposing rats to frequent social and physical stressors for 21 days. In addition, blood samples were collected to determine corticosterone and serum VD levels. Also, behavioral tests were conducted, including the sucrose preference test (SPT), the forced swimming test (FST), the tail suspension test (TST), the open field test (OFT), and the elevated plus maze test (EPM). Our results show that VD3 had effects similar to fluoxetine on the depressive behavior of the rats when measured by three behavioral tests, namely SPT, FST, and OFT ( p < 0.001). Additionally, VD3 had a protective effect against depression similar to that of fluoxetine. Corticosterone levels were lower in the CUMS group that received vitamin D and the CUMS group that received both vitamin D and fluoxetine than in the CUMS group ( p < 0.000). In conclusion, VD3 has a protective effect against anxiety and depressive behaviors produced by CUMS in rats.

The energy homeostasis-associated (Enho) gene, the transcript for the Adropin peptide, is usually linked to energy homeostasis, adiposity, glycemia, and insulin resistance. Studies on Enho expression in stressful conditions are lacking. This work aimed to investigate Enho mRNA expression and energy homeostasis in acute stress (AS) versus chronic unpredictable mild stress (CUMS) rat models. A total of thirty male Wistar rats (180-220 g) were fed a balanced diet with free access to water. Rats were divided into three equal groups ( n = 10): (a) the normal control (NC) group; (b) the AS group, where one episode of stress for 2 h was applied; and (c) the CUMS group, in which rats were exposed to a variable program of mild stressors for 4 weeks. Energy homeostasis was analyzed by the PhenoMaster system for the automatic measuring of food intake (FI), respiratory O 2 volume (VO 2 ), CO 2 volume (VCO 2 ), respiratory quotient (RQ), and total energy expenditure (TEE). Finally, liver, whole brain, and adipose (WAT) tissue samples were collected, total RNA was prepared, and RT-PCR analysis of the Enho gene was performed. The CUMS group showed higher VO 2 consumption and VCO 2 production, and a higher RQ than the AS group. Furthermore, the TEE and FI were higher in the CUMS group compared to the AS group. Enho gene expression in the liver, brain, and WAT was significantly higher in the CUMS group than in the AS and NC groups. We can conclude that in the chew-fed AS rats, hypophagia was evident, with a shift in the RQ toward fat utilization, with no changes in body weight despite the increase in Enho mRNA expression in all studied tissues. In the CUMS group, the marked rise in Enho mRNA expression may have contributed to weight loss despite increased FI and TEE.

Vitamin D (VD) deficiency is frequently reported in heart transplant (HT) recipients and routinely supplemented. However, the efficacy of VD supplementation on bone mineral density (BMD) and its association with all-cause mortality is underinvestigated. The VD levels and BMD were studied for two years, and the association of VD and BMD with all-cause mortality risk was investigated. Ninety-six HT patients (38.18 ± 12.10 years old; 74% men) were followed up during VD, Ca, and Mg supplementation. Anthropometric measurements, BMD by Dual-energy X-ray absorptiometry (DEXA) scan, VD concentrations, and related biochemical parameters were analyzed before, 1 year, and 2 years after HT. Despite significant improvement of VD 3 and 25-hydroxy VD (25OHVD) levels especially in the men, BMD parameters were insignificantly changed. After 2 years, the all-cause mortality rate was 15.6%. High pretransplant levels of 25OHVD failed to improve the survival probability. Cox's regression showed a 32.7% increased hazard ratio for each unit increase in body mass index (95% CI: 1.015-1.733, p = 0.038), in the VD-deficient group rather than in the VD-sufficient one. In conclusion, VD supplementation improves the biochemical status, especially in VD-deficient HT. However, its impact on the BMD and mortality was not as usually expected. Further investigation of the disturbed VD metabolism in HT is warranted.