👤 Seyma Nur Ercan

This review examines the role of adipokines and gene polymorphisms in the development of depression and obesity. It is of great importance to understand the mechanisms that may be effective in the development of obesity and depression as their incidence increases. Adipokines are released from adipose tissues and primarily regulate the connection between the metabolic and inflammatory effects of obesity and the brain cells and adipose tissue. Adipokines may potentially contribute to the pathophysiology of depression by influencing the HPA axis and neurotransmitters. According to some estimates, the genetic overlap between obesity and depression is as high as 12 percent. Furthermore, these genes may be linked to significant interconnected signaling networks that have a role in the etiology of both disorders. Obesity and depression are both on the rise globally, and it is thought that there is a bidirectional relationship between these two conditions. Obesity and obesity-induced depression seriously limit the psychosocial functionality of individuals and impair their quality of life. Having a high body mass index (BMI) raises the likelihood of developing depression. On the other hand, as the BMI elevates in people suffering from depression, the possibility of developing obesity also rises. Show less

Non syndromic monogenic obesity is a rare cause of early onset severe obesity in the childhood period. This form may not be distinguishable from other forms of severe obesity without genetic analysis, particularly if patients do not exibit any physical abnormalities or developmental delay. The aim of this study was to screen 41 different obesity-related genes in children with non-syndromic early onset severe obesity. Children with severe (body mass index-standard deviation score >3) and early onset (<7 years) obesity were screened by next-generation sequencing based, targeted DNA custom panel for 41 known-obesity-related genes and the results were confirmed by Sanger technique. Six novel variants were identified in five candidate genes in seven out of 105 children with severe obesity; two in We identified six novel and four previously described variants in six obesity-related genes in 11 out of 105 childrens with early onset severe obesity. The prevalence of monogenic obesity was 10.4% in our cohort. Show less

Cyclodextrins (CD) are natural macrocyclic oligosaccharides linked by α(1,4) glycosidic bonds. Hydrophobic cavity of CDs are able to incorporate small molecules, ions, macromolecules which makes them excellent delegates for forming nanoparticulate carriers upon chemical modification to render amphiphilicity to CDs. In this study, blank 6OCaproβCD nanoparticle was prepared and administered to MCF-7 breast cancer cells. The effects of these nanoparticles on the cells were investigated in depth through biochemical and proteomic tests following 48 h of incubation. Proteomics studies revealed that apoptosis-related protein levels of hnRNP and CBX1 were increased while HDGF was not affected supporting the idea that 6OCaproβCD nanoparticles prevent cell proliferation. Gene expression studies were generally in correlation with protein levels since gene expression was significantly stimulated while protein levels were lower compared to the control group suggesting that a post-transcriptional modification must have occurred. Furthermore, 6OCaproβCD was observed to not trigger multidrug resistance as proved with RT-PCR that effectuates another exquisite characteristic of 6OCaproβCD nanoparticle as carrier of chemotherapeutic drugs. Metabolomic pathways of CD effect on MCF7 cells were elucidated with HMDB as serine biosynthesis, transmembrane transport of small molecules, metabolism of steroid hormones, estrogen biosynthesis and phospholipid biosynthesis. In conclusion, 6OCaproβCD is a promising nanoparticulate carrier for chemotherapeutic drugs with intrinsic apoptotic effect to be employed in treatment of breast cancer and further studies should be conducted in order to comprehend the exact mechanism of action. Show less