Recently, leptin has been shown to play a regulatory role for differentiation within the myeloid and erythroid cell lineage, whereas results of its regulatory effects on lymphocytes and related tumor cells have been contradictory. To investigate whether leptin plays a role in acute lymphoblastic leukemia (ALL), we investigated the levels of leptin in plasma with enzyme-linked immunosorbent assays and the expression of the leptin receptor on malignant lymphoblasts with reverse transcriptase polymerase chain reaction (RT-PCR). At diagnosis, the leptin levels of bone marrow-derived plasma in children with ALL were found to be significantly lower than the levels of healthy control subjects (0.92 +/- 0.79 ng/mL versus 3.01 +/- 2.27 ng/mL, respectively). Notably, at complete hematologic remission (at day 33 of chemotherapy), leptin levels had normalized to 2.6 +/- 2.4 ng/mL. To elucidate the underlying mechanism of this phenomenon, we analyzed the expression of the leptin receptor on the mononuclear cell populations of the patients. RT-PCR analysis revealed gene expression rates of 33% at diagnosis versus 71% at remission, compared with 100% for healthy control subjects. Results of immunohistochemical staining supported these findings by showing that the tumor clones themselves do not express the leptin receptor. Finally, some hypotheses that might explain the decrease of leptin levels in the presence of the tumor clone are discussed.
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Front Biosci (Landmark Ed)
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University of Hospital Würzburg, 97080 Würzburg, Germany.
Background: The inheritance of the short allele, encoding the serotonin transporter (SERT) in humans, increases susceptibility to neuropsychiatric and metabolic disorders, with aging and female sex further exacerbating these conditions. Both central and peripheral mechanisms of the compromised serotonin (5-HT) system play crucial roles in this context. Previous studies on SERT-deficient (Sert) mice, which model human SERT deficiency, have demonstrated emotional and metabolic disturbances, exacerbated by exposure to a high-fat Western diet (WD).
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Laboratory of Neuroendocrinology and In Situ Hybridization, Department of Anatomy, Histology and Embryology, Semmelweis University, H1094 Budapest, Hungary.
The ability to reproduce depends on metabolic status. In rodents, the ventral premammillary nucleus (PMv) integrates metabolic and reproductive signals. While leptin (adiposity-related) signaling in the PMv is critical for female fertility, male reproductive functions are strongly influenced by glucose homeostasis.
View Article and Find Full Text PDFBiomolecules
December 2024
Research Department, Royal College of Surgeons of Ireland, Adliya, Busaiteen 15503, Bahrain.
Objective: Polycystic ovary syndrome (PCOS) is a prevalent metabolic disorder with an increased risk for cardiovascular disease (CVD) that is enhanced by obesity. This study sought to determine whether a panel of cardiovascular risk proteins (CVRPs) would be dysregulated in overweight/obese PCOS patients, highlighting potential biomarkers for CVD in PCOS.
Methods: In this exploratory cross-sectional study, plasma levels of 54 CVRPs were analyzed in women with PCOS (n = 147) and controls (n = 97).
PLoS One
January 2025
Department of Nutritional Physiology, National Institute of Medical and Nutritional Sciences "Salvador Zubirán", Mexico City, Mexico.
Childhood obesity increases the risk of developing metabolic diseases in adulthood, since environmental stimuli during critical windows of development can impact on adult metabolic health. Studies demonstrating the effect of prepubertal diet on adult metabolic disease risk are still limited. We hypothesized that a prepubertal control diet (CD) protects the adult metabolic phenotype from diet-induced obesity (DIO), while a high-fat diet (HFD) would predispose to adult metabolic alterations.
View Article and Find Full Text PDFDent J (Basel)
December 2024
Oral Biology & Diagnostic Sciences, Dental College of Georgia, Augusta University, Augusta, GA 30912, USA.
The incidence of obesity has dramatically increased worldwide. Obesity has been shown to exacerbate the progression of periodontal disease. Studies suggest a sex difference in periodontitis, whereby males are more sensitive to periodontal inflammation compared to females.
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