Rapid weight loss can increase the risk of acute kidney injury in wrestlers

Objective Restrictive diets, forced starvation or voluntary weight loss are attracting more and more attention from scientists. Overall trends show that about 80% of combat sports athletes use specific methods of reducing body mass. Rapid weight loss could be a risk factor for kidney-related adverse outcomes. This study aimed to examine the impact of high-intensity specific training combined with rapid weight loss in the first and without rapid weight loss in the second phases on body composition and biochemical markers of kidney function. Methods The study was conducted on 12 male wrestlers. Kidney function markers were measured, including blood urea nitrogen, serum creatinine, uric acid and serum Cystatin-C. Alterations in analysed markers were noted in both phases of the research. Results According to the data, a significant increase was noted in blood urea nitrogen (p=0.002), uric acid (p=0.000) and serum creatinine (p=0.006) during the first phase in comparison with the second phase. The levels of serum Cystatin-C were slightly elevated after both phases compared with the initial measurement. Conclusion It is evident that high-intensity specific training combined with rapid weight loss significantly affects the increase in kidney function markers compared with identical training without rapid weight loss. The findings in this study suggest that rapid body mass reduction is associated with an increased risk of acute kidney injury in wrestlers

IGFBP3 Colocalizes with and Regulates Hypocretin (Orexin)

Background: The sleep disorder narcolepsy is caused by a vast reduction in neurons producing the hypocretin (orexin) neuropeptides. Based on the tight association with HLA, narcolepsy is believed to result from an autoimmune attack, but the cause of hypocretin cell loss is still unknown. We performed gene expression profiling in the hypothalamus to identify novel genes dysregulated in narcolepsy, as these may be the target of autoimmune attack or modulate hypocretin gene expression. Methodology/Principal Findings: We used microarrays to compare the transcriptome in the posterior hypothalamus of (1) narcoleptic versus control postmortem human brains and (2) transgenic mice lacking hypocretin neurons versus wild type mice. Hypocretin was the most downregulated gene in human narcolepsy brains. Among many additional candidates, only one, insulin-like growth factor binding protein 3 (IGFBP3), was downregulated in both human and mouse models and coexpressed in hypocretin neurons. Functional analysis indicated decreased hypocretin messenger RNA and peptide content, and increased sleep in transgenic mice overexpressing human IGFBP3, an effect possibly mediated through decrease

Upregulation of Insulin-Like Growth Factor Binding Protein 3 in Astrocytes of Transgenic Mice That Express Borna Disease Virus Phosphoprotein▿†

In a previous study, we demonstrated that transgenic mice that express Borna disease virus (BDV) phosphoprotein (P) in astrocytes show striking neurobehavioral abnormalities resembling those in BDV-infected animals. To understand the molecular disturbances induced by the expression of P in astrocytes, we performed microarray analysis with cultured astroglial cells transiently expressing P. We showed that expression of insulin-like growth factor binding protein 3 mRNA increases not only in P-expressing cultured cells but also in astrocytes from the cerebella of P transgenic mice (P-Tg). Furthermore, we demonstrated that insulin-like growth factor signaling is disturbed in the P-Tg cerebellum, a factor that might be involved in the increased vulnerability of Purkinje cell neurons in the brain