We investigated leptin effects on lymphocyte interactions with hepatic-stellate-cells (HSCs). Leptin showed pro-fibrotic effects on HSCs with oxidative status imbalance. In co-cultures, leptin activates HSCs and consequently adhered HCV-lymphocytes more than healthy ones. Leptin also increased healthy and HCV lymphocyte proliferations; increased their reactive-oxygen-species; decreased antioxidants (reduced-glutathione) levels while inhibited apoptosis only of HCV-lymphocytes. The leptin-treated HCV-lymphocytes activated HSCs, increase interleukin-4 while decreased their apoptosis. Leptin-receptor-deficient (db-db)-HSCs did not adhere lymphocytes. db/db-lymphocytes however showed fewer adherences to HSCs when compared to WT-counterparts. This study presents immune and oxidative modulatory effects of leptin on lymphocytes and their consequent interaction with HSCs.
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http://dx.doi.org/10.1016/j.mito.2012.10.012 | DOI Listing |
Mitochondrial retrograde signaling (MRS) pathways relay the functional status of mitochondria to elicit homeostatic or adaptive changes in nuclear gene expression. Budding yeast have "intergenomic signaling" pathways that sense the amount of mitochondrial DNA (mtDNA) independently of oxidative phosphorylation (OXPHOS), the primary function of genes encoded by mtDNA. However, MRS pathways that sense the amount of mtDNA in mammalian cells remain poorly understood.
View Article and Find Full Text PDFJ Bacteriol
January 2025
Institute for Microbiology, Martin Luther University Halle-Wittenberg, Halle (Saale), Saxony-Anhalt, Germany.
Formic acid is an important source of reductant and energy for many microorganisms. Formate is also produced as a fermentation product, e.g.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Xicheng District, Beijing, China.
Alzheimer's disease (AD) is a degenerative disease characterized by progressive cognitive dysfunction. The strong link between nutrition and the occurrence and progression of AD pathology has been well documented. Poor nutritional status accelerates AD progress by potentially aggravating amyloid beta (Aβ) and tau deposition, exacerbating oxidative stress response, modulating the microbiota-gut-brain axis, and disrupting blood-brain barrier function.
View Article and Find Full Text PDFBackground: Childhood obesity and the rate of its spread is a serious threat to the reproductive health of the nation, especially among boys, being a background for delaying sexual development and further disrupting fertility.
Aim: To study the peculiarities of the ratio of the level of leptin and a number of toxic and essential chemical trace elements in biological environments in adolescent boys aged 13-14 years with obesity and delayed sexual development.
Materials And Methods: Three groups of adolescents aged 13-14 years were studied and formed: the main ones - with constitutional exogenous obesity of 1-2 degrees (1-20 boys without secondary signs of puberty; 2 - 24 boys with 2-4 stages of puberty according to Tanner) and comparisons (3 - 15 boys with normal body weight and without deviations in puberty).
Myc hyperactivation coordinately regulates numerous metabolic processes to drive lymphomagenesis. Here, we elucidate the temporal and functional relationships between the medley of pathways, factors, and mechanisms that cooperate to control redox homeostasis in Myc-overexpressing B cell lymphomas. We find that Myc overexpression rapidly stimulates the oxidative pentose phosphate pathway (oxPPP), nucleotide synthesis, and mitochondrial respiration, which collectively steers cellular equilibrium to a more oxidative state.
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