Omentin-1 gene expression is gender specific influenced by PPARγ

Dracheva, K. V.; Pobozheva, I.; Пантелеева, А. А.; Brovin, D. L.; Polyakova, E.; Belyeva, O; Беркович, О. А.; Баранова, Е. И.; Pchelina, Sofya; Miroshnikova, V. V.

doi:10.1016/j.atherosclerosis.2021.06.580

Cited by 1 publication

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“…Indeed, a study on adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) mice, which showed markedly decreased NAD+ concentrations in WAT, demonstrated the suppression of adiponectin activation and peroxisome proliferator-activated receptor (PPAR) signaling pathways [ 59 ]. The latter mechanism may directly stimulate the secretion of adiponectin and omentin-1 through an increase in the number of small adipocytes [ 16 , 60 ]. PPARs are also involved in the control of genes involved in anti-inflammatory and anti-oxidant pathways, which in turn may regulate adipokines secretion via reduced TNF-α and IL-6 levels [ 61 , 62 ].…”

Section: Discussionmentioning

confidence: 99%

The Effect of the Ketogenic Diet on Adiponectin, Omentin and Vaspin in Children with Drug-Resistant Epilepsy

Chyra¹,

Roczniak

Świętochowska

et al. 2022

Nutrients

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Background: Changes in adipokine secretion may be involved in the anti-epileptic effect of a ketogenic diet (KD) in drug-resistant epilepsy (DRE). Objectives: The assessment of the influence of KD on serum adiponectin, omentin-1, and vaspin in children with DRE. Methods: Anthropometric measurements (weight, height, BMI, and waist-to-hip circumference ratio) were performed in 72 children aged 3–9 years, divided into 3 groups: 24 children with DRE treated with KD, 26—treated with valproic acid (VPA), and a control group of 22 children. Biochemical tests included fasting glucose, insulin, beta-hydroxybutyric acid, lipid profile, aminotransferases activities, and blood gasometry. Serum levels of adiponectin, omentin-1 and vaspin were assayed using commercially available ELISA tests. Results: Serum levels of adiponectin and omentin-1 in the KD group were significantly higher and vaspin—lower in comparison to patients receiving VPA and the control group. In all examined children, serum adiponectin and omentin-1 correlated negatively with WHR and serum triglycerides, insulin, fasting glucose, and HOMA-IR. Vaspin levels correlated negatively with serum triglycerides and positively with body weight, BMI, fasting glucose, insulin, and HOMA-IR. Conclusion: One of the potential mechanisms of KD in children with drug-resistant epilepsy may be a modulation of metabolically beneficial and anti-inflammatory adipokine levels.

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