Anna Lenartowicz
Research Subjects
Anna Lenartowicz has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Alina Kuryłowicz
Department of Human Epigenetics, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland
1 shared publication - Artur Binda
Department of General, Oncological and Bariatric Surgery, Medical Centre of Postgraduate Education, 00-401 Warsaw, Poland
1 shared publication - Bartłomiej Noszczyk
Department of Plastic Surgery, Medical Centre of Postgraduate Education, 00-401 Warsaw, Poland
1 shared publication - Jakub Podraza
The Faculty of Biology and Biotechnology, Warsaw University of Life Sciences, 02-787 Warsaw, Poland
1 shared publication - Klaudia Gutowska
II Department of Obstetrics and Gynecology, Warsaw Medical University, 00-315 Warsaw, Poland
1 shared publication - Marta Izabela Jonas
Department of Human Epigenetics, Mossakowski Medical Research Centre, Polish Academy of Sciences, 02-106 Warsaw, Poland
1 shared publication
Latest Publications
- Open Access
- 7 May 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (10) , 5058
The Role of microRNA in the Regulation of Cortisol Metabolism in the Adipose Tissue in the Course of Obesity
The similarity of the clinical picture of metabolic syndrome and hypercortisolemia supports the hypothesis that obesity may be associated with impaired expression of genes related to cortisol action and metabolism in adipose tissue. The expression of genes encoding the glucocorticoid receptor alpha (GR), cortisol metabolizing enzymes (HSD11B1, HSD11B2, H6PDH), and adipokines, as well as selected microRNAs, was measured by real-time PCR in adipose tissue from 75 patients with obesity, 19 patients following metabolic surgery, and 25 normal-weight subjects. Cortisol levels were analyzed by LC-MS/MS in 30 pairs of tissues. The mRNA levels of all genes studied were significantly (p < 0.05) decreased in the visceral adipose tissue (VAT) of patients with obesity and normalized by weight loss. In the subcutaneous adipose tissue (SAT), GR and HSD11B2 were affected by this phenomenon. Negative correlations were observed between the mRNA levels of the investigated genes and selected miRNAs (hsa-miR-142-3p, hsa-miR-561, and hsa-miR-579). However, the observed changes did not translate into differences in tissue cortisol concentrations, although levels of this hormone in the SAT of patients with obesity correlated negatively with mRNA levels for adiponectin. In conclusion, although the expression of genes related to cortisol action and metabolism in adipose tissue is altered in obesity and miRNAs may be involved in this process, these changes do not affect tissue cortisol concentrations.
- 7 May 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 25 (10) , 5058
Open AccessThe Role of microRNA in the Regulation of Cortisol Metabolism in the Adipose Tissue in the Course of Obesity
The similarity of the clinical picture of metabolic syndrome and hypercortisolemia supports the hypothesis that obesity may be associated with impaired expression of genes related to cortisol action and metabolism in adipose tissue. The expression of genes encoding the glucocorticoid receptor alpha (GR), cortisol metabolizing enzymes (HSD11B1, HSD11B2, H6PDH), and adipokines, as well as selected microRNAs, was measured by real-time PCR in adipose tissue from 75 patients with obesity, 19 patients following metabolic surgery, and 25 normal-weight subjects. Cortisol levels were analyzed by LC-MS/MS in 30 pairs of tissues. The mRNA levels of all genes studied were significantly (p < 0.05) decreased in the visceral adipose tissue (VAT) of patients with obesity and normalized by weight loss. In the subcutaneous adipose tissue (SAT), GR and HSD11B2 were affected by this phenomenon. Negative correlations were observed between the mRNA levels of the investigated genes and selected miRNAs (hsa-miR-142-3p, hsa-miR-561, and hsa-miR-579). However, the observed changes did not translate into differences in tissue cortisol concentrations, although levels of this hormone in the SAT of patients with obesity correlated negatively with mRNA levels for adiponectin. In conclusion, although the expression of genes related to cortisol action and metabolism in adipose tissue is altered in obesity and miRNAs may be involved in this process, these changes do not affect tissue cortisol concentrations.