Estrogen affects adipose tissue function. Therefore, this study aimed at assessing changes in the transcriptional activity of estrogen receptor (ER) α and β genes (ESR1 and ESR2, respectively) in the adipose tissues of obese individuals before and after weight loss and verifying whether epigenetic mechanisms were involved in this phenomenon. ESR1 and ESR2 mRNA and miRNA levels were evaluated using real-time PCR in visceral (VAT) and subcutaneous adipose tissue (SAT) of 78 obese (BMI > 40 kg/m²) and 31 normal-weight (BMI = 20–24.9 kg/m²) individuals and in 19 SAT samples from post-bariatric patients. ESR1 and ESR2 methylation status was studied using the methylation-sensitive digestion/real-time PCR method. Obesity was associated with a decrease in mRNA levels of both ERs in SAT (p < 0.0001) and ESR2 in VAT (p = 0.0001), while weight loss increased ESR transcription (p < 0.0001). Methylation levels of ESR1 and ESR2 promoters were unaffected. However, ESR1 mRNA in the AT of obese subjects correlated negatively with the expression of hsa-miR-18a-5p (r_s = −0.444), hsa-miR-18b-5p (r_s = −0.329), hsa-miR-22-3p (r_s = −0.413), hsa-miR-100-5p (r_s = −0.371), and hsa-miR-143-5p (r_s = −0.289), while the expression of ESR2 in VAT correlated negatively with hsa-miR-576-5p (r_s = −0.353) and in SAT with hsa-miR-495-3p (r_s = −0.308). In conclusion, obesity-associated downregulation of ER mRNA levels in adipose tissue may result from miRNA interference.

Loss of physiological nocturnal blood pressure (BP) decline is an independent predictor of cardiovascular risk and mortality. The aim of the study was to investigate the influence of body composition and fat distribution on 24-hour BP pattern and nocturnal dipping of mean arterial pressure (MAP) in patients with obesity. The study comprised 436 patients, 18 to 65 years old (306 women), with BMI ≥30 kg/m². Body composition was assessed with dual-energy X-ray absorptiometry (DXA) and blood pressure was assessed by 24-hour BP monitoring. The prevalence of hypertension was 64.5% in patients with BMI <40 kg/m² and increased to 78.7% in individuals with BMI ≥50 kg/m² (p = 0.034). The whole-body DXA scans showed that the hypertensive patients were characterized by a greater lean body mass (LBM) and a higher abdominal-fat-to-total-fat-mass ratio (AbdF/FM), while the normotensive participants had greater fat mass, higher body fat percentage and more peripheral fat. Loss of physiological nocturnal MAP decline was diagnosed in 50.2% of the patients. The percentage of non-dippers increased significantly: from 38.2% in patients with BMI <40 kg/m² to 50.3% in those with BMI 40.0–44.9 kg/m², 59.0% in patients with BMI 45.0–49.9 kg/m², 71.4% in those with BMI 50.0–54.9 kg/m² and 83.3% in patients with BMI ≥55 kg/m² (p = 0.032, p = 0.003, p<0.001, and p = 0.002 vs. BMI <40 kg/m², respectively). The multivariable regression analysis showed that patients at the highest quartiles of body weight, BMI, LBM and AbdF/FM had significantly reduced nocturnal MAP dipping compared with patients at the lowest quartiles, respectively.

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.

The advanced glycosylation end-product receptor (AGER) is involved in the development of metabolic inflammation and related complications in type 2 diabetes mellitus (T2DM). Tissue expression of the AGER gene (AGER) is regulated by epigenetic mediators, including a long non-coding RNA AGER-1 (lncAGER-1). This study aimed to investigate whether human obesity and T2DM are associated with an altered expression of AGER and lncAGER-1 in adipose tissue and, if so, whether these changes affect the local inflammatory milieu. The expression of genes encoding AGER, selected adipokines, and lncAGER-1 was assessed using real-time PCR in visceral (VAT) and subcutaneous (SAT) adipose tissue. VAT and SAT samples were obtained from 62 obese (BMI > 40 kg/m²; N = 24 diabetic) and 20 normal weight (BMI = 20–24.9 kg/m²) women, while a further 15 SAT samples were obtained from patients who were 18 to 24 months post-bariatric surgery. Tissue concentrations of adipokines were measured at the protein level using an ELISA-based method. Obesity was associated with increased AGER mRNA levels in SAT compared to normal weight status (p = 0.04) and surgical weight loss led to their significant decrease compared to pre-surgery levels (p = 0.01). Stratification by diabetic status revealed that AGER mRNA levels in VAT were higher in diabetic compared to non-diabetic women (p = 0.018). Elevated AGER mRNA levels in VAT of obese diabetic patients correlated with lncAGER-1 (p = 0.04, r_s = 0.487) and with interleukin 1β (p = 0.008, r_s = 0.525) and resistin (p = 0.004, r_s = 0.6) mRNA concentrations. In conclusion, obesity in women is associated with increased expression of AGER in SAT, while T2DM is associated with increased AGER mRNA levels and pro-inflammatory adipokines in VAT.

Purpose: SASI (single anastomosis sleeve ileal) bypass can lead to nutritional deficiencies, including disorders of iron metabolism and anemia. This study aims to evaluate the effect of SASI bypass on weight loss, anemia, and iron deficiency in patients with obesity during the follow-up period. Methods: This study is a retrospective analysis of prospectively collected data from patients who underwent SASI bypass at our hospital between January 2020 and February 2022. Results: The mean age of the patients was 42 years (range 22–58). The average duration of the follow-up period was 26 months. The mean percentage of excess weight loss (%EWL) was 90.1%, and total weight loss (%TWL) was 30.5%. During the postoperative observation period, anemia was identified in ten patients (25%), comprising 70% with normocytic anemia, 10% with microcytic anemia, and two macrocytic anemia cases (20%). Iron deficiency was observed in two patients (5%). Conclusion: SASI bypass is an effective bariatric procedure in weight loss outcomes. However, there may be an increased risk of anemia and iron metabolism disruptions associated with this procedure. The common limb length (250 vs. 300 cm) did not significantly impact hemoglobin, iron, TIBC, ferritin levels, or anemia incidence among patients undergoing SASI bypass. The decrease in postoperative ferritin levels signifies a depletion in tissue iron reserves, thereby emphasizing the necessity for surveillance of iron homeostasis parameters following SASI bypass.

Introduction: The aim of the study is to assess the effect of shortening the excluded loop of the small intestine to 150 cm on the effectiveness of one anastomosis gastric bypass (OAGB) in remission of type 2 diabetes with I^o obesity. Material and methods: The study included 25 patients with a body mass index (BMI) 30–35 kg/m², with a diagnosis of diabetes mellitus type 2 (T2DM), and undergoing OAGB with excluded 150 cm of the small intestine. Results: There were no deaths in the study group, bleeding during the postoperative period requiring reoperation, anastomotic leakage/leakage throught mechanical stitching. The mean a glycated haemoglobin (HbA1C) level 12 months after surgery was 6.16 ± 0.96%, corresponding to a 2.29 ± 3.3% decrease. In more than 85% of the patients taking insulin before surgery, the insulin was discontinued in the postoperative period. Additionally, the level of glycaemia was assessed in patients on the day of surgery (163 ± 58 mg/dl) and on the day of discharge from the hospital (4.7 ± 1.3 days)—it was lower by over 18% (133 ± 39.2 mg). Over the period of 12 months following OAGB, there was a reduction in the mean BMI value from 33.5 ± 2 to 25.5 ± 2.5 kg/m² and improvement in lipid parameters and mean values of blood pressure. Conclusion: OAGB with excluded 150 cm of the small intestine has beneficial effect on the remission of T2DM in patients with a BMI of 30–35kg/m² and is associated with an acceptable level of complications. The achieved weight loss after surgery is satisfactory.