scholarly journals Enhanced GIP Secretion in Obesity Is Associated with Biochemical Alteration and miRNA Contribution to the Development of Liver Steatosis

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 476
Author(s):  
Joanna Góralska ◽  
Urszula Raźny ◽  
Anna Polus ◽  
Agnieszka Dziewońska ◽  
Anna Gruca ◽  
...  
Keyword(s):  
Odds Ratio ◽  
Liver Steatosis ◽  
Potential Contribution ◽  
Fibroblast Growth ◽  
Epigenetic Factors ◽  
Cytokeratin 18 ◽  
Biochemical Alteration ◽  
Fatty Liver Index ◽  
Fatty Acids Metabolism ◽  
Expression Pathways

Nutrient excess enhances glucose-dependent insulinotropic polypeptide (GIP) secretion, which may in turn contribute to the development of liver steatosis. We hypothesized that elevated GIP levels in obesity may affect markers of liver injury through microRNAs. The study involved 128 subjects (body mass index (BMI) 25–40). Fasting and postprandial GIP, glucose, insulin, and lipids, as well as fasting alanine aminotransferase (ALT), γ-glutamyltransferase (GGT), cytokeratin-18, fibroblast growth factor (FGF)-19, and FGF-21 were determined. TaqMan low density array was used for quantitative analysis of blood microRNAs. Fasting GIP was associated with ALT [β = 0.16 (confidence interval (CI): 0.01–0.32)], triglycerides [β = 0.21 (95% CI: 0.06–0.36], and FGF-21 [β = 0.20 (95%CI: 0.03–0.37)]; and postprandial GIP with GGT [β = 0.17 (95%CI: 0.03–0.32)]. The odds ratio for elevated fatty liver index (>73%) was 2.42 (95%CI: 1.02–5.72) for high GIP versus low GIP patients. The miRNAs profile related to a high GIP plasma level included upregulated miR-136-5p, miR-320a, miR-483-5p, miR-520d-5p, miR-520b, miR-30e-3p, and miR-571. Analysis of the interactions of these microRNAs with gene expression pathways suggests their potential contribution to the regulation of the activity of genes associated with insulin resistance, fatty acids metabolism, and adipocytokines signaling. Exaggerated fasting and postprandial secretion of GIP in obesity are associated with elevated liver damage markers as well as FGF-21 plasma levels. Differentially expressed microRNAs suggest additional, epigenetic factors contributing to the gut–liver cross-talk.

scholarly journals Initiation of Conceptus Elongation Coincides with an Endometrium Basic Fibroblast Growth Factor (FGF2) Protein Increase in Heifers

2020 ◽  
Vol 21 (5) ◽  
pp. 1584 ◽  
Author(s):  
Daniel Chiumia ◽  
Katy Schulke ◽  
Anna E. Groebner ◽  
Nadine Waldschmitt ◽  
Horst-Dieter Reichenbach ◽  
...  
Keyword(s):  
Growth Factors ◽  
Fibroblast Growth Factors ◽  
Transcript Abundance ◽  
Potential Contribution ◽  
Protein Abundance ◽  
Fibroblast Growth ◽  
Mrna Transcript ◽  
Pregnancy Status ◽  
A Minor

Fibroblast growth factors (FGF) play an important role during embryo development. To date, the role of FGF and the respective receptors (FGFR) during the preimplantation phase in cattle are not fully characterized. We examined FGF1, FGF2, FGFR1, FGFR2, and FGFR3 in cyclic and early pregnant heifers at Days 12, 15, and 18 after insemination (Day 0). Endometrial FGF1 mRNA transcript abundance in heifers varied significantly with respect to the day after insemination, the pregnancy status, and their interaction. The expression was higher in nonpregnant than in pregnant heifers at Day 18. The conceptus transcripts abundance of FGFR2 and FGFR3 were significantly lower at Day 15 than 18. In the endometrium, FGF1 protein abundance significantly decreased from Day 12 onwards and FGF2 protein abundance showed a minor, but a significant increase at Day 15 in comparison to Days 12 and 18. We concluded that the decrease in FGF1 mRNA expression in pregnant heifers at Day 18 points towards a potential contribution of FGF1 in the preimplantation process. Additionally, successful embryo elongation might require a spatiotemporal FGF2 protein increase in the endometrium.

scholarly journals Endocan: A Biomarker for Hepatosteatosis in Patients with Metabolic Syndrome

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Hande Erman ◽  
Engin Beydogan ◽  
Seher Irem Cetin ◽  
Banu Boyuk
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Liver ◽  
Liver Steatosis ◽  
Cutoff Point ◽  
Healthy Controls ◽  
Roc Curve Analysis ◽  
Cross Sectional ◽  
Nonalcoholic Fatty Liver ◽  
Fatty Liver Index ◽  
Hepatic Steatosis Index

Background. Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases, which has recently been mentioned as an independent cardiovascular risk factor. Objectives. Endocan is a novel molecule of endothelial dysfunction. We aimed to evaluate the associations of serum endocan levels with the hepatic steatosis index (HSI), fatty liver index (FLI), and degrees of hepatosteatosis in patients with metabolic syndrome with NAFLD. Design and Setting. This cross-sectional prospective study was performed in the outpatient clinic of an internal medicine department. Methods. The study included 40 patients with metabolic syndrome with NAFLD as noted using hepatic ultrasound and 20 healthy controls. Secondary causes of fatty liver were excluded. FLI and HSI calculations were recorded. Serum endocan level values were obtained after overnight fasting. Results. Higher values of HSI and FLI were found in the NAFLD groups than in the control groups (p<0.001). Five (12.5%) of 20 patients with liver steatosis had grade 1 liver steatosis, 15 (37.5%) patients had grade 2 liver steatosis, and 20 (50%) patients had grade 3 liver steatosis. Serum endocan levels were lower in patients with NAFLD compared with the healthy controls (146.56±133.29 pg/mL vs. 433.71±298.01 pg/mL, p<0.001). ROC curve analysis suggested that the optimum endocan value cutoff point for NAFLD was 122.583 pg/mL (sensitivity: 71.79%, specificity: 90%, PPV: 93.3%, and NPV: 62.1%). Conclusion. Serum endocan concentrations are low in patients with NAFLD, and the optimum cutoff point is 122.583 pg/mL. HSI and FLI were higher in patients with NAFLD; however, there was no correlation with serum endocan.

scholarly journals Elevated intracellular level of basic fibroblast growth factor correlates with stage of chronic lymphocytic leukemia and is associated with resistance to fludarabine

Blood ◽  
1996 ◽  
Vol 87 (3) ◽  
pp. 1056-1063 ◽  
Author(s):  
T Menzel ◽  
Z Rahman ◽  
E Calleja ◽  
K White ◽  
EL Wilson ◽  
...  
Keyword(s):  
Growth Factor ◽  
High Risk ◽  
Chronic Lymphocytic Leukemia ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Lymphocytic Leukemia ◽  
Potential Contribution ◽  
Fibroblast Growth ◽  
High Risk Disease ◽  
Cellular Source

Chronic lymphocytic leukemia (CLL) is characterized by delayed senescence and slow accumulation of monoclonal, small lymphocytes. Basic fibroblast growth factor (bFGF) is a pleiotropic cytokine that plays a role in hematopoiesis and apoptosis. Elevated bFGF levels have been detected in urine from patients with a variety of neoplastic diseases including various leukemias; however, the cellular source of the bFGF has not been determined. In this study, the intracellular bFGF level in lymphocytes of 36 patients with B-CLL and 15 normal donors was determined using an enzyme-linked immunoassay. In cells derived from patients with high-risk disease, the median level of intracellular bFGF was 381.5 pg/2 x 10(5) cells, compared with a median of 90.5 pg/2 x 10(5) cells in patients with intermediate disease. In patients with low- risk disease, the median bFGF level was 4.9 pg/2 x 10(5) cells, and in normal controls, it was 6.0 pg/2 x 10(5) cells. The difference in the bFGF levels was significant for the comparison between low- and intermediate-risk (P = .00119), low- and high-risk (P < .0001), and intermediate- and high-risk disease (P = .0001). Immunofluorescent stains of peripheral blood mononuclear cells confirmed CLL lymphocytes as a cellular source of bFGF. To evaluate the potential contribution of elevated intracellular bFGF levels to the phenotype of CLL cells, leukemic cells were cultured in vitro with an apoptotic stimulus (fludarabine). CLL cells with high intracellular levels of bFGF appeared to be more resistant to fludarabine treatment. The addition of bFGF to fludarabine-treated CLL cells resulted in a delay of apoptosis and prolonged survival. These data suggest that bFGF may contribute to the resistance of CLL cells to an apoptotic stimulus.

scholarly journals The value of the triglyceride-glucose index in the diagnosis of insulin resistance in early forms of non-alcoholic fatty liver disease

2021 ◽  
pp. 43-48
Author(s):  
A. A. Shipovskaya ◽  
N. A. Larina ◽  
I. V. Kurbatova ◽  
O. P. Dudanova
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Cytokeratin 18 ◽  
Alcoholic Fatty Liver ◽  
Triglyceride Glucose Index ◽  
Tnf Α ◽  
Alcoholic Fatty Liver Disease

The goal. To determine the value of the triglyceride glucose index (TGI) for the diagnosis of insulin resistance (IR) in early forms of non-alcoholic fatty liver disease (NAFLD).Materials and methods. 99 patients with NAFLD were examined: 38 (38.4%) with liver steatosis (LS) and 61 (61.6%) with steatohepatitis (SH). TGI was determined by the formula — In [fasting TG (mg / dl) × fasting glucose (mg / dl) / 2], patients with LS and SH were divided into quartiles (Q1-Q4) by increasing TGI levels with an assessment of liver tests, insulin levels (“Insulin TEST System”, Monobind Inc., USA), HOMA-IR, fragments of cytokeratin-18 (FCK-18) ("TPS ELISA, Biotech”, Sweden) and TNF-α (“Human TNFα Platinum” ELISA, eBioscience, Austria).Results. In patients with LS with a TGI increase from Q1 to Q4, HOMA-IR increased from 1.12 ± 0.48 to 6.02 ± 3.15 (p <0.05), a direct relationship was found between these indicators — r = 0.52 (p = 0.03). TGI also correlated with waist circumference — r = 0.81 (p = 0.01), cholesterol — r = 0.51 (p = 0.002), alkaline phosphatase — r = 0.41 (p = 0.02). In patients with SH, from Q1 to Q4, HOMA-IR increased from 3.15 ± 1.8 to 6.2 ± 3.04 (p <0.05), but there was no significant correlation between HOMA-IR and TGI. The levels of FCK-18 increased from Q1 to Q4-139.82 ± 72.45 to 359.75 ± 189.03 U / L (p <0.05) and TNF-α — from 6.38 ± 1.25 pg / ml up to 7.75 ± 1.09 pg / ml (p <0.05). There was a connection between TGI and the level of a marker of hepatocyte apoptosis — FCK-18 — r = 0.43 (p = 0.004).Conclusion. In liver steatosis, TGI has demonstrated its diagnostic role as a surrogate marker of insulin resistance, correlating with HOMA-IR. In steatohepatitis, TGI reflected the degree of hepatocytic apoptosis, correlating with fragments of cytokeratin-18.

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