Gene Expression of Leptin, Resistin, and Adiponectin in the White Adipose Tissue of Obese Patients with Non-Alcoholic Fatty Liver Disease and Insulin Resistance

2006 ◽  
Vol 16 (9) ◽  
pp. 1118-1125 ◽  
Author(s):  
Ancha Baranova ◽  
Shobha Gowder ◽  
Karen Schlauch ◽  
Hazem Elariny ◽  
Rochelle Collantes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
White Adipose Tissue ◽  
Fatty Liver Disease ◽  
Obese Patients ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals Evaluation of potential gene expression as early markers of insulin resistance and non-alcoholic fatty liver disease in the Indonesian population

2018 ◽  
Vol 23 (2) ◽  
pp. 84
Author(s):  
Eunice Limantara ◽  
Felicia Kartawidjajaputra ◽  
Antonius Suwanto
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Model Assessment ◽  
Gene Expressions ◽  
Alcoholic Fatty Liver ◽  
Early Markers ◽  
Alcoholic Fatty Liver Disease

Early detection of insulin resistance (IR) or non-alcoholic fatty liver disease (NAFLD) is crucial to preventing future risks of developing chronic diseases. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), Liver Fat Score (LFS), and Fatty Liver Index (FLI) are generally employed to measure severity stages of IR and NAFLD. The study of gene expressions could explain the molecular mechanisms that occur early on in IR and NAFLD; thus providing potential early markers for both diseases. This study was conducted to evaluate the gene expressions that could potentially be early markers of IR and NAFLD. All participants (n = 21) had normal blood glucose and were categorized as without hepatosteatosis (n = 10), at higher risk of hepatosteatosis (n = 6), and hepatosteatosis (n = 5). Gene expression analysis was performed using the 2-∆∆CT relative quantification method. There were significant differences in galnt2 (p < 0.002) and sirt1 (p < 0.010) expression between the first and the third tertiles of HOMA-IR; and in ptpn1 (p < 0.012) expression between the first and the second tertiles of LFS. In conclusion, the expressions of galnt2 and sirt1 could be used as early markers of IR, while the expression of ptpn1 could be employed as an early marker of NAFLD.

scholarly journals Omentin-1 Levels and Non-alcoholic Fatty Liver Disease in Obese Adolescents

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Emine Turkkan ◽  
Huseyin Dag ◽  
Okan Dikker ◽  
Nevin Cetin Dag ◽  
Alper Kacar ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
Obese Patients ◽  
Alcoholic Fatty Liver ◽  
Obese Adolescents ◽  
Significant Difference ◽  
Alcoholic Fatty Liver Disease

Background: Omentin-1 is an adipocytokine secreted from visceral adipose tissue that is thought to increase insulin sensitivity. Non-alcoholic fatty liver disease (NAFLD) is a comparatively extensive problem in obese adolescents. Decreased omentin-1 levels have been reported in obese patients, but the relationship between NAFLD and omentin-1 is contradictory. Objectives: We aimed to evaluate the omentin-1 levels in the sera of obese adolescents with and without NAFLD and compare them with each other. Methods: In this study, a total of 88 adolescents (56 obese and 32 normal-weight) were enrolled. Abdominal ultrasonography (US) identified 28 obese adolescents with grade 2-3 hepatosteatosis constituting the NAFLD group and 28 without hepatosteatosis on US constituting the non-NAFLD group. The control group included 32 age- and gender-matched cases without hepatosteatosis and with normal percentile body mass index (BMI). Serum omentin-1 levels were evaluated and compared. Results: The mean age of the research group was 12.72 ± 1.91 years. Unsurprisingly, BMI, glycated hemoglobin (HbA1c), liver transaminases (AST, ALT), total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL), homeostatic model assessment for insulin resistance (HOMA-IR), and insulin rates were noticeably elevated in obese adolescents compared to controls (P < 0.05). However, omentin-1 and high-density lipoprotein cholesterol (HDL) levels were remarkably lower in the obese group (P < 0.05). No significant difference was found between the NAFLD and non-NAFLD groups regarding omentin-1, HbA1c, glucose, urea, creatinine, AST, C-reactive protein (CRP), total cholesterol, triglyceride, HDL, LDL, thyroid stimulating hormone, 25-hydroxyvitamin D3, HOMA-IR, and insulin. The BMI and ALT grades of the non-NAFLD group were notably lower than the NAFLD group (P < 0.05). While there was no significant difference between omentin-1 and other parameters in obese adolescents without NAFLD (P > 0.05), we found a significant difference between omentin-1 and BMI, AST, ALT, HOMA-IR, and insulin values in obese adolescents with NAFLD (P < 0.05). Conclusions: Omentin-1 levels were decreased in obese adolescents regardless of the presence of NAFLD. However, in obese patients with NAFLD, there was a significant difference between omentin-1 and several markers of obesity and insulin resistance.

scholarly journals Evaluation of adipose tissue and liver radiodensity in overweight or obese patients with non-alcoholic fatty liver disease

2019 ◽  
Author(s):  
Radosław Kempiński ◽  
Katarzyna Neubauer ◽  
Agnieszka Hałoń ◽  
Przemysław Podgórski ◽  
Robert Dudkowiak ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Obese Patients ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals Supplementation with a Specific Combination of Metabolic Cofactors Ameliorates Non-Alcoholic Fatty Liver Disease and, Hepatic Fibrosis, and Insulin Resistance in Mice

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3532
Author(s):  
Sergio Quesada-Vázquez ◽  
Marina Colom-Pellicer ◽  
Èlia Navarro-Masip ◽  
Gerard Aragonès ◽  
Josep M. Del Bas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Fibrosis ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Alcoholic Fatty Liver ◽  
Specific Combination ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) have emerged as the leading causes of chronic liver disease in the world. Obesity, insulin resistance, and dyslipidemia are multifactorial risk factors strongly associated with NAFLD/NASH. Here, a specific combination of metabolic cofactors (a multi-ingredient; MI) containing precursors of glutathione (GSH) and nicotinamide adenine dinucleotide (NAD+) (betaine, N-acetyl-cysteine, L-carnitine and nicotinamide riboside) was evaluated as effective treatment for the NAFLD/NASH pathophysiology. Six-week-old male mice were randomly divided into control diet animals and animals exposed to a high fat and high fructose/sucrose diet to induce NAFLD. After 16 weeks, diet-induced NAFLD mice were distributed into two groups, treated with the vehicle (HFHFr group) or with a combination of metabolic cofactors (MI group) for 4 additional weeks, and blood and liver were obtained from all animals for biochemical, histological, and molecular analysis. The MI treatment reduced liver steatosis, decreasing liver weight and hepatic lipid content, and liver injury, as evidenced by a pronounced decrease in serum levels of liver transaminases. Moreover, animals supplemented with the MI cocktail showed a reduction in the gene expression of some proinflammatory cytokines when compared with their HFHFr counterparts. In addition, MI supplementation was effective in decreasing hepatic fibrosis and improving insulin sensitivity, as observed by histological analysis, as well as a reduction in fibrotic gene expression (Col1α1) and improved Akt activation, respectively. Taken together, supplementation with this specific combination of metabolic cofactors ameliorates several features of NAFLD, highlighting this treatment as a potential efficient therapy against this disease in humans.

scholarly journals MicroRNA-155 Deficiency Leads to Decreased Atherosclerosis, Increased White Adipose Tissue Obesity, and Non-alcoholic Fatty Liver Disease

2016 ◽  
Vol 292 (4) ◽  
pp. 1267-1287 ◽  
Author(s):  
Anthony Virtue ◽  
Candice Johnson ◽  
Jahaira Lopez-Pastraña ◽  
Ying Shao ◽  
Hangfei Fu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
White Adipose Tissue ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease
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