scholarly journals Effect of adipose tissue insulin resistance on metabolic parameters and liver histology in obese patients with nonalcoholic fatty liver disease

Hepatology ◽  
2012 ◽  
Vol 55 (5) ◽  
pp. 1389-1397 ◽  
Author(s):  
Romina Lomonaco ◽  
Carolina Ortiz-Lopez ◽  
Beverly Orsak ◽  
Amy Webb ◽  
Jean Hardies ◽  
...  
2011 ◽  
Vol 43 (1) ◽  
pp. 73-77 ◽  
Author(s):  
Giampaolo Bianchi ◽  
Elisabetta Bugianesi ◽  
Jan Frystyk ◽  
Lise Tarnow ◽  
Allan Flyvbjerg ◽  
...  

2018 ◽  
Author(s):  
Giovanni Tarantino ◽  
Susan Costantini ◽  
Vincenzo Citro ◽  
Paolo Conforti ◽  
Francesca Capone ◽  
...  

SUMMARYBackgroundIntramuscular triglycerides (IMTGs) represent an important energy supply and a dynamic fat-storage depot that can expand during periods of elevated lipid availability and a fatty ac-id source. Ultrasonography (US) of human skeletal muscles is a practical and reproducible method to assess both IMTG presence and entity.Although a crosstalk between cytokines in skeletal muscle and adipose tissue has been suggested in obesity, condition leading to hepatic steatosis (HS) or better defined as nonalcoholic fatty liver disease and cancer, there are still questions to be answered about the role of interferons (IFNs), alpha as well as gamma, and IMTG in obesity. We aimed at discovering any correlation between IFNs and IMTG.MethodsWe analysed anthropometric data, metabolic parameters and imaging features of a population of obese subjects with low-prevalence of co-morbidities but HS. The levels of serum IFNs were detected by a magnetic bead-based multiplex immunoassays.ResultsSerum concentrations of IFN-alpha2 were increased, while serum levels of IFN-gamma were decreased confronted with those of controls; the severity of IMTG, revealed at US as Heckmatt scores, was inversely predicted by IFN-alpha2 serum concentrations; IMTG scores were not predicted by serum levels of IFN-gamma; IMTG scores were predicted by HS severity, ascertained at US; HS severity was predicted by visceral adipose tissue, assessed by US, but the latter was not instrumental to IMTG.Discussion & ConclusionThis study has added some pieces of observation about the cytokine network regulating the interplay between IMTG and obesity in obese patients with HS.


2012 ◽  
Vol 11 (4) ◽  
pp. 478-486 ◽  
Author(s):  
Narendra S. Choudhary ◽  
Ajay Duseja ◽  
Naveen Kalra ◽  
Ashim Das ◽  
Radha K. Dhiman ◽  
...  

2005 ◽  
Vol 152 (1) ◽  
pp. 113-118 ◽  
Author(s):  
Claudio Pagano ◽  
Giorgio Soardo ◽  
Walter Esposito ◽  
Francesco Fallo ◽  
Lorenza Basan ◽  
...  

Objectives: Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease. Design and methods: We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis. Results: Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93±0.45 vs 15.67±1.60 ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16±0.78 vs 5.69±0.49 ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values. Conclusions: These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.


Obesity ◽  
2010 ◽  
Vol 18 (12) ◽  
pp. 2268-2273 ◽  
Author(s):  
Valentina Medici ◽  
MohamedR. Ali ◽  
Suk Seo ◽  
Christopher A. Aoki ◽  
Lorenzo Rossaro ◽  
...  

2011 ◽  
Vol 12 (4) ◽  
pp. 498-503 ◽  
Author(s):  
Stergios A Polyzos ◽  
Jannis Kountouras ◽  
Efthimia Zafeiriadou ◽  
Kalliopi Patsiaoura ◽  
Evangelia Katsiki ◽  
...  

Aim: The renin–angiotensin–aldosterone system has been implicated in the pathogenesis of insulin resistance and nonalcoholic fatty liver disease (NAFLD). The beneficial effect of spironolactone in a mouse model with diabetes and NAFLD has recently been reported. The main aim was assessment of the effect of spironolactone on serum metabolic parameters and insulin resistance in patients with NAFLD. Methods: This study includes preliminary results of a single-centre randomised controlled trial of treatment with vitamin E (group 1, 10 patients) versus spironolactone plus vitamin E (group 2, 10 patients) in biopsy-proven NAFLD. Serum transaminases, lipids, potassium, sodium, glucose and insulin were measured, and homeostatic model assessment-insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI) were calculated before and 8 weeks after baseline assessment. Results: Insulin was decreased within group 2 (15.3 ± 2.7 at baseline vs. 10.3 ± 5.0 at week 8, p = 0.013). Although no difference in glucose was observed, HOMA-IR significantly decreased (4.4 ± 0.9 vs. 2.8 ± 0.5, respectively, p = 0.047). QUICKI was increased, but not statistically significantly. Conclusions: Spironolactone and vitamin E combined therapy seems to exhibit a favourable effect on serum insulin and HOMA-IR in patients with NAFLD. If validated in a large-scale clinical trial, it may prove an inexpensive therapeutic approach for the management of NAFLD patients.


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