scholarly journals The Angiogenesis Inhibitor ALS-L1023 from Lemon-Balm Leaves Attenuates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease through Regulating the Visceral Adipose-Tissue Function

2017 ◽  
Vol 18 (4) ◽  
pp. 846 ◽  
Author(s):  
Jeongjun Kim ◽  
Haerim Lee ◽  
Jonghoon Lim ◽  
Jaeho Oh ◽  
Soon Shin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Angiogenesis Inhibitor ◽  
High Fat ◽  
Lemon Balm ◽  
Nonalcoholic Fatty Liver ◽  
Visceral Adipose

scholarly journals Visceral adipose tissue visfatin in nonalcoholic fatty liver disease

2010 ◽  
Vol 9 (3) ◽  
pp. 266-270 ◽  
Author(s):  
Radhika Gaddipati ◽  
Sasikala Mitnala ◽  
Nagarajarao Padaki ◽  
Rathindra Mohan Mukherjee ◽  
Anuradha Sekaran ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Visceral Adipose Tissue ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Visceral Adipose

scholarly journals Betaine improved adipose tissue function in mice fed a high-fat diet: a mechanism for hepatoprotective effect of betaine in nonalcoholic fatty liver disease

2010 ◽  
Vol 298 (5) ◽  
pp. G634-G642 ◽  
Author(s):  
Zhigang Wang ◽  
Tong Yao ◽  
Maria Pini ◽  
Zhanxiang Zhou ◽  
Giamila Fantuzzi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Diet ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Betaine Supplementation

Adipose tissue dysfunction, featured by insulin resistance and/or dysregulated adipokine production, plays a central role not only in disease initiation but also in the progression to nonalcoholic steatohepatitis and cirrhosis. Promising beneficial effects of betaine supplementation on nonalcoholic fatty liver disease (NAFLD) have been reported in both clinical investigations and experimental studies; however, data related to betaine therapy in NAFLD are still limited. In this study, we examined the effects of betaine supplementation on hepatic fat accumulation and injury in mice fed a high-fat diet and evaluated mechanisms underlying its hepatoprotective effects. Male C57BL/6 mice weighing 25 ± 0.5 (SE) g were divided into four groups (8 mice/group) and started on one of four treatments: control diet, control diet supplemented with betaine, high-fat diet, and high-fat diet supplemented with betaine. Betaine was supplemented in the drinking water at a concentration of 1% (wt/vol) (anhydrous). Our results showed that long-term high-fat feeding caused NAFLD in mice, which was manifested by excessive neutral fat accumulation in the liver and elevated plasma alanine aminotransferase levels. Betaine supplementation alleviated hepatic pathological changes, which were concomitant with attenuated insulin resistance as shown by improved homeostasis model assessment of basal insulin resistance values and glucose tolerance test, and corrected abnormal adipokine (adiponectin, resistin, and leptin) productions. Specifically, betaine supplementation enhanced insulin sensitivity in adipose tissue as shown by improved extracellular signal-regulated kinases 1/2 and protein kinase B activations. In adipocytes freshly isolated from mice fed a high-fat diet, pretreatment of betaine enhanced the insulin signaling pathway and improved adipokine productions. Further investigation using whole liver tissues revealed that betaine supplementation alleviated the high-fat diet-induced endoplasmic reticulum stress response in adipose tissue as shown by attenuated glucose-regulated protein 78/C/EBP homologous protein (CHOP) protein abundance and c-Jun NH2-terminal kinase activation. Our findings suggest that betaine might serve as a safe and efficacious therapeutic tool for NAFLD by improving adipose tissue function.

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