Key result
Betaine supplementation alleviated hepatic pathological changes, attenuated insulin resistance, and corrected abnormal adipokine productions in mice fed a high-fat diet.
Why the study?
Does betaine supplementation alleviate hepatic fat accumulation and injury in mice fed a high-fat diet?
Does betaine supplementation alleviate hepatic fat accumulation and injury in mice fed a high-fat diet?
Betaine supplementation protects against high-fat diet-induced NAFLD in mice by improving adipose tissue function and reducing endoplasmic reticulum stress.
Answers are grounded in this paper and cite their sources.
Betaine may prevent and reverse hepatic steatosis plus insulin resistance in high-fat mouse models; leaves open translation to human NAFLD therapy.
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 NH(2)-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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Wang et al. (2010) studied Nonalcoholic fatty liver disease (NAFLD) (n=32). Betaine supplementation vs. High-fat diet without betaine and control diets was evaluated on Hepatic fat accumulation, injury, and insulin resistance. Betaine supplementation alleviated hepatic pathological changes, attenuated insulin resistance, and corrected abnormal adipokine productions in mice fed a high-fat diet.
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