Guanidinoacetic acid ameliorates hepatic steatosis and inflammation and promotes white adipose tissue browning in middle-aged mice with high-fat-diet-induced obesity

Apr 3, 2024Food & function

Guanidinoacetic acid reduces liver fat and inflammation and helps convert fat to energy in middle-aged mice with high-fat diet obesity

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Regenerative Health on OpenScience ↗PubMed ↗DOI ↗

Abstract

Dietary supplementation of guanidinoacetic acid (GAA) significantly inhibited inguinal white adipose tissue hypertrophy in high-fat diet-fed mice.

GAA supplementation reduced levels of systemic inflammatory factors, including IL-4, TNF-α, IL-1β, and IL-6.
Hepatic steatosis and lipid deposition in high-fat diet-fed mice were improved, indicated by decreased levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol.
GAA increased levels of high-density lipoprotein cholesterol in the liver.
The expression of browning markers and mitochondrial-related genes in inguinal white adipose tissue increased with GAA supplementation.
GAA may promote browning of inguinal white adipose tissue by activating the AMPK/Sirt1 signaling pathway.

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Guanidinoacetic acid (GAA) is a naturally occurring amino acid derivative that plays a critical role in energy metabolism. In recent years, a growing body of evidence has emerged supporting the importance of GAA in metabolic dysfunction. Hence, we aimed to investigate the effects of GAA on hepatic and adipose tissue metabolism, as well as systemic inflammatory responses in obese middle-aged mice models and attempted to explore the underlying mechanism. We found that dietary supplementation of GAA inhibited inguinal white adipose tissue (iWAT) hypertrophy in high-fat diet (HFD)-fed mice. In addition, GAA supplementation observably decreased the levels of some systemic inflammatory factors, including IL-4, TNF-α, IL-1β, and IL-6. Intriguingly, GAA supplementation ameliorated hepatic steatosis and lipid deposition in HFD-fed mice, which was revealed by decreased levels of TG, TC, LDL-C, PPARγ, SREBP-1c,,,, andand increased levels of HDL-C in the liver. Moreover, GAA supplementation increased the expression of browning markers and mitochondrial-related genes in the iWAT. Further investigation showed that dietary GAA promoted the browning of the iWATactivating the AMPK/Sirt1 signaling pathway and might be associated with futile creatine cycling in obese mice. These results indicate that GAA has the potential to be used as an effective ingredient in dietary interventions and thus may play an important role in ameliorating and preventing HFD-induced obesity and related metabolic diseases. FASN ACC FABP1APOB via

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Guanidinoacetic acid ameliorates hepatic steatosis and inflammation and promotes white adipose tissue browning in middle-aged mice with high-fat-diet-induced obesity

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