Yin Zhi Huang, a traditional Chinese herbal formula, ameliorates diet-induced obesity and hepatic steatosis by activating the AMPK/SREBP-1 and the AMPK/ACC/CPT1A pathways

Abstract

Background: Yin Zhi Huang (YZH) is a formula composed of Artemisia scoparia, Gardeniae fructus, Scutellaria baicalensis Georgi, and Lonicerae Japonicae Flos. Most of the components are eaten as food in Asia. Here, we evaluated the role of YZH on a high-fat diet (HFD)-induced obesity and hepatic steatosis.Methods: Male C57BL/6J mice were fed with normal-chow diet, HFD, and HFD with low-or high-dose YZH for 16 weeks. Body weight gain, adipose mass, and plasma lipids levels were measured to evaluate the effect of YZH on obesity. Liver weight and staining methods on liver tissues were used to determine hepatic steatosis. The expression of involved genes and proteins were screened with qRT-PCR and immunoblotting, respectively. Results:The results showed that YZH significantly reduced body weight gain, adipose mass, and the size of adipocytes, while did not affect food intake in HFD-fed mice. H&E staining, bodipy staining, and oil red O staining displayed that YZH alleviates hepatic lipid accumulation. It also effectively restored elevated plasma levels of triglycerides (TG), total cholesterol (TC), alanine aminotransferase, and aspartate aminotransferase in HFD-fed mice. Mechanistically, these effects of YZH have associated with a decrease of AMPK/SREBP-1 pathway-mediated de novo lipogenesis and an increase of AMPK/ACC/CPT1A pathwaymediated mitochondrial fatty acid β oxidation.Conclusions: YZH supplementation ameliorated diet-induced obesity and hepatic steatosis by decreasing AMPK/SREBP-1 pathway-mediated de novo lipogenesis and increasing AMPK/ACC/CPT1A pathwaymediated mitochondrial fatty acid β oxidation.

Madecassoside Inhibits Body Weight Gain via Modulating SIRT1-AMPK Signaling Pathway and Activating Genes Related to Thermogenesis

“…Apart from regulating the gene transcription of white adipose tissue (WAT) to adapt to the systemic energy regulation, it can also affect the differentiation and remodeling of brown adipose tissue (BAT) by regulating the activity of PGC-1α and PPAR-γ factors ( 29 – 31 ). AMPK acts as an energy regulator, and requires activation to exert anti-obesity effects in the surrounding tissues ( 32 , 33 ). ACC is the downstream factor of AMPK, and it often plays an essential role on fatty acid metabolism ( 34 ).…”

MicroRNA Profiling Reveals an Abundant ssc-miRNA-148a-3p that Promotes Proliferation and Differentiation during Intramuscular Adipogenesis in Chinese Guizhou Congjiang Pigs Breeds by targeting PPARGC1A

“…In an insulin resistance C57BL/6J mice model, Yin Zhi Huang has associated with a decrease of AMPK/SREBP-1 pathway-mediated de novo lipogenesis and an increase of AMPK/ACC/CPTI pathwaymediated mitochondrial fatty acid β oxidation to ameliorate insulin resistance and facilitate lipid metabolism [64]. In current study, we found that miR-148a-3p inhibited AMPK to phosphorylate ACC activating its' ability to convert malonyl-CoA from acetyl-CoA consequently decreased CPT1C content to reduce mitochondrial fatty acid oxidation.…”

The role of liver kinase B1 in tumor progression through regulation of lipid metabolism

“…ACC accelerates FAO in two CPT1dependent manners. On the one hand, phosphorylation of ACC inactivates the ability to mediate malonyl-coA production, which promotes FAO with increased CPT1A content [58]. On the other hand, the formation of a complex between ACCα and CPT1A attenuates in the case of glucose deficiency, which boosts FAO by facilitating the transport of FA [59].…”