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Tags: Metabolism

Adiponectin is a protein hormone first characterized in differentiating mouse 3T3-L1 adipocytes. It was found to be produced primarily by adipocytes in human, mouse and rat, and circulates at high levels in the blood (approximately 0.01% of all plasma protein). It modulates several metabolic processes and is involved in different metabolic pathologies such as diabetes, atherosclerosis, and obesity. There is an inverse correlation between adiponectin levels and body fat percentage in adults and it is thought that some of its weight reduction effects, notably increased tissue fat oxidation, are a result of an increase in insulin sensitivity and a decrease in plasma glucose. Adiponectin tends to automatically self-associate into a homotrimer. Trimers can then also self-associate and form hexamers or dodecamers. The presence of these high molecular weight multimers seems to be linked with a lower risk of diabetes but a higher propensity for coronary artery disease. They bind to different receptors with distinct tissue specificities and different affinities within the body but ultimately, activation of these receptors by adiponectin affects the activity of AMP kinase, a critical regulator of the cellular metabolic rate.

Non-alcoholic fatty liver disease (NAFLD) covers a whole range of liver disorders including steatosis, non-alcoholic steatohepatitis (i.e. a combination of necrosis and inflammation of the liver), fibrosis, cirrhosis and even liver failure. It is highly prevalent in patients already suffering from diabetes, insulin resistance and obesity and is now considered as a hepatic materialization of the metabolic disturbance. Levels of adiponectin were found to be significantly decreased in patients suffering from NAFLD. Taking these facts into consideration, the discovery of drugs capable of mimicking the effects of adiponectin such as AdipoRon or modulating its expression could prove decisive in the treatment of metabolic disorders including NAFLD. Unfortunately, there is currently no approved treatment for NAFLD as it is considered to be reversible through lifestyle changes including diet and exercise. These modifications can be difficult to manage for some patients and therefore, a drug-based therapy is needed for long term effectiveness.

In a recent study, researchers investigated the effects of ursolic acid in high-fat diet-induced NAFLD rats. Ursolic acid is a natural compound found in a number of plants including basil, lavender, peppermint, rosemary, oregano and thyme, and forms an integral part of a balanced diet. Several seminal studies demonstrated positive effects against inflammation, oxidation, mutation, cancer, atherosclerosis and hyperlipidemia. It was previously showed that incorporation of ursolic acid into a high-fat diet prevented increase of body weight and fat accumulation by facilitating the hydrolysis of triglycerides. In the study, Dr. Li and colleagues from Harbin Medical University observed that the addition of ursolic acid into a high-fat diet led to the reversal of high-fat diet fatty liver and liver injury, the reduction of body and fat/body weight ratio, and the improvement of the expression of triglyceride- and free fatty acid-associated genes (e.g. PPARα, DGAT, FAT/CD36, SREBP-1c, ACC and FAS). Using Enzo’s ELISA kits against TNFα, MCP-1, leptin and adiponectin, they determined a direct correlation between increased amounts of ursolic acid and the diminution of high-fat diet changes in serum biochemical parameters. Finally, they showed that these beneficial effects occurred via PPARα-associated pathway. Altogether, these data suggest that ursolic acid is a promising therapeutic contender against NAFLD.

Enzo Life Sciences offers comprehensive tools for advancing your metabolic research and for discovering, analyzing and quantifying metabolic biomarkers including ELISA kits and enzymatic assays, some of which are described below:

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References:

  • S. Li, et al. Therapeutic role of ursolic acid on ameliorating hepatic steatosis and improving metabolic disorders in high-fat diet-induced non-alcoholic fatty liver disease rats. PLoS One (2014) 9: e86274.

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