Adiponectin helps protect against alcoholic liver steatosis by activating various signalling pathways involving, silent mating type information regulation 2 homolog 1 (Sirtuin, SIRT1), AMP-activated protein kinase, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, peroxisome proliferator-activated receptor alpha and sterol regulatory element binding protein 1.197 These pathways collectively reduce lipogenesis, enhance fat oxidation and prevent lipid accumulation in the liver.197 However, chronic alcohol consumption leads to a decrease in adiponectin levels.197 Leptin is another important adipokine that regulates energy balance by suppressing energy intake and increasing energy expenditure.198 Alcohol exposure lowers leptin levels, which can worsen alcohol-related diseases.198 Administration of leptin has been shown to mitigate alcohol-induced hepatic steatosis.198 Additionally, fibroblast growth factor 21, an adipokine secreted by WAT, can be induced by alcohol consumption, further promoting lipolysis.199 Alcohol exposure also causes significant changes in cytokine levels and leads to an influx of immune cells, such as macrophages, CD4 + T cells and dendritic cells, into adipose tissue, contributing to inflammation.13 For example, TNF- secreted by adipose tissue can induce apoptosis in hepatocytes and activate KCs, further exacerbating the inflammatory response associated with ALD.13 200 In summary, the gut-liver axis plays a critical role in maintaining homeostasis, but alcohol disrupts intestinal barrier integrity, leading to increased permeability and the translocation of microbial products like LPS into the portal circulation
[DOI] [PubMed] [Google Scholar] Ochiai T., Soeda S., Ohno S., Tanaka H., Shoyama Y., Shimeno H
Membranes 10:89
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The increased expression of SAT1 promotes the depletion of spermidine and spermine, which leads to mitochondria-mediated apoptosis, and increases the sensitivity of drug-resistant cells to cisplatin-induced apoptosis (Mandal et al., 2015)
