Abstract
Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.
Highlights
Adipose tissue is recognized as a highly dynamic endocrine tissue exhibiting extensive physiological functions [1] and is composed of mature adipocytes and a stromal vascular fraction, where adipose-derived stem cells, blood cells, fibroblasts, and nerves reside [2]
Adipose tissue constitutes a central node in the interorgan crosstalk network and mediates the regulation of multiple organs and tissues through adipokines [3], biologically active molecules causing pleiotropic effects, including modulation of angiogenesis, metabolism, and inflammation [4]
The serum levels of leptin and resistin and the leptin-to-adiponectin ratio were significantly higher in patients with chronic Hepatitis C virus (HCV) infection than in controls, and low serum levels of resistin were associated with the presence of fibrosis independent of potential confounders [115]
Summary
Adipose tissue is recognized as a highly dynamic endocrine tissue exhibiting extensive physiological functions [1] and is composed of mature adipocytes and a stromal vascular fraction, where adipose-derived stem cells, blood cells, fibroblasts, and nerves reside [2]. The emerging functional characterization of adipokines suggests a close link between the endocrine and immune systems of adipose tissue. This link is emphasized by the altered expression pattern of adipokines in adipose tissue adjacent to sites of inflammation [5]. The excessive accumulation of adipose tissue due to hyperplasia and hypertrophy [6], is currently considered a global epidemicand is related to low-grade systemic inflammation. This state of inflammation is characterized by alterations in adipokine regulation [7]. The current review systematically highlights important findings about altered adipokine profiles in the context of diseases of the digestive tract, including the liver, pancreas, esophagus, stomach, small intestine, and colon, with a perspective on the clinical implications and associated mechanistic approaches
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