Non-alcoholic fatty liver disease and colorectal cancer

Abstract

As a significant cause of cancer death worldwide, colorectal cancer (CRC) is still one of the most common cancers in the world. The most efficient strategies to reduce CRC incidence include identifying risk factors for CRC and performing a preventive colonoscopy in high-risk populations. Some well-established risk factors for CRC development include hereditary syndromes and inflammatory bowel disease. Of note, in recent years, attention has been given to new evidence indicating that more than 75%-95% of CRC occurs in individuals with little or no genetic risk. For these individuals, the risk for CRC is associated with their lifestyle and dietary factors, including central obesity, overweight and physical inactivity. Recently, evidence demonstrated a connection between non-alcoholic fatty liver disease (NAFLD) and CRC. Insulin resistance and metabolic syndrome (MetS) are common risks that NAFLD and colorectal neoplasms share. The incidence of NAFLD is increasing in parallel with an increasing prevalence of MetS and obesity. Consequently, the question arises: will the incidence of CRC increase together with this dramatic increase in obesity, MetS and ultimately NAFLD prevalence? Recent studies of adenomatous polyps, CRC and NAFLD are discussed in this manuscript.

The association between nonalcoholic fatty liver disease and esophageal, stomach, or colorectal cancer: National population-based cohort study

“…Because of the pathogenic factors of NAFLD, including insulin resistance and abdominal obesity, that could influence colorectal neoplasm development [14], several studies have investigated the association between NAFLD and colorectal neoplasms [14,15]. NAFLD (diagnosed by imaging study) independently increased the risk of overall colorectal neoplasm occurrence and severity at the time of the surveillance colonoscopy [16][17][18]. In a retrospective study in Chinese females, combined NAFLD and metabolic syndrome was an independent risk factor for colorectal cancer-specific mortality [19].…”

circRNA_0046366 inhibits hepatocellular steatosis by normalization of PPAR signaling

“…Patients with hepatic steatosis are also susceptible to some aspects of metabolic syndrome ( e.g ., type 2 diabetes and hyperlipidemia)[ 9 , 10 ] and related diseases ( i.e . cardiovascular events, cerebrovascular diseases, and extrahepatic cancer)[ 11 , 12 ]. Although it is being recognized as a public health burden, clinical intervention for hepatic steatosis is deficient because of the limited understanding of its underlying mechanisms.…”

Circular RNA Profiling and Bioinformatic Modeling Identify Its Regulatory Role in Hepatic Steatosis

“…Serving as the hallmark of nonalcoholic fatty liver disease (NAFLD), hepatic steatosis predisposes patients to nonalcoholic steatohepatitis (NASH), liver fibrosis/cirrhosis, and the final outcome of hepatocellular carcinoma (HCC) [4]. High incidence of extrahepatic death and disability (i.e., cardiovascular events, cerebral apoplexy, and cancers) also takes place in the population with hepatic steatosis [5–7]. Recent decades have witnessed a dramatic prevalence of hepatic steatosis increase worldwide, ranging in 24%–46% in the western countries and 7.9%–54% in the Asia-Pacific area [8–11], which suggests the coming emergency and serious burden of public health.…”