Non-Alcoholic Fatty Liver Disease and Cardiovascular Comorbidities: Pathophysiological Links, Diagnosis, and Therapeutic Management

Abstract

Non-alcoholic fatty liver disease (NAFLD) has a growing prevalence in recent years. Its association with cardiovascular disease has been intensively studied, and certain correlations have been identified. The connection between these two entities has lately aroused interest regarding therapeutic management. In order to find the best therapeutic options, a detailed understanding of the pathophysiology that links (NAFLD) to cardiovascular comorbidities is needed. This review focuses on the pathogenic mechanisms that are behind these two diseases and on the therapeutic management available at this time.

Effects of the 5:2 intermittent fasting diet on non-alcoholic fatty liver disease: A randomized controlled trial

“…Although genetic factors also play a pivotal role in the development of NAFLD, a major contribution to its pathogenesis is attributed to modifiable risk factors, i.e., obesity, metabolic syndrome, and diabetes ( 2 , 3 ). As patients diagnosed with NAFLD are prone to developing liver cirrhosis as well as hepatocellular carcinoma, urgent measures are needed to combat the spread of the NAFLD epidemic ( 4 – 7 ), particularly as there are no approved pharmacotherapies for this chronic hepatic disorder.…”

Sphingosine kinase 1 mediates sexual dimorphism in fibrosis in a mouse model of NASH

“…Non-alcoholic fatty liver disease (NAFLD) encompasses a set of pathologies associated with ectopic lipid accumulation in hepatocytes [ 1 ]. NAFLD can progress to non-alcoholic steatohepatitis (NASH), an inflammatory condition which is increasing in prevalence in parallel with other diseases connected to lipid metabolism, such as type 2 diabetes and cardiovascular disease [ 2 ]. NASH is characterized by hepatic necrosis, increased inflammatory signaling, immune cell infiltration, and the potential to progress to fibrosis, cirrhosis, hepatocellular carcinoma, and ultimately liver failure [ 1 , 3 , 4 ].…”

A Glimpse at the Size of the Fetal Liver—Is It Connected with the Evolution of Gestational Diabetes?

“…The authors concluded that this "liver-sparing" phenomenon might be linked with the elevated cardiovascular risk of offspring born from these pregnancies [91]. Moreover, liver and cardiovascular disorders seem to share pathophysiological links also in adulthood, as previously reviewed by Jichitu et al (2021) [92]. More recently, Opheim et al (2020) revealed that the blood flow to the fetal liver was negatively associated with the maternalfetal gradient of glucose and positively associated with the fraction of blood shunted via the ductus venosus in pregnant females with a normal BMI but not in those suffering from overweight.…”

“…Overall, the analyzed research papers point out a possible connection between fetal liver indices and GDM; however, the base of evidence is too small to conclude that these parameters can serve as predictors of GDM in pregnancy. Consequently, further research is needed to clarify the relationship between fetal liver indices and GDM and, if our hypothesis is confirmed, to delineate cutoff values for the variables that could predict the development of GDM [5,24,37,68,69,[85][86][87][88][89][90][91][92][93]. Only one study, conducted by Perovic et al (2014), proposed an FLL of 39 mm as a predictor of GDM [37].…”

“…In the analyzed papers, the most investigated fetal liver indices were FLL (n = 5) and FLV (n = 5). Overall, the subjects with GDM had higher FLL and FLV versus comparators, with several studies revealing associations between FLL and (or) FLV and anthropometric (BMI or BW in particular) or carbohydrate metabolism indices (FPG or HbA1c) [5,24,37,68,69,[85][86][87][88][89][90][91][92][93]. Interestingly, Boito et al (2007) demonstrated that if glycemia is adequately controlled and if GDM is appropriately treated, the FLV is similar between GDM and NGT pregnancies [86].…”