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Gabriela Oprea-Călin, Petru Aurel Babeș, Dan Valentin Andronescu and Crăița-Isabela Andronescu

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the commonest liver condition in the world, accounting for 20-30% of the adult population, and encompasses a spectrum of liver disorders characterized by fat accumulation within the liver, associated or not with varying degrees of hepatic inflammation and liver fibrosis through to cirrhosis. The prevalence of NAFLD increases significantly in the presence of obesity (60-80%) and type 2 diabetes (60%). NAFLD is associated with metabolic disorders (type 2 diabetes, obesity and hyperlipidemia) grouped together as the metabolic syndrome (MetS). It is now regarded as the hepatic manifestation of this syndrome and is closely linked to insulin resistance (IR).The presence of NAFLD predicts the development of type 2 diabetes independent of established risk factors. NAFLD patients should therefore be screened for diabetes, including by the Oral Glucose Tolerance Test (OGTT) if there any abnormalities of fasting blood glucose (FBG) and given appropriate lifestyle advice. Early diagnosis with the institution of lifestyle measures could help prevent or retard the onset of these metabolic disorders. Type 2 diabetes causes more severe non-alcoholic steatohepatitis (NASH), and patients with diabetes have an increased risk for cirrhosis and the development of hepatocellular carcinoma (HCC)

Open access

Decebal Popescu, Dan Andronescu and Petru Aurel Babeș

Abstract

Most studies in the past decades show that screening of Helicobacter Pylori (HP) together with monitoring the inflammatory markers, plasma glucose and HbA1c levels can help prevent or delay type 2 diabetes mellitus. There is a double interrelation between HP infection and diabetes; thus diabetic patients are more susceptible to infection with HP via multiple mechanisms (decreased cellular and humoral immunity induced by diabetes, reducing gastrointestinal motility and secretion of hydrochloric acid, impaired glucose metabolism with the advent of chemical modifications of the gastric mucosa, the last two mechanisms favoring the intestinal colonization with HP). At the same time, those infected with HP can develop diabetes. The purpose of this paper is reviewing the data from the medical literature on the role of the chronic infection with HP on the induction of type 2 diabetes. The studies presented below lead us to the conclusion that the chronic infection with HP, in addition to local specific effects (simple gastritis, peptic ulcer and malignant diseases), also has extradigestive effects. The one approached in our work is that HP is being able to induce type 2 diabetes by complex mechanisms related to insulin resistance, chronic low-grade inflammation, decreased insulin secretion, and influences on glucose and lipid absorption.