Nonalcoholic fatty liver disease (NAFLD) includes steatosis and nonalcoholic steatohepatitis (NASH), which can be complicated by cirrhosis and hepatocellular carcinoma [1]. NAFLD affects over 30 % of the general population and is associated with type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. NAFLD prevalence in T2DM patients is about 70 % using ultrasonography (US). NAFLD and T2DM share insulinresistance, which in the liver increases gluconeogenesis and glycogenolysis, resulting in hyperglycemia. The pancreatic beta islet cells adapt to hyperglycemia by increasing insulin secretion. Hyperinsulinemia upregulates several lipogenic transcription factors, promoting hepatic lipid synthesis. The association between NAFLD and T2DM seems to be the result of a “common soil”. Several studies showed that NAFLD predicts T2DM and vice versa, and that each condition may act as a progression factor for the other. There is evidence of a high risk of NASH and its progression to hepatocellular carcinoma in T2DM patients [6]. Conversely, recent studies showed that NAFLD not only predicts diabetes, but also contributes to poor glycemic control and chronic complications [8]. Despite its clear link with T2DM, the association of NAFLD with family history of diabetes has been poorly investigated. A recent cross-sectional study in nondiabetic individuals with NAFLD demonstrated that family history of diabetes increased the risk of NASH and fibrosis. The aim of this study was to evaluate the prevalence of NAFLD in healthy first degree relatives of T2DM patients (T2DM-rel) and in healthy subjects without family history of T2DM and to assess the risk factors associated with NAFLD development.

Two-hour postload glycemia is associated to an increased risk of NAFLD in healthy subjects with family history of type 2 diabetes: a case control study

FILARDI, TIZIANA;
2016-01-01

Abstract

Nonalcoholic fatty liver disease (NAFLD) includes steatosis and nonalcoholic steatohepatitis (NASH), which can be complicated by cirrhosis and hepatocellular carcinoma [1]. NAFLD affects over 30 % of the general population and is associated with type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. NAFLD prevalence in T2DM patients is about 70 % using ultrasonography (US). NAFLD and T2DM share insulinresistance, which in the liver increases gluconeogenesis and glycogenolysis, resulting in hyperglycemia. The pancreatic beta islet cells adapt to hyperglycemia by increasing insulin secretion. Hyperinsulinemia upregulates several lipogenic transcription factors, promoting hepatic lipid synthesis. The association between NAFLD and T2DM seems to be the result of a “common soil”. Several studies showed that NAFLD predicts T2DM and vice versa, and that each condition may act as a progression factor for the other. There is evidence of a high risk of NASH and its progression to hepatocellular carcinoma in T2DM patients [6]. Conversely, recent studies showed that NAFLD not only predicts diabetes, but also contributes to poor glycemic control and chronic complications [8]. Despite its clear link with T2DM, the association of NAFLD with family history of diabetes has been poorly investigated. A recent cross-sectional study in nondiabetic individuals with NAFLD demonstrated that family history of diabetes increased the risk of NASH and fibrosis. The aim of this study was to evaluate the prevalence of NAFLD in healthy first degree relatives of T2DM patients (T2DM-rel) and in healthy subjects without family history of T2DM and to assess the risk factors associated with NAFLD development.
2016
NASH
Plasma Glucose Level
Normal Glucose Tolerance
Nondiabetic Individual
Pancreatic Beta Islet Cell
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12078/19693
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