Elevated levels of serum advanced glycation end products in patients with non‐alcoholic steatohepatitis

Hyogo, Hideyuki; Yamagishi, Sho‐ichi; Iwamoto, Keiko; Arihiro, Koji; Takeuchi, Masayoshi; Satō, Takashi; Ochi, Hidenori; Nonaka, Michihiro; Nabeshima, Yoshitaka; Inoue, Motoki; Ishitobi, Tomokazu; Chayama, Kazuaki; Tazuma, Susumu

doi:10.1111/j.1440-1746.2007.04943.x

Cited by 177 publications

(186 citation statements)

References 43 publications

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“…via soluble factors that are released from these non-HSC cell types. This could still have relevance for patients with insulin resistance and NASH who display elevated serum and tissue levels of AGE [1,50] . Whether the observed RAGE upregulation may contribute to fibrosis via these indirect pathways needs to be investigated in further studies using either coculture experiments, gene modified animals, or the administration of AGEs to animals with experimental liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Role of the receptor for advanced glycation end products inhepatic fbrosis

Lohwasser¹,

Neureiter²,

Popov³

et al. 2009

WJG

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Section: Discussionmentioning

confidence: 99%

Role of the receptor for advanced glycation end products inhepatic fbrosis

Lohwasser¹,

Neureiter²,

Popov³

et al. 2009

WJG

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“…The previously reported relations between skin autofluorescence and age (p<0.01) [13,17,27], microalbuminuria (p<0.01) [29] and tobacco (p<0.05) [17] were also present in our patients. Liver-toxic glyceraldehyde-derived AGEs [30] are increased in the serum of progressive Non Alcoholic Steato Hepatite vs simple steatosis [31], but may not be detected by autofluorescence, or may not accumulate in the skin like in the liver. Our result do not argue for an important deleterious effect of AGEs in NAFLD, but further work on this hypothesis seems necessary, due to the limitations of our study.…”

Section: Discussionmentioning

confidence: 99%

Steatosis, Glycation and Liver Fibrosis in Patients with Diabetes

Marty¹,

Jb²

2015

J Diabetes Metab

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Introduction: Non Alcoholic Fatty Liver Disease (NAFLD) is frequent and progresses to fibrosis among patients with diabetes. The roles of hepatic steatosis and of the accumulation of Advanced Glycation Endproducts (AGEs) can now be analyzed by new non-invasive methods. Patients and methods:Among hospitalized patients with diabetes, we assessed liver fibrosis by liver stiffness measurement (LSM), steatosis by the attenuation coefficient of an ultrasonic wave (CAP) and AGE accumulation by skin autofluorescence (sAF). The patients with severe fibrosis were compared to the others by ANOVA and Chi-2, and the relations between fibrosis, steatosis, and skin AF were studied by regression analysis.Results: 178 patients were included: 60% male, age 59 ± 11 years, BMI 31 ± 6 kg/m 2 , 79% with Type 2 Diabetes (T2D), poorly controlled (HbA1C 9.0 ± 2.4%). sAF were available in all patients, LSM in 139 and CAP in 93 subjects. Severe fibrosis (LSM>8.7 kPa) was evidenced in 32 (23%) patients, mainly T2D (n=31/32), with higher BMI and waist circumference (p<0.0001). They had higher CAP: 319 ± 53 dB/m (No fibrosis: 268 ± 59, p<0.005), whereas their sAF did not differ. LSM was correlated to the CAP (r=0.40, p<0.0001) and the waist circumference (r=0.46, p<0.0001), but not to sAF. CAP was related to waist circumference and triglycerides level (r=0.70 in multivariate analysis). Conclusion:More steatosis and similar skin autofluorescence in patients with diabetes and severe liver fibrosis support that steatosis promotes fibrosis, and suggests that AGEs do not accelerate this progression. Steatosis, Glycation and Liver Fibrosis in Patients with Diabetes IntroductionNon Alcoholic Fatty Liver Diseases (NAFLD) causes serious hepatic damage and can lead to fibrosis, cirrhosis and liver cancer [1]. Their natural history includes two phases: first the accumulation of triglycerides due to insulin resistance makes a vulnerable steatotic liver, and then a second hit, involving oxidative stress, leads to inflammation and fibrosis [2] . These events are not clinically apparent, and diagnosis is delayed. NAFLD is a cause of "cryptogenetic" cirrhosis [3]. A direct histological follow-up is rarely performed because the liver biopsy is an invasive procedure, indicated only when advanced lesions are suspected, whereas a simple steatosis is benign [4]. Whether triglycerides by themselves are toxic for the liver is even uncertain, some reports suggest that their accumulation may be a mechanism of defense against liver injury [5,6]. Noninvasive procedures of evaluation of liver fibrosis and steatosis, by Fibroscan (Liver Stiffness Measurement LSM and Controlled Attenuation Parameter CAP) seem adapted to study early stages of NAFLD in high risk populations, like patients with diabetes [7]. Are the levels of steatosis high in patients with diabetes and hepatic fibrosis? NAFLD are especially frequent among patients with diabetes [8]; mainly Type 2, but Type 1 Diabetes is also concerned [9]. They progress more to liver fibrosis, rates of severe fibr...

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“…Presence of AGEs has been shown in the liver of patients with non-alcoholic steatohepatitis using immunohistochemical methods, and serum AGE levels were found related with the severity of hepatic disorder (18)(19)(20).…”

Section: Hepatic Diseasesmentioning

confidence: 98%

Dietary glycotoxins and infant formulas

Kutlu

2016

Turk Pediatri Ars

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Advanced glycation end products constitute a complex group of compounds derived from the nonenzymatic glycation of proteins, lipids, and nucleic acids formed endogenously, but also from exogenous supplies such as tobacco smoking (glycotoxins). Accumulating evidence underlies the beneficial effect of the dietary restriction of glycotoxins in animal studies and also in patients with diabetic complications and metabolic diseases. Composition of infant formulas and their processing methods render an extraordinary favorable milieu for the formation of glycotoxins, and the content of glycotoxins in infant formula exceeds that of breast milk by hundred folds. Data from a limited number of short-term small studies in healthy infants do not provide direct evidence of acute negative health effects of glycotoxins in early infancy. However, the effects in sensitive groups on the state of future health in adulthood remain unclear. (Turk Pediatri Ars 2016; 51: 179-85)

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Elevated levels of serum advanced glycation end products in patients with non‐alcoholic steatohepatitis

Abstract: The present data suggest that the sustained increase of glyceraldehyde-derived AGE could at least in part contribute to the pathogenesis of NASH. The serum glyceraldehyde-derived AGE level may be a useful biomarker for discriminating NASH from simple steatosis.

Cited by 177 publications

References 43 publications

Role of the receptor for advanced glycation end products inhepatic fbrosis

Role of the receptor for advanced glycation end products inhepatic fbrosis

Steatosis, Glycation and Liver Fibrosis in Patients with Diabetes

Dietary glycotoxins and infant formulas

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