Advanced Glycation End-Products in Patients With Chronic Alcohol Misuse

Kalousová, Marta; Zima, Tomáš; Popov, Petr; Špaček, P.; Braun, M.; Soukupová, J; Pelinková, Květa; Kientsch-Engel, Rosemarie

doi:10.1093/alcalc/agh058

Cited by 41 publications

(16 citation statements)

References 27 publications

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“…However, while leptin is sensitive to several physiological stimuli including feeding status (fasted vs. fed) and body weight, nutrient status was infrequently reported or controlled for and correlations between body weight and leptin were not always performed. Similar to the inconclusive results reported for circulating leptin in animal models, the serum leptin concentration from humans appears to be unrelated to alcohol intake [80,87,95,96,97,98,99], although exceptions do exist [27,100,101,102]. In alcoholic patients, leptin has been reported to be increased, decreased or unchanged, and serum leptin was also not altered by either alcohol withdrawal for 15 days [27] or the severity of liver disease [87,95,96].…”

Section: Adipokinessupporting

confidence: 65%

Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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Chronic alcohol consumption perturbs lipid metabolism as it increases adipose tissue lipolysis and leads to ectopic fat deposition within the liver and the development of alcoholic fatty liver disease. In addition to the recognition of the role of adipose tissue derived fatty acids in liver steatosis, alcohol also impacts other functions of adipose tissue and lipid metabolism. Lipid balance in response to long-term alcohol intake favors adipose tissue loss and fatty acid efflux as lipolysis is upregulated and lipogenesis is either slightly decreased or unchanged. Study of the lipolytic and lipogenic pathways has identified several regulatory proteins modulated by alcohol that contribute to these effects. Glucose tolerance of adipose tissue is also impaired by chronic alcohol due to decreased glucose transporter-4 availability at the membrane. As an endocrine organ, white adipose tissue (WAT) releases several adipokines that are negatively modulated following chronic alcohol consumption including adiponectin, leptin, and resistin. When these effects are combined with the enhanced expression of inflammatory mediators that are induced by chronic alcohol, a pro-inflammatory state develops within WAT, contributing to the observed lipodystrophy. Lastly, while chronic alcohol intake may enhance thermogenesis of brown adipose tissue (BAT), definitive mechanistic evidence is currently lacking. Overall, both WAT and BAT depots are impacted by chronic alcohol intake and the resulting lipodystrophy contributes to fat accumulation in peripheral organs, thereby enhancing the pathological state accompanying chronic alcohol use disorder.

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Section: Adipokinessupporting

confidence: 65%

Alcohol, Adipose Tissue and Lipid Dysregulation

Steiner

Lang

2017

Biomolecules

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“…Kalousová et al (2004) reported markedly increased AGE in chronic alcoholics compared to healthy controls [304]. Moreover, their results also supported the notion that AGE production may be prevented or even diminished by antioxidant supplementation with vitamin B derivatives [305,306], and/or vitamins A, C, and E [307].…”

Section: Lifestyle Factorsmentioning

confidence: 81%

The effects of oxidative stress on female reproduction: a review

Agarwal

Aponte-Mellado

Premkumar

et al. 2012

Reprod Biol Endocrinol

1,395

1,188

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Oxidative stress (OS), a state characterized by an imbalance between pro-oxidant molecules including reactive oxygen and nitrogen species, and antioxidant defenses, has been identified to play a key role in the pathogenesis of subfertility in both males and females. The adverse effects of OS on sperm quality and functions have been well documented. In females, on the other hand, the impact of OS on oocytes and reproductive functions remains unclear. This imbalance between pro-oxidants and antioxidants can lead to a number of reproductive diseases such as endometriosis, polycystic ovary syndrome (PCOS), and unexplained infertility. Pregnancy complications such as spontaneous abortion, recurrent pregnancy loss, and preeclampsia, can also develop in response to OS. Studies have shown that extremes of body weight and lifestyle factors such as cigarette smoking, alcohol use, and recreational drug use can promote excess free radical production, which could affect fertility. Exposures to environmental pollutants are of increasing concern, as they too have been found to trigger oxidative states, possibly contributing to female infertility. This article will review the currently available literature on the roles of reactive species and OS in both normal and abnormal reproductive physiological processes. Antioxidant supplementation may be effective in controlling the production of ROS and continues to be explored as a potential strategy to overcome reproductive disorders associated with infertility. However, investigations conducted to date have been through animal or in vitro studies, which have produced largely conflicting results. The impact of OS on assisted reproductive techniques (ART) will be addressed, in addition to the possible benefits of antioxidant supplementation of ART culture media to increase the likelihood for ART success. Future randomized controlled clinical trials on humans are necessary to elucidate the precise mechanisms through which OS affects female reproductive abilities, and will facilitate further explorations of the possible benefits of antioxidants to treat infertility.

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“…Advanced glycation end products (AGEs), a heterogeneous group of irreversible reactive derivatives formed by non-enzymatic glycation and oxidation of proteins and lipids, elicit oxidative stress generation, subsequently evoke inflammation [2], and have been implicated in pulmonary [3] and renal fibrosis [4]. AGE levels are elevated in nonalcoholic steatohepatitis patients (NASH) [5] and chronic alcohol misuse patients [6,7]. There are no data on AGE levels in hepatitis C patients; however, AGE levels independently correlate with IR [8].…”

Section: Introductionmentioning

confidence: 99%