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Mechanisms of Diabetes-Induced Liver Damage: The role of oxidative stress and inflammation

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TLDR
This review summarises the biochemical, histological and macromolecular changes that contribute to oxidative liver damage among diabetic individuals.
Abstract
Diabetes mellitus is a non-communicable disease that occurs in both developed and developing countries. This metabolic disease affects all systems in the body, including the liver. Hyperglycaemia, mainly caused by insulin resistance, affects the metabolism of lipids, carbohydrates and proteins and can lead to non-alcoholic fatty liver disease, which can further progress to non-alcoholic steatohepatitis, cirrhosis and, finally, hepatocellular carcinomas. The underlying mechanism of diabetes that contributes to liver damage is the combination of increased oxidative stress and an aberrant inflammatory response; this activates the transcription of pro-apoptotic genes and damages hepatocytes. Significant involvement of pro-inflammatory cytokines-including interleukin (IL)-1β, IL-6 and tumour necrosis factor-α-exacerbates the accumulation of oxidative damage products in the liver, such as malondialdehyde, fluorescent pigments and conjugated dienes. This review summarises the biochemical, histological and macromolecular changes that contribute to oxidative liver damage among diabetic individuals.

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TL;DR: The interaction between diabetes, oxidative stress and inflammation, factors promoting prevalence of diabetes mellitus, mechanisms involved in hyperglycaemia-induced oxidative stress with particular focus on type 2 diabetes and selected diabetic complications are examined.
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Dapagliflozin slows the progression of the renal and liver fibrosis associated with type 2 diabetes

TL;DR: It is demonstrated that dapagliflozin not only improves hyperglycemia but also slows the progression of diabetes-associated glomerulosclerosis and liver fibrosis by improving hyper glycemia-induced tissue inflammation and oxidative stress.
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Dacryodes edulis enhances antioxidant activities, suppresses DNA fragmentation in oxidative pancreatic and hepatic injuries; and inhibits carbohydrate digestive enzymes linked to type 2 diabetes.

TL;DR: Results indicate the anti-oxidative, anti-diabetic and anti-obesogenic potentials of D. edulis leaves, which gives credence to its antidiabetic folkloric claims.
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Review article: drug‐induced liver injury in the context of nonalcoholic fatty liver disease – a physiopathological and clinical integrated view

TL;DR: Nonalcoholic fatty disease is the most common liver disease, since it is strongly associated with obesity and metabolic syndrome pandemics, and drugs may trigger fatty liver and inflammation per se by mimicking NAFLD pathophysiological mechanisms.
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The Link Between Tau and Insulin Signaling: Implications for Alzheimer's Disease and Other Tauopathies

TL;DR: The deleterious consequences of Tau pathology-induced insulin resistance to the brain and/or peripheral tissues are highlighted, suggesting that these are key events mediating cognitive decline in Alzheimer’s disease (AD) and other tauopathies.
References
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Journal ArticleDOI

Diabetes, oxidative stress, and antioxidants: a review

TL;DR: There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.
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Human fatty liver disease: old questions and new insights.

TL;DR: Recent mechanistic insights into nonalcoholic fatty liver disease are discussed, focusing primarily on those that have emerged from human genetic and metabolic studies.
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Harrison’s Principles of Internal Medicine

Preeti N. Malani
- 07 Nov 2012 - 
Journal ArticleDOI

Advanced glycation endproducts—role in pathology of diabetic complications

TL;DR: The chemistry of glycation and AGEs is introduced and the mechanisms by which they mediate their toxicity are examined and the role of A GEs in the pathogenesis of retinopathy, cataract, atherosclerosis, neuropathy, nephropathy, diabetic embryopathy and impaired wound healing are considered.
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