Standardisation of diet and exercise in clinical trials of NAFLD-NASH: Recommendations from the Liver Forum

Glass, Oliver; Filozof, Claudia; Noureddin, Mazen; Berner-Hansen, Mark; Schabel, Elmer; Omokaro, Stephanie O.; Schattenberg, Jörn M.; Barradas, Katherine; Miller, Veronica; Francque, Sven; Abdelmalek, Manal F.

doi:10.1016/j.jhep.2020.04.030

Cited by 63 publications

(63 citation statements)

References 41 publications

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“…Although often clinically silent, NAFLD can progress to non-alcoholic steatohepatitis, cirrhosis and end-stage liver disease over time (Pais et al, 2016). NAFLD-related liver failure has become the second leading cause of liver transplantation in western countries (Glass et al, 2020). Lifestyle modification is the mainstay of treatment, including dietary changes and exercise, with the primary goal being weight loss.…”

Section: Introductionmentioning

confidence: 99%

Naringin Attenuates High Fat Diet Induced Non-alcoholic Fatty Liver Disease and Gut Bacterial Dysbiosis in Mice

et al. 2020

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Section: Introductionmentioning

confidence: 99%

Naringin Attenuates High Fat Diet Induced Non-alcoholic Fatty Liver Disease and Gut Bacterial Dysbiosis in Mice

et al. 2020

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“…Although there is no approved cure for NASH and a game-changing clinical approach has not yet been identified, several studies to ameliorate NASH are being performed in clinical trials [ 17 , 18 ]. In fact, an emerging trend in NAFLD or NASH treatment is represented by healthy lifestyle modifications, including diet and exercise [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Pharmaceutical Efficacy of Gypenoside LXXV on Non-Alcoholic Steatohepatitis (NASH)

Lee¹,

Kim

et al. 2020

Biomolecules

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Ginsenosides have offered a wide array of beneficial roles in the pharmacological regulation of hepatic metabolic syndromes, including non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD), and obesity. Of the numerous ginsenosides, Rg3 has been widely investigated, but there have been few studies of gypenosides (Gyp). Particularly, no study on Gyp LXXV has been reported to date. Here, to firstly explore the pharmacological effects of Gyp LXXV against NASH and the related mechanism, methionine- and choline-deficient (MCD) diet-induced NASH mice and hepatic cells (stellate cells, hepatic macrophages, and hepatocytes) were selected. Gyp LXXV exhibited markedly alleviated MCD diet-induced hepatic injury, inflammation, and fibrosis by down-regulating hepatic fibrosis markers such as α-smooth muscle actin(α-SMA), collagen1, transforming growth factors-β (TGF-β1), tumor necrosis factor-α (TNF-α), MCP-1, interleukin (IL)-1β, nuclear factor κB (NFκB), and GRP78. Remarkably, histopathological studies confirmed that 15 mg/kg of Gyp LXXV administration to MCD diet-induced mice led to effective prevention of liver injury, lipid accumulation, and activation of hepatic macrophages, indicating that Gyp LXXV might be a potential anti-NASH drug.

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“…Although the modulation of the caloric intake and increase of physical activity are the cornerstones of the treatment of metabolic disorders [241][242][243], some experimental and clinical investigations were aimed at finding out novel drugs that could be useful for the prevention and/or treatment of steatosis. Thus, a variety of TRβ-specific agonists have been prepared and shown to cause significant decrease of cholesterolemia and body weight [244][245][246][247][248].…”

Section: The 35-t2 and Lipid Metabolismmentioning

confidence: 99%

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

Giammanco

Schiera

Liegro

2020

IJMS

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Since the realization that the cellular homologs of a gene found in the retrovirus that contributes to erythroblastosis in birds (v-erbA), i.e. the proto-oncogene c-erbA encodes the nuclear receptors for thyroid hormones (THs), most of the interest for THs focalized on their ability to control gene transcription. It was found, indeed, that, by regulating gene expression in many tissues, these hormones could mediate critical events both in development and in adult organisms. Among their effects, much attention was given to their ability to increase energy expenditure, and they were early proposed as anti-obesity drugs. However, their clinical use has been strongly challenged by the concomitant onset of toxic effects, especially on the heart. Notably, it has been clearly demonstrated that, besides their direct action on transcription (genomic effects), THs also have non-genomic effects, mediated by cell membrane and/or mitochondrial binding sites, and sometimes triggered by their endogenous catabolites. Among these latter molecules, 3,5-diiodo-L-thyronine (3,5-T2) has been attracting increasing interest because some of its metabolic effects are similar to those induced by T3, but it seems to be safer. The main target of 3,5-T2 appears to be the mitochondria, and it has been hypothesized that, by acting mainly on mitochondrial function and oxidative stress, 3,5-T2 might prevent and revert tissue damages and hepatic steatosis induced by a hyper-lipid diet, while concomitantly reducing the circulating levels of low density lipoproteins (LDL) and triglycerides. Besides a summary concerning general metabolism of THs, as well as their genomic and non-genomic effects, herein we will discuss resistance to THs and the possible mechanisms of action of 3,5-T2, also in relation to its possible clinical use as a drug.

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Standardisation of diet and exercise in clinical trials of NAFLD-NASH: Recommendations from the Liver Forum

Cited by 63 publications

References 41 publications

Naringin Attenuates High Fat Diet Induced Non-alcoholic Fatty Liver Disease and Gut Bacterial Dysbiosis in Mice

Naringin Attenuates High Fat Diet Induced Non-alcoholic Fatty Liver Disease and Gut Bacterial Dysbiosis in Mice

Pharmaceutical Efficacy of Gypenoside LXXV on Non-Alcoholic Steatohepatitis (NASH)

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

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