A call to action for fatty liver disease

Mantovani, Alessandro; Valenti, Luca

doi:10.1111/liv.14907

Cited by 13 publications

(17 citation statements)

References 36 publications

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“…Several explanations have been proposed to explain the loss of hepatic fat with fibrosis progression and development of portal hypertension, including alterations in hepatic vasculature and mitochondrial metabolism, reduced exposure to insulin and stimulation of catabolic pathways, 7 and increased levels of adiponectin, the insulin‐sensitizing adipokine which is cleared by the liver 11 . Conversely, despite the progressive reduction in hepatic fat, severe fibrosis is consistently linked to insulin resistance and to a higher incidence of diabetes 5,12,13 …”

Section: Figurementioning

confidence: 99%

“…11 Conversely, despite the progressive reduction in hepatic fat, severe fibrosis is consistently linked to insulin resistance and to a higher incidence of diabetes. 5,12,13 In a seminal paper recently published in Nature, Ng et al reported new findings that may provide an explanation for this paradox. 14 The study aimed at the identification of somatic mutations occurring in non-malignant liver tissues (n=29) from individuals with advanced alcoholic and nonalcoholic FLD, which were extensively sampled (vs controls with a normal liver (n=5).…”

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confidence: 99%

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A genetic hypothesis for burnt‐out steatohepatitis

Valenti

Romeo

Pajvani

2021

Liver International

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A genetic hypothesis for burnt-out steatohepatitisEnvironmental stressors such as obesity and insulin resistance, exposure to hepatotoxins, and hepatitis C virus infection increase hepatocyte lipid content, with a significant change in triglyceride, cholesterol as well as other lipid species. Resultant fatty liver disease (FLD) variably progresses to steatohepatitis, cirrhosis and hepatocellular carcinoma (HCC). 1 Evidence for shared determinants of FLD and end-stage liver complications first arose from human genetics, 2 that the main risk variants for FLD had a proportional impact on fibrosis and HCC, and fibrosis/HCC development was very closely linked to the impact on the lipid content of hepatocytes. 3,4 However, this theory is challenged by the observation that hepatic fat accumulation and biochemical markers of liver damage and inflammation tend to decrease with the progression of liver fibrosis. [5][6][7] Programme Horizon 2020 (under grant agreement No. 777377) for the project LITMUS (LV). The European Union, programme 'Photonics' under grant agreement '101016726' (LV). Gilead_IN-IT-989-5790 (LV).

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Section: Figurementioning

confidence: 99%

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confidence: 99%

A genetic hypothesis for burnt‐out steatohepatitis

Valenti

Romeo

Pajvani

2021

Liver International

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“…Seeing the multiple pathways implicated in the pathogenesis of NAFLD and its complications, as well as the single response from single-agent therapies across RCTs available so far, it is also reasonable to hypothesize that the combination of different therapies (e.g., GLP-1 receptor agonists plus SGLT-2 inhibitors) will be more appropriate for treating NAFLD patients [86,87,89]. In this context, as suggested by several experts in the field, a holistic approach in managing and treating NAFLD patients seems to be fundamental [75,85].…”

Section: Discussionmentioning

confidence: 99%

“…In this context, as suggested by several experts in the field [13], a potential comprehensive CVD risk assessment may include (Table 2): (a) evaluation of coexisting risk factors (such as a prior history of CVD, family history of premature CVDs or T2DM, cigarette smoking, presence of T2DM, dyslipidemia, hypertension, obesity, metabolic syndrome, chronic kidney disease and erectile dysfunction), (b) physical examination (such as body weight, height, body mass index, waist circumference, blood pressure, arterial bruits and pulse examination), (c) laboratory tests (such as blood count, lipid profile, fasting plasma glucose, HbA1c, serum creatinine, transaminases, albumin, urinalysis, albuminuria) and (d) cardiovascular examination tests (such as resting electrocardiogram, carotid artery ultrasonography, and exercise stress test if coexisting CVD, CKD, T2DM or >2 CVD risk factors). In addition, the current evidence on this topic also calls attention to a holistic approach in managing and treating NAFLD patients [75,85].…”

Section: Cvd Risk Assessment In Patients With Nafldmentioning

confidence: 99%

Non-Alcoholic Fatty Liver Disease and Risk of Macro- and Microvascular Complications in Patients with Type 2 Diabetes

Mantovani

Dalbeni

Beatrice

et al. 2022

JCM

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Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome. To date, NAFLD is the most frequent chronic liver disease seen day by day in clinical practice across most high-income countries, affecting nearly 25–30% of adults in the general population and up to 70% of patients with T2DM. Over the last few decades, it clearly emerged that NAFLD is a “multisystemic disease” and that the leading cause of death among patients with NAFLD is cardiovascular disease (CVD). Indeed, several observational studies and some meta-analyses have documented that NAFLD, especially its advanced forms, is strongly associated with fatal and non-fatal cardiovascular events, as well as with specific cardiac complications, including sub-clinical myocardial alteration and dysfunction, heart valve diseases and cardiac arrhythmias. Importantly, across various studies, these associations remained significant after adjustment for established cardiovascular risk factors and other confounders. Additionally, several observational studies and some meta-analyses have also reported that NAFLD is independently associated with specific microvascular conditions, such as chronic kidney disease and distal or autonomic neuropathy. Conversely, data regarding a potential association between NAFLD and retinopathy are scarce and often conflicting. This narrative review will describe the current evidence about the association between NAFLD and the risk of macro- and microvascular manifestations of CVD, especially in patients with T2DM. We will also briefly discuss the biological mechanisms underpinning the association between NAFLD and its advanced forms and macro- and microvascular CVD.

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“…Metabolic dysfunction-associated fatty liver disease (MAFLD), formerly known as nonalcoholic fatty liver disease (NAFLD), due to its high global prevalence, causes a huge economic burden to society [ 1 ]. Unhealthy habits such as sedentary and less active lifestyles and unhealthy dietary patterns are closely related to a high incidence rate of MAFLD [ 2 ], which can be diagnosed accurately by certain evaluating criteria like obesity, type 2 diabetes mellitus (T2DM), or metabolic disorders [ 3 ]. The prevalence of fatty liver disease (FLD) and osteoporosis is increasing in elderly people [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

Wang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Introduction. Many Asian cohort studies have shown that nonalcoholic fatty liver disease (NAFLD), now renamed as metabolic dysfunction-associated fatty liver disease (MAFLD), increases the risk of osteoporosis, yet the effect of MAFLD on elderly patients with osteopenia (OPe) has not been reported. Objective. This study aimed to explore the influence of MAFLD on the function of macrophages in patients with OPe. Methods. A total of 107 elderly OPe patients with or without MAFLD who visited the Huadong Hospital Affiliated to Fudan University (Shanghai, China) between January 1st, 2021, and September 30th, 2021, were evaluated for an interviewer-assisted questionnaire, as well as clinical and biological assessments. Results. Comparing two groups of elderly patients with the same bone mass level, we found that the six-minute walking distance ( P = 0.012 ) and short physical performance battery (SPPB) score ( P = 0.0029 ) of the elderly OPe patients with MAFLD are worse than those in OPe patients without MAFLD. Our results confirmed that the mitochondrial reactive oxygen species (mtROS) in peripheral blood of OPe patients with MAFLD was significantly higher than those without. We also observed the mitochondrial metabolism level of peripheral blood-derived macrophages in the included patients and peripheral blood macrophages in patients with MAFLD with more unbalanced mitochondrial dynamics of macrophages, more weakened mitochondrial respiratory capacity, and greater mitochondrial microstructure damage, when compared with the elderly patients without MAFLD. Conclusions. To conclude, our data revealed that MAFLD itself may aggravate the inflammatory state in elderly OPe people due to mitochondrial homeostasis imbalance of peripheral blood macrophages. Damaged monocyte-macrophages might trigger attenuation of the walking ability of OPe patients.

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A call to action for fatty liver disease

Cited by 13 publications

References 36 publications

A genetic hypothesis for burnt‐out steatohepatitis

A genetic hypothesis for burnt‐out steatohepatitis

Non-Alcoholic Fatty Liver Disease and Risk of Macro- and Microvascular Complications in Patients with Type 2 Diabetes

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

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