Non‐alcoholic fatty liver disease and type 2 diabetes: An update

Lee, C H; Lui, David Tak Wai; Lam, Ksl

doi:10.1111/jdi.13756

Cited by 51 publications

(34 citation statements)

References 118 publications

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“…Obesity is associated with insulin resistance in peripheral glucose, called insulin resistance, and can lead to the development of T2DM and contribute to the development of hepatic steatosis and cardiovascular risk [35][36][37]. Diabetes and obesity are well-known risk factors in the evolution of liver disorders [38][39][40].…”

Section: Discussionmentioning

confidence: 99%

The Influence of Metabolic Factors in Patients with Chronic Viral Hepatitis C Who Received Oral Antiviral Treatment

Gavril

Mitu

et al. 2023

Metabolites

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Hepatic diseases pose a significant public health concern. Regardless of the severity of hepatic fibrosis, treatment is recommended for all chronic hepatitis C virus (HCV) subjects. However, fibrosis and steatosis assessment remains crucial for evaluating the prognosis, progression, and hepatic disease monitoring, particularly following the treatment with direct-acting antivirals (DAAs). The aim of our study was to evaluate the impact of metabolic factors and the extent of hepatic fibrosis and fat accumulation in chronic HCV infection subjects. Additionally, another objective was to investigate modifications regarding fibrosis and steatosis three months after a successful sustained viral response (SVR). A total of 100 patients with compensated cirrhosis and chronic hepatitis C (CHC) were included in our study. These patients received treatment with DAA and underwent Fibromax assessment before and three months post SVR. After DAA treatment, a significant decrease was observed in the degree of hepatic fibrosis and hepatic steatosis. This regression was evident three months following the achievement of SVR. Chronic viral hepatitis C may trigger risk factors for metabolic syndromes, such as obesity and type 2 diabetes mellitus. Conclusions: It is crucial to monitor metabolic factors and take timely measures to prevent or treat metabolic syndrome in patients with chronic viral hepatitis C.

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Section: Discussionmentioning

confidence: 99%

The Influence of Metabolic Factors in Patients with Chronic Viral Hepatitis C Who Received Oral Antiviral Treatment

Gavril

Mitu

et al. 2023

Metabolites

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“…NAFLD is present in >70% of individuals with type 2 diabetes [ 60 ]. Impairment of glucose and lipid metabolism, which has been accelerated by the worldwide increase in the prevalence of obesity and type 2 diabetes, is most likely behind the increase in patients with NAFLD [ 61 ].…”

Section: Stamp2 In Type 2 Diabetes Inflammatory Diseases and Cancersmentioning

confidence: 99%

The Role of STAMP2 in Pathogenesis of Chronic Diseases Focusing on Nonalcoholic Fatty Liver Disease: A Review

Kim

Yoo

2022

Biomedicines

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Nonalcoholic fatty liver disease (NAFLD) is a major health issue. NAFLD can progress from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). NASH can progress to cirrhosis or hepatocellular carcinoma. Unfortunately, there is no currently approved pharmacologic therapy for NAFLD patients. The six transmembrane protein of prostate 2 (STAMP2), a metalloreductase involved in iron and copper homeostasis, is well known for its critical role in the coordination of glucose/lipid metabolism and inflammation in metabolic tissues. We previously demonstrated that hepatic STAMP2 could be a suitable therapeutic target for NAFLD. In this review, we discuss the emerging role of STAMP2 in the dysregulation of iron metabolism events leading to NAFLD and suggest therapeutic strategies targeting STAMP2.

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“…With the worldwide spread of a sedentary lifestyle and the Western diet, non-alcoholic fatty liver disease (NAFLD)—characterized by excessive fat accumulation in hepatocytes caused by factors other than alcohol abuse—is becoming a global health problem with approximately 30% of the world suffering from the disease ( 1 ). As NAFLD progresses, its pathology ranges from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), fibrosis, and ultimately to hepatocellular carcinoma (HCC) ( 2 ). The “multiple-hit” hypothesis for the pathogenesis of NAFLD has gradually been replaced by the “two-hit” hypothesis.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D improves hepatic steatosis in NAFLD via regulation of fatty acid uptake and β-oxidation

Lian

Zhang

et al. 2023

Front. Endocrinol.

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IntroductionThe study aimed to explore the association of serum 25(OH)D3 and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD) patients and to determine whether the effect of vitamin D (VD) is mediated by activation of the peroxisome proliferator-activated receptor α (PPARα) pathway.MethodsThe study contained a case-control study, in vivo and in vitro experiments. A case-control study was conducted to compare serum parameters between NAFLD patients and controls and to evaluate the association of 25(OH)D3 and NAFLD. In vivo study, male Wistar rats were randomly divided into control and model groups, fed a standard chow diet and a high-fat diet (HFD), respectively, for 7 weeks to generate an NAFLD model. Then, the rats were treated with VD and a PPARα antagonist (MK886) for 7 weeks. Tissue and serum were collected and assessed by biochemical assays, morphological analysis, histological analysis, and western blot analysis. In vitro, HepG2 cells were incubated with oleic acid (OA) to induce steatosis, which was evaluated by staining. HepG2 cells were pretreated with MK886 followed by calcitriol treatment, and differences in lipid metabolism-related proteins were detected by western blot.ResultsNAFLD patients were characterized by impaired liver function, dyslipidemia, and insulin resistance. Serum 25(OH)D3 was negatively associated with alanine aminotransferase (ALT) in NAFLD. VD deficiency was a risk factor for patients with no advanced fibrosis. Adequate VD status (25(OH)D3 >20 ng/mL) had a protective effect in patients after adjustment for confounding variables. NAFLD rats showed hyperlipidemia with severe hepatic steatosis, systematic inflammation, and lower serum 25(OH)D3. VD treatment ameliorated hepatic steatosis both in NAFLD rats and OA-induced HepG2 cells. Further, MK886 inhibited the anti-steatosis effect of VD.ConclusionThe study revealed that an adequate VD level may act as a protective factor in NAFLD and that VD may alleviate hepatic steatosis via the PPARα signaling pathway.

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Non‐alcoholic fatty liver disease and type 2 diabetes: An update

Cited by 51 publications

References 118 publications

The Influence of Metabolic Factors in Patients with Chronic Viral Hepatitis C Who Received Oral Antiviral Treatment

The Influence of Metabolic Factors in Patients with Chronic Viral Hepatitis C Who Received Oral Antiviral Treatment

The Role of STAMP2 in Pathogenesis of Chronic Diseases Focusing on Nonalcoholic Fatty Liver Disease: A Review

Vitamin D improves hepatic steatosis in NAFLD via regulation of fatty acid uptake and β-oxidation

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