The Relationship between the Growth Hormone/Insulin-like Growth Factor System and the Histological Features of Nonalcoholic Fatty Liver Disease

Chishima, Sayaka; Kogiso, Tomomi; Matsushita, Noriko; Hashimoto, Etsuko; Tokushige, Katsutoshi

doi:10.2169/internalmedicine.56.7626

Cited by 39 publications

(36 citation statements)

References 40 publications

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“…Noninvasive Biomarkers for the Diagnosis of Liver Fibrosis and Cirrhosis DOI: http://dx.doi.org /10.5772/intechopen.84351 in patients with NAFLD and CHC and the relation to the histologic severity of NAFLD. IGFBP-3 levels were lower in patients with cirrhosis caused by NAFLD, whereas the levels did not decrease according to fibrosis grade in patients with HCVinduced chronic liver disease [46]. Our results concurred with those of that study.…”

Section: Discussionsupporting

confidence: 93%

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Noninvasive Biomarkers for the Diagnosis of Liver Fibrosis and Cirrhosis

Rosique-Oramas¹,

Martínez-Castillo²,

Guzmán³

et al. 2019

Liver Cirrhosis - Debates and Current Challenges

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The clinical importance of monitoring liver fibrosis lies in the morbidity and mortality of the chronic liver diseases in relation to the stage and progression of fibrosis. Whether the fibrosis stabilizes or regresses depends on the specific treatment. Liver biopsy, the current standard for the diagnosis, has implicit limitations due to sampling heterogeneity. There are noninvasive imaging methods, such as transient elastography that measures the stiffness of the liver, but it has some limitations (feasibility and unreliability), particularly in obese patients. FibroTest is the most widely used noninvasive serological method worldwide which is efficacious in the extreme stages of fibrosis, but these methods cannot discern intermediate stages. Liver fibrosis is a dynamic response that involves multiple cellular and molecular events with an excessive deposit of extracellular matrix. Even though there is much information on the pathophysiology of fibrosis, that knowledge is still incomplete, greatly hindering the development of both an accurate treatment and a noninvasive diagnostic method with adequate sensitivity for all the stages of fibrosis. It is known that IGFBP participates in liver homeostasis, and thus these proteins can be used as serum biomarkers during the progression of liver fibrosis in chronic hepatitis C.

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Section: Discussionsupporting

confidence: 93%

“…Since 1995, many studies have been conducted on IGFBPs in patients with liver cirrhosis due to different causes. Results have shown a decrease in IGFBP-3 concentrations and an increase in IGF-I [46,47]. IGFBPs are also thought to be associated with a high risk for liver cancer [48] and with poor prognosis [26].…”

Section: Discussionmentioning

confidence: 99%

Noninvasive Biomarkers for the Diagnosis of Liver Fibrosis and Cirrhosis

Rosique-Oramas¹,

Martínez-Castillo²,

Guzmán³

et al. 2019

Liver Cirrhosis - Debates and Current Challenges

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“…In respect of the role of the GH-IGF-I axis in the pathogenesis of general NAFLD/NASH, it has been reported that serum levels of GH, IGF-I, and IGF-binding protein 3 (IGFBP-3) were associated with hepatic steatosis and fibrosis in patients with NAFLD, even in the non-GH-deficient population [ 39 ]. Elevated levels of GH, and decreased levels of IGF-I and IGFBP-3, suggesting a presence of GH resistance, were associated with the severity of the disease in patients with NAFLD but not in patients with HCV-related chronic liver disease [ 40 ]. Lower serum IGF-I levels were associated with the severity of inflammation, hepatocyte ballooning [ 41 ], and fibrosis [ 42 ] in patients with NAFLD.…”

Section: Nafld Is An Important Complication In Adult Ghdmentioning

confidence: 99%

The Role of Growth Hormone and Insulin-Like Growth Factor-I in the Liver

Takahashi

2017

IJMS

140

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Adult growth hormone deficiency (GHD) is characterized by metabolic abnormalities associated with visceral obesity, impaired quality of life, and increased mortality. Patients with adult GHD show increased prevalence of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH), and growth hormone (GH) replacement therapy has been shown to improve these conditions. It has also been demonstrated that a decrease in the GH insulin-like growth factor-I (IGF-I) axis is closely associated with the progression of general NAFLD, suggesting a physiological role of these hormones for the maintenance of the liver. NASH histologically demonstrates inflammation, necrosis, and fibrosis, in addition to steatosis (and is a serious disease because it can progress to liver cirrhosis and hepatocellular carcinoma in a subset of cases). While fibrosis determines the prognosis of the patient, efficacious treatment for fibrosis is crucial; however, it has not yet been established. Recent studies have clarified the essential roles of GH and IGF-I in the liver. GH profoundly reduces visceral fat, which plays an important role in the development of NAFLD. Furthermore, GH directly reduces lipogenesis in the hepatocytes. IGF-I induces cellular senescence and inactivates hepatic stellate cells, therefore ameliorating fibrosis. IGF-I treatment has been shown to improve animal models of NASH and cirrhosis, suggesting potential clinical applications of IGF-I in these conditions. In this review, I will focus on the important roles of GH and IGF-I in the liver, their underlying mechanisms, and their potential therapeutic applications.

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“…Steatosis is also associated with alterations of the GH/IGF-1 axis. While data on plasma GH are inconsistent [ 42 , 43 ], studies agree on a decrease in plasma IGF-1 in NAFLD [ 42 , 43 , 44 ]. The liver being the main organ contributing to plasma IGF-1 concentration, this suggests that NAFLD alters IGF-1 production.…”

Section: Hepatic Endoplasmic Reticulum Stress and Muscle Homeostasmentioning

confidence: 99%

Muscle Loss in Chronic Liver Diseases: The Example of Nonalcoholic Liver Disease

Bandt¹,

Jegatheesan²,

Tennoune-El-Hafaia³

2018

Nutrients

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Recent publications highlight a frequent loss of muscle mass in chronic liver diseases, including nonalcoholic fatty liver disease (NAFLD), and its association with a poorer prognosis. In NAFLD, given the role of muscle in energy metabolism, muscle loss promotes disease progression. However, liver damage may be directly responsible of this muscle loss. Indeed, muscle homeostasis depends on the balance between peripheral availability and action of anabolic effectors and catabolic signals. Moreover, insulin resistance of protein metabolism only partially explains muscle loss during NAFLD. Interestingly, some data indicate specific alterations in the liver–muscle axis, particularly in situations such as excess fructose/sucrose consumption, associated with increased hepatic de novo lipogenesis (DNL) and endoplasmic reticulum stress. In this context, the liver will be responsible for a decrease in the peripheral availability of anabolic factors such as hormones and amino acids, and for the production of catabolic effectors such as various hepatokines, methylglyoxal, and uric acid. A better understanding of these liver–muscle interactions could open new therapeutic opportunities for the management of NAFLD patients.

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The Relationship between the Growth Hormone/Insulin-like Growth Factor System and the Histological Features of Nonalcoholic Fatty Liver Disease

Cited by 39 publications

References 40 publications

Noninvasive Biomarkers for the Diagnosis of Liver Fibrosis and Cirrhosis

Noninvasive Biomarkers for the Diagnosis of Liver Fibrosis and Cirrhosis

The Role of Growth Hormone and Insulin-Like Growth Factor-I in the Liver

Muscle Loss in Chronic Liver Diseases: The Example of Nonalcoholic Liver Disease

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