Lower levels of insulin‐like growth factor‐1 standard deviation score are associated with histological severity of non‐alcoholic fatty liver disease

Sumida, Yoshio; Yasuda, Yoshikazu; Tanaka, Saiyu; Mori, Kumiko; Kanemasa, Kazuyuki; Imai, Shoichi; Taketani, Hiroyoshi; Hara, Tasuku; Seko, Yuya; Ishiba, Hiroshi; Okajima, Akira; Yamaguchi, Kanji; Moriguchi, Michihisa; Mitsuyoshi, Hironori; Yasui, Kohichiroh; Minami, Masahito; Itoh, Yoshito

doi:10.1111/hepr.12408

Cited by 66 publications

(48 citation statements)

References 52 publications

(110 reference statements)

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“…On the other hand, the relationship between insulin resistance and NAFLD has also been recognized [40]. Low IGF-1 levels is associated with liver steatosis [41]. A previous study showed that insulin resistance has a negative correlation with muscle mass and has a positive correlation with liver fat accumulation [17].…”

Section: Discussionmentioning

confidence: 99%

The relationship between hepatic steatosis and skeletal muscle mass index in men with type 2 diabetes

et al. 2016

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Section: Discussionmentioning

confidence: 99%

The relationship between hepatic steatosis and skeletal muscle mass index in men with type 2 diabetes

et al. 2016

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“…Likewise, cessation of GH treatment in GH-deficient (GHD) children after achieving adult height leads to development of NAFLD and dyslipidemia in 29% of patients surveyed 10 years after therapy (2). Importantly, reductions in circulating GH (2,5) or its mediator, IGF-1 (6–8), associate with NAFLD even after adjusting to BMI (9). Obese patients manifest GH resistance and can show declines in GH (10,11) that may be as low as those observed in GHD subjects (12,13).…”

Section: Introductionmentioning

confidence: 99%

Growth Hormone Control of Hepatic Lipid Metabolism

et al. 2016

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In humans, low levels of growth hormone (GH) and its mediator, IGF-1, associate with hepatic lipid accumulation. In mice, congenital liver-specific ablation of the GH receptor (GHR) results in reductions in circulating IGF-1 and hepatic steatosis, associated with systemic insulin resistance. Due to the intricate relationship between GH and IGF-1, the relative contribution of each hormone to the development of hepatic steatosis is unclear. Our goal was to dissect the mechanisms by which hepatic GH resistance leads to steatosis and overall insulin resistance, independent of IGF-1. We have generated a combined mouse model with liver-specific ablation of GHR in which we restored liver IGF-1 expression via the hepatic IGF-1 transgene. We found that liver GHR ablation leads to increases in lipid uptake, de novo lipogenesis, hyperinsulinemia, and hyperglycemia accompanied with severe insulin resistance and increased body adiposity and serum lipids. Restoration of IGF-1 improved overall insulin sensitivity and lipid profile in serum and reduced body adiposity, but was insufficient to protect against steatosis-induced hepatic inflammation or oxidative stress. We conclude that the impaired metabolism in states of GH resistance results from direct actions of GH on lipid uptake and de novo lipogenesis, whereas its actions on extrahepatic tissues are mediated by IGF-1.

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“…In addition, insulin-like growth factor (IGF)-1 and insulin share common downstream components [35], which makes it plausible that IR has an negative effect on IGF-1-dependent protection against skeletal muscle loss [36]. Simultaneously, there exists a negative relationship between IGF-1 and hepatic fibrosis [37].…”

Section: Discussionmentioning

confidence: 99%

Sarcopenia Contributes to the Progression of Nonalcoholic Fatty Liver Disease- Related Fibrosis: A Meta-Analysis

Pan

Han

Zou

et al. 2018

Dig Dis

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Backgrounds and Aims: Previous studies have investigated that sarcopenia is associated with nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis, and fibrosis in NAFLD. The study aims to investigate the risk for NAFLD, especially NAFLD-related significant fibrosis among subjects with sarcopenia. Methods: We searched electronic databases until 30, September 2017 and reviewed literature extensively. Effect estimates were pooled using random effect models regarding the risk for NAFLD and fixed effect models concerning the risk for significant fibrosis among sarcopenia patients. Sensitivity analysis was performed for the risk of NAFLD. Results: We identified 6 studies. Our results showed that subjects with sarcopenia exhibited an increased risk for NAFLD compared to those without sarcopenia (OR 1.29, 95% CI 1.12–1.49) with heterogeneity among the individual studies (I² = 61%). And the risk for NAFLD-related significant fibrosis appeared to be more pronounced in sarcopenia patients (OR 1.57, 95% CI 1.29–1.90) with an I² of 0%. Sensitivity analysis revealed that neither the direction nor the magnitude of the estimated pooled results for NAFLD was obviously affected. Furthermore, the pooled ORs were both close to initial analysis when omitting the study by Hong et al. [Hepatology 2014; 59: 1772–1778] (OR 1.24, 95% CI 1.11–1.39, I² = 47%) or by Hashimoto et al. [Endocr J 2016; 63: 877–884] (OR 1.33, 95% CI 1.11–1.59, I² = 67%), which were considered sources of heterogeneity. Conclusions: Our analysis demonstrated that sarcopenia served not only as a risk factor for the onset of NAFLD but also related to the progression of NAFLD-related significant fibrosis.

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Lower levels of insulin‐like growth factor‐1 standard deviation score are associated with histological severity of non‐alcoholic fatty liver disease

Abstract: Low levels of circulating IGF-1 may have a role in the development of advanced NAFLD, independent of insulin resistance. Supplementation with GH/IGF-1 may be a candidate for the treatment of NASH.

Cited by 66 publications

References 52 publications

The relationship between hepatic steatosis and skeletal muscle mass index in men with type 2 diabetes

The relationship between hepatic steatosis and skeletal muscle mass index in men with type 2 diabetes

Growth Hormone Control of Hepatic Lipid Metabolism

Sarcopenia Contributes to the Progression of Nonalcoholic Fatty Liver Disease- Related Fibrosis: A Meta-Analysis

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