Role of growth hormone, insulin-like growth factor 1 and insulin-like growth factor-binding protein 3 in development of non-alcoholic fatty liver disease

Ichikawa, Tatsuki; Nakao, Kazuwa; Hamasaki, Koji; Furukawa, Ryuji; Tsuruta, Shotarou; Ueda, Yasuo; Taura, Naota; Shibata, Hidetaka; Fujimoto, Masumi; Toriyama, Kan; Eguchi, Katsumi

doi:10.1007/s12072-007-9007-4

Cited by 104 publications

(93 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Introduction of the parameter permitted us to additionally manifest the relatively more or less pronounced negative correlations of the parameter with several clinical data (age, grading, AFP concentration, staging). In our patients, we were not able to confirm the apparently evident coexistence of lowered S-IGF-1 and serum IGF-1/IGFBP-3 values and the highest IGFBP-3 levels with liver steatosis, reported earlier by other authors in their studies on isolated fatty degeneration of the liver (22) or non-alcoholic fatty liver disease and portal fibrosis (49). In the present study, quantitative evaluation of tissue IGFBP-3 expression in HCV-infected livers demonstrated a notably significant overexpression of the protein in CH-C patients as compared to the control and HCC patients.…”

Section: Discussioncontrasting

confidence: 99%

The insulin-like growth factor-1 and expression of its binding protein-3 in chronic hepatitis C and hepatocellular carcinoma

Adamek¹,

Kasprzak²,

Mikos³

et al. 2013

Oncology Reports

View full text Add to dashboard Cite

Section: Discussioncontrasting

confidence: 99%

The insulin-like growth factor-1 and expression of its binding protein-3 in chronic hepatitis C and hepatocellular carcinoma

Adamek¹,

Kasprzak²,

Mikos³

et al. 2013

Oncology Reports

View full text Add to dashboard Cite

“…We did, however, observe a significant inverse correlation between intrahepatic fat and serum IGF1. This is in line with studies on rodents and human subjects, where intrahepatic fat is determined by reduced GH secretion and action (32,33,34). Moreover, treatment of acromegalic patients with a GH antagonist increases intrahepatic fat content (22).…”

Section: European Journal Of Endocrinologysupporting

confidence: 88%

GH signaling in skeletal muscle and adipose tissue in healthy human subjects: impact of gender and age

Vestergaard

Vendelbo

Pedersen

et al. 2014

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: The mechanisms underlying the impact of age and gender on the GH-IGF1 axis remain unclear. We tested the hypothesis that age and gender have impacts on GH signaling in human subjects in vivo. Design: A total of 20 healthy non-obese adults ('young group' !30 years (5F/5M) and 'old group' O60 years (5F/5M)) were studied after: i) an i.v. GH bolus (0.5 mg) and ii) saline. Methods: Muscle and fat biopsies were obtained after 30 and 120 min. Total and phosphorylated STAT5B proteins, gene expression of IGF1, SOCS1, SOCS2, SOCS3 and CISH, body composition, VO 2max , and muscle strength were measured. Results: In the GH-unstimulated state, women displayed significantly elevated levels of CISH mRNA in muscle (PZ0.002) and fat (PZ0.05) and reduced levels of IGF1 mRNA in fat. Phosphorylated STAT5B (pSTAT5b) was maximally increased in all subjects 30 min after GH exposure and more pronounced in women when compared with men (PZ0.01). IGF1, SOCS1, SOCS2, SOCS3, and CISH mRNA expression increased significantly in muscle after 120 min in all subjects with no impact of age and gender. GH-induced pSTAT5b correlated inversely with lean body mass (LBM; rZK0.56, PZ0.01) and positively with the CISH mRNA response (rZ0.533, PZ0.05). Conclusion: i) GH signaling in muscle and fat after a single GH bolus in healthy human subjects is age independent, ii) we hypothesize that constitutive overexpression of CISH may contribute to the relative GH resistance in women, and iii) experimental studies on the impact of sex steroid administration and physical training on GH signaling in human subjects in vivo are required.

show abstract

“…Conversely, a smaller study of 55 patients with NAFLD found no association between grade of fibrosis and GH concentrations. Perhaps unsurprisingly, as IGF1 is predominantly produced by the liver, there was a negative correlation between IGF1 and fibrosis stage (58) and low levels of circulating IGF1 in patients with NAFLD has been replicated in other studies (59). Using dynamic tests, peak levels of GH and IGF1 are reduced in patients with NAFLD (60), and in patients with pituitary disease, GH deficiency appears to be associated with increased hepatic lipid content (61).…”

Section: Oestrogensmentioning

confidence: 83%

Mechanisms in endocrinology: Non-alcoholic fatty liver disease in common endocrine disorders

Hazlehurst

Tomlinson

2013

European Journal of Endocrinology

View full text Add to dashboard Cite

Non-alcoholic fatty liver disease (NAFLD) is a spectrum of disease spanning from simple benign steatosis to steatohepatitis with fibrosis and scarring that can eventually lead to cirrhosis. Its prevalence is rising rapidly and is developing into the leading indication for liver transplantation worldwide. Abnormalities in endocrine axes have been associated with NALFD, including hypogonadism, hypothyroidism, GH deficiency and hypercortisolaemia. In some instances, correction of the endocrine defects has been shown to have a beneficial impact. While in patients with type 2 diabetes the association with NAFLD is well established and recognised, there is a more limited appreciation of the condition among common endocrine diseases presenting with hormonal excess or deficiency. In this review, we examine the published data that have suggested a mechanistic link between endocrine abnormalities and NAFLD and summarise the clinical data endorsing these observations.

show abstract

Role of growth hormone, insulin-like growth factor 1 and insulin-like growth factor-binding protein 3 in development of non-alcoholic fatty liver disease

Abstract: GH, IGF-1 and IGFBP-3 are associated with hepatic fibrosis and steatosis in NAFLD. Low levels of IGF-1 might be associated with fibrosis while low level of GH with hepatic steatosis.

Cited by 104 publications

References 41 publications

The insulin-like growth factor-1 and expression of its binding protein-3 in chronic hepatitis C and hepatocellular carcinoma

The insulin-like growth factor-1 and expression of its binding protein-3 in chronic hepatitis C and hepatocellular carcinoma

GH signaling in skeletal muscle and adipose tissue in healthy human subjects: impact of gender and age

Mechanisms in endocrinology: Non-alcoholic fatty liver disease in common endocrine disorders

Contact Info

Product

Resources

About