Abstract
BackgroundNon-alcoholic fatty liver disease (NAFLD), which is characterized by hepatic steatosis, can be reversed by early treatment. Several case reports have indicated that the administration of recombinant growth hormone (GH) could improve fatty liver in GH-deficient patients. Here, we investigated whether chronic exogenous GH levels could improve hepatic steatosis induced by a high-fat diet in rats, and explored the underlying mechanisms.ResultsHigh-fat diet-fed rats developed abdominal obesity, fatty liver and insulin resistance. Chronic exogenous GH improved fatty liver, by reversing dyslipidaemia, fat accumulation and insulin resistance. Exogenous GH also reduced serum tumour necrosis factor-alpha (TNF-alpha) levels, and ameliorated hepatic lipid peroxidation and oxidative stress. Hepatic fat deposition was also reduced by exogenous GH levels, as was the expression of adipocyte-derived adipokines (adiponectin, leptin and resistin), which might improve lipid metabolism and hepatic steatosis. Exogenous GH seems to improve fatty liver by reducing fat weight, improving insulin sensitivity and correcting oxidative stress, which may be achieved through phosphorylation or dephosphorylation of a group of signal transducers and activators of hepatic signal transduction pathways.ConclusionsChronic exogenous GH has positive effects on fatty liver and may be a potential clinical application in the prevention or reversal of fatty liver. However, chronic secretion of exogenous GH, even at a low level, may increase serum glucose and insulin levels in rats fed a standard diet, and thus increase the risk of insulin resistance.
Highlights
Non-alcoholic fatty liver disease (NAFLD), which is characterized by hepatic steatosis, can be reversed by early treatment
Body composition, liver wet weight and hepatic index (HI) The daily food intake was virtually identical among the four groups of rats (Fig. 1); the high-fat diet caused significant body weight gain compared with the control diet and the body weight of the CH group was significantly greater than that of the CS group at week 12 (p < 0.01) (Table 1)
In the high-fat diet fed rats, exogenous growth hormone (GH) levels reduced the body weight gain compared with the control group (GH vs. CH, p < 0.05) (Table 1), even though food intake was marginally increased in the GH group
Summary
Non-alcoholic fatty liver disease (NAFLD), which is characterized by hepatic steatosis, can be reversed by early treatment. Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder characterized by fatty infiltration of the liver in the absence of alcohol consumption. It is the most common cause of chronic liver disease and represents a spectrum of liver diseases, which include simple fatty liver, steatohepatitis, and cirrhosis [1]. Hepatic steatosis is a hallmark of NAFLD and is caused by the accumulation of lipids, triglycerides, in the liver. Usually considered as an early stage of NAFLD, is generally benign, relatively non-aggressive and reversible. The symptoms are not obvious and the disease is often overlooked
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