Key result
Short-term growth hormone administration in diet-induced obesity rats reduced hepatic FASN and CD36 mRNA expression and increased CPT1A mRNA expression, improving liver lipid metabolism.
Why the study?
Long-term growth hormone treatment increases lipolytic activity but decreases insulin sensitivity, whereas short-term administration may have no impact on insulin sensitivity.
Does short-term growth hormone administration improve liver lipid metabolism in diet-induced obesity rats?
Does short-term growth hormone administration improve liver lipid metabolism in diet-induced obesity rats?
Short-term growth hormone supplementation improves liver lipid metabolism and may slow the progression of NAFLD in a diet-induced obesity rat model.
Hypothesis-generating for growth hormone effects on hepatic lipid genes in obesity; leaves open human translation.
Obesity has been linked to metabolic syndrome, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD). Obesity causes a decrease in growth hormone (GH) levels and an increase in insulin levels. Long-term GH treatment increased lipolytic activity as opposed to decreasing insulin sensitivity. Nonetheless, it is possible that short-term GH administration had no impact on insulin sensitivity. In this study, the effect of short-term GH administration on liver lipid metabolism and the effector molecules of GH and insulin receptors were investigated in diet-induced obesity (DIO) rats. Recombinant human GH (1 mg/kg) was then administered for 3 days. Livers were collected to determine the hepatic mRNA expression and protein levels involved in lipid metabolism. The expression of GH and insulin receptor effector proteins was investigated. In DIO rats, short-term GH administration significantly reduced hepatic fatty acid synthase (FASN) and cluster of differentiation 36 (CD36) mRNA expression while increasing carnitine palmitoyltransferase 1A (CPT1A) mRNA expression. Short-term GH administration reduced hepatic FAS protein levels and downregulated gene transcription of hepatic fatty acid uptake and lipogenesis, while increasing fatty acid oxidation in DIO rats. DIO rats had lower hepatic JAK2 protein levels but higher IRS-1 levels than control rats due to hyperinsulinemia. Our findings suggest that short-term GH supplementation improves liver lipid metabolism and may slow the progression of NAFLD, where GH acts as the transcriptional regulator of related genes.
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Likitnukul et al. (2023) studied Diet-induced obesity. Recombinant human GH vs. Control rats was evaluated on Hepatic mRNA expression and protein levels involved in lipid metabolism. Short-term growth hormone administration in diet-induced obesity rats reduced hepatic FASN and CD36 mRNA expression and increased CPT1A mRNA expression, improving liver lipid metabolism.
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