scholarly journals Hepatic steatosis, GH deficiency and the effects of GH replacement: a Liverpool magnetic resonance spectroscopy study

2012 ◽  
Vol 166 (6) ◽  
pp. 993-1002 ◽  
Author(s):  
Chris J Gardner ◽  
Andrew J Irwin ◽  
Christina Daousi ◽  
Ian A McFarlane ◽  
Franklin Joseph ◽  
...  

ObjectiveNon-alcoholic fatty liver disease (NAFLD) is reported to be more common in patients with GH deficiency (GHD) than in the general population. We aimed to determine: i) liver fat in patients with GHD compared with age and body mass index (BMI)-matched controls; and ii) effect of 6 months of GH replacement (GHR) on liver fat.Participants and methodsThe study included 28 GHD patients and 24 controls. 12 patients were studied before and after 6 months of GHR. Anthropometry, liver enzymes and lipid profiles were measured, and body composition and intrahepatocellular lipid (IHCL) were determined by magnetic resonance imaging and spectroscopy.ResultsAge and BMI (median (inter-quartile range)) of patients and controls were 52.6 (14) vs 52.6 (12) years (P=0.9) and 27.8 (24.7, 34.7) vs 27.9 (25.1, 32.1) kg/m2(P=0.9). IGF1 was lower in the patients (11.5 vs 16.0 nmol/l,P=0.002). There was no difference in liver transaminases, lipids or IHCL between patients and controls (2.8 (1.3, 8.6) vs 5.0 (1.5, 12.7),P=0.72), despite significantly higher visceral fat in GHD patients. Thirty-two percent of patients and 50% of controls had NAFLD (defined as IHCL >5.6%), and the relationship between IHCL and BMI was the same in each group. GHR significantly reduced abdominal subcutaneous and visceral fat in all patients; however, GHR did not reduce liver fat.ConclusionsNAFLD is equally common in patients with GHD and matched controls. GHR is associated with a hierarchical reduction in fat deposition (fat loss: visceral > subcutaneous > liver). Further studies involving GHD patients with NAFLD are required to conclude the role of GHR in treating NAFLD.

2013 ◽  
Vol 44 (4) ◽  
pp. 789-795 ◽  
Author(s):  
M. J. Taylor ◽  
B. Godlewska ◽  
J. Near ◽  
D. Christmas ◽  
J. Potokar ◽  
...  

BackgroundThe development of depressive symptomatology is a recognized complication of treatment with the cytokine interferon-α (IFN-α) and has been seen as supporting inflammatory theories of the pathophysiology of major depression. Major depression has been associated with changes in glutamatergic activity and recent formulations of IFN-induced depression have implicated neurotoxic influences that could also lead to changes in glutamate function. The present study used magnetic resonance spectroscopy (MRS) to measure glutamate and its major metabolite glutamine in patients with hepatitis C who received treatment with pegylated IFN-α and ribavirin.MethodMRS measurements of glutamate and glutamine were taken from a 25 × 20 × 20 mm voxel including the pregenual anterior cingulate cortex in 12 patients before and after 4–6 weeks of treatment with IFN.ResultsIFN treatment led to an increase in cortical levels of glutamine (p = 0.02) and a significant elevation in the ratio of glutamine to glutamate (p < 0.01). Furthermore, changes in glutamine level correlated significantly with ratings of depression and anxiety at the time of the second scan.ConclusionsWe conclude that treatment with IFN-α is associated with MRS-visible changes in glutamatergic metabolism. However, the changes seen differ from those reported in major depression, which suggests that the pathophysiology of IFN-induced depression may be distinct from that of major depression more generally.


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