1.
Applying Lipidomics to Non-Alcoholic Fatty Liver Disease: A Clinical Perspective.
Huang, J, Sigon, G, Mullish, BH, Wang, D, Sharma, R, Manousou, P, Forlano, R
Nutrients. 2023;(8)
Abstract
The prevalence of Non-alcoholic fatty liver disease (NAFLD) and associated complications, such as hepatocellular carcinoma (HCC), is growing worldwide, due to the epidemics of metabolic risk factors, such as obesity and type II diabetes. Among other factors, an aberrant lipid metabolism represents a crucial step in the pathogenesis of NAFLD and the development of HCC in this population. In this review, we summarize the evidence supporting the application of translational lipidomics in NAFLD patients and NAFLD associated HCC in clinical practice.
2.
The effects of dietary supplementation with inulin and inulin-propionate ester on hepatic steatosis in adults with non-alcoholic fatty liver disease.
Chambers, ES, Byrne, CS, Rugyendo, A, Morrison, DJ, Preston, T, Tedford, C, Bell, JD, Thomas, L, Akbar, AN, Riddell, NE, et al
Diabetes, obesity & metabolism. 2019;21(2):372-376
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Plain language summary
Non-alcoholic fatty liver disease (NAFLD) is characterised by an accumulation of fat within the liver, and is strongly associated with obesity. Recent investigations suggest that diet, the gut microbiota and liver fat storage could be linked through a mechanism involving short chain fatty acids (SCFA), in particular the SCFA propionate, which are produced by the gut bacteria. The aim of this randomised controlled study was to evaluate whether an inulin-propionate ester (IPE) has benefits in patients with NAFLD. Subjects with NAFLD received either 20 g/d of inulin (control) or IPE for 42 days. 18 subjects completed the trial. Intrahepatocellular lipids IHCL (a marker of fat accumulation in the liver) increased post supplementation in both groups with no significant difference between control and IPE group. There was a change in insulin resistance (HOMA-IR) which was significantly different between groups, with a non-significant increase in the inulin-control group and decrease in the IPE group. There were no within- or between-group differences in body composition. The authors discuss these unexpected results and suggest that the SCFA acetate, from inulin fermentation by gut bacteria, may have led to an increase in IHCL which was attenuated by the propionate.
Abstract
The short chain fatty acid (SCFA) propionate, produced through fermentation of dietary fibre by the gut microbiota, has been shown to alter hepatic metabolic processes that reduce lipid storage. We aimed to investigate the impact of raising colonic propionate production on hepatic steatosis in adults with non-alcoholic fatty liver disease (NAFLD). Eighteen adults were randomized to receive 20 g/d of an inulin-propionate ester (IPE), designed to deliver propionate to the colon, or an inulin control for 42 days in a parallel design. The change in intrahepatocellular lipid (IHCL) following the supplementation period was not different between the groups (P = 0.082), however, IHCL significantly increased within the inulin-control group (20.9% ± 2.9% to 26.8% ± 3.9%; P = 0.012; n = 9), which was not observed within the IPE group (22.6% ± 6.9% to 23.5% ± 6.8%; P = 0.635; n = 9). The predominant SCFA from colonic fermentation of inulin is acetate, which, in a background of NAFLD and a hepatic metabolic profile that promotes fat accretion, may provide surplus lipogenic substrate to the liver. The increased colonic delivery of propionate from IPE appears to attenuate this acetate-mediated increase in IHCL.
3.
Muscle cramps in cirrhosis: the therapeutic value of quinine. Is it underused?
Corbani, A, Manousou, P, Calvaruso, V, Xirouchakis, I, Burroughs, AK
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2008;(9):794-9
Abstract
Muscle cramps are a common and recurring symptom in patients with cirrhosis. Although, the pathophysiology has not been specifically studied in cirrhosis, this is thought to be the same for cramps in general, originating in the motorneurone, with high frequency firing of motor unit action potentials. However precise pathophysiological mechanisms are not known. Risk factors in cirrhosis have been little studied. Neither aetiology, nor pre-ascitic or ascitic stage, nor electrolyte disturbances, nor use of diuretic therapy has been found to have a statistical association with cramps in patients with cirrhosis. Effective treatments, from this literature review, are albumin, which however is expensive and has little applicability as preventative therapy and oral quinine or quinidine. Quinine is little used in Italy but licensed in the UK for the therapy of muscle cramps. There is evidence for the efficacy of quinine in patients without cirrhosis and in healthy subjects. In cirrhosis quinidine (isomer of quinine) has also been shown to be effective versus placebo. Its major effect is in the prevention of cramps. More widespread use of quinine and further studies are needed, particularly in Italy and other countries, in which its use has been limited, as it is effective therapy in many patients with cirrhosis.