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Acute responses of hepatic fat content to consuming fat, glucose and fructose alone and in combination in non-obese non-diabetic individuals with non-alcoholic fatty liver disease.
Kovar, J, Dusilova, T, Sedivy, P, Bruha, R, Gottfriedova, H, Pavlikova, P, Pitha, J, Smid, V, Drobny, M, Dezortova, M, et al
Journal of physiology and pharmacology : an official journal of the Polish Physiological Society. 2021;72(1)
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Non-alcoholic fatty liver disease (NAFLD) is often associated with obesity or conditions related to obesity, such as type 2 diabetes. Steatosis is one of the four stages of NAFLD, where there is a small layer of fat build-up on the liver. Currently, one in three people in the UK has simple fatty liver or steatosis. A fascinating aspect of this study is exploring the long-term cumulative effects of daily fat intake when consumed with glucose or fructose and in the pathogenesis of steatosis. In this randomised controlled study, the researchers examined the immediate impact of high-fat loads on hepatic fat content (HFC) when administered with glucose or fructose in eight healthy overweight males with NFALD. The experiments lasted only eight hours. HFC was only transiently elevated by co-administration of glucose and high-fat loading. However, fructose co-administration with multiple high-fat loads promoted HFC. Small sample size and short duration are the limitations of this study. Long-term robust studies are needed to confirm the findings. Yet, healthcare professionals can use this study to distinguish between the immediate effects of fructose or glucose when combined with multiple doses of high fat on HFC in healthy and NAFLD subjects.
Abstract
We have recently demonstrated that a high-fat load can induce immediate increase in hepatic fat content (HFC) and that such an effect can be modified differently by co-administration of fructose or glucose in healthy subjects. Therefore, we addressed the question how consumption of these nutrients affects changes in HFC in subjects with non-alcoholic fatty liver disease (NAFLD). Eight male non-obese non-diabetic patients with NAFLD underwent 6 experiments each lasting 8 hours: 1. fasting, 2. high-fat load (150 g of fat (dairy cream) at time 0), 3. glucose (three doses of 50 g at 0, 2, and 4 hours), 4. high-fat load with three doses of 50 g of glucose, 5. fructose (three doses of 50 g at 0, 2, and 4 hours), 6. high-fat load with three doses of 50 g of fructose. HFC was measured using magnetic resonance spectroscopy prior to meal administration and 3 and 6 hours later. Plasma triglycerides, non-esterified fatty acids, glucose and insulin were monitored throughout each experiment. HFC increased by 10.4 ± 6.9% six hours after a high-fat load and by 15.2 ± 12.5% after high-fat load with fructose. When co-administering glucose with fat, HFC rose only transiently to return to baseline at 6 hours. Importantly, NAFLD subjects accumulated almost five times more fat in their livers than healthy subjects with normal HFC. Consumption of a high-fat load results in fat accumulation in the liver of NAFLD patients. Fat accumulation after a fat load is diminished by glucose but not fructose co-administration.
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Fructose, high-fructose corn syrup, sucrose, and nonalcoholic fatty liver disease or indexes of liver health: a systematic review and meta-analysis.
Chung, M, Ma, J, Patel, K, Berger, S, Lau, J, Lichtenstein, AH
The American journal of clinical nutrition. 2014;100(3):833-49
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There have been increasing concerns on the relationship between non-alcoholic fatty liver disease (NAFLD) and fructose or high-fructose corn syrup (HFCS). The objective of this systematic review was to assess the effect of dietary fructose in different forms on NAFLD and various biomarkers of liver health. This review included 21 published intervention studies and found a diet supplemented with fructose or glucose increases liver fat and aspartate aminotransferase (AST) concentrations when compared with a maintenance diet in healthy adults. Based on the available research, the authors point out the relationship between liver health markers and fructose, but also recognise this association may be confounded by excess energy intake. Due to the lack of robust findings, they conclude there is insufficient evidence on HFCS and NAFLD.
Abstract
BACKGROUND Concerns have been raised about the concurrent temporal trend between simple sugar intakes, especially of fructose or high-fructose corn syrup (HFCS), and rates of nonalcoholic fatty liver disease (NAFLD) in the United States. OBJECTIVE We examined the effect of different amounts and forms of dietary fructose on the incidence or prevalence of NAFLD and indexes of liver health in humans. DESIGN We conducted a systematic review of English-language, human studies of any design in children and adults with low to no alcohol intake and that reported at least one predetermined measure of liver health. The strength of the evidence was evaluated by considering risk of bias, consistency, directness, and precision. RESULTS Six observational studies and 21 intervention studies met the inclusion criteria. The overall strength of evidence for observational studies was rated insufficient because of high risk of biases and inconsistent study findings. Of 21 intervention studies, 19 studies were in adults without NAFLD (predominantly healthy, young men) and 1 study each in adults or children with NAFLD. We found a low level of evidence that a hypercaloric fructose diet (supplemented by pure fructose) increases liver fat and aspartate aminotransferase (AST) concentrations in healthy men compared with the consumption of a weight-maintenance diet. In addition, there was a low level of evidence that hypercaloric fructose and glucose diets have similar effects on liver fat and liver enzymes in healthy adults. There was insufficient evidence to draw a conclusion for effects of HFCS or sucrose on NAFLD. CONCLUSIONS On the basis of indirect comparisons across study findings, the apparent association between indexes of liver health (ie, liver fat, hepatic de novo lipogenesis, alanine aminotransferase, AST, and γ-glutamyl transpeptase) and fructose or sucrose intake appear to be confounded by excessive energy intake. Overall, the available evidence is not sufficiently robust to draw conclusions regarding effects of fructose, HFCS, or sucrose consumption on NAFLD.