Beyond the Paradigm of Weight Loss in Non-Alcoholic Fatty Liver Disease: From Pathophysiology to Novel Dietary Approaches.
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ABSTRACT:
SUBMITTER: Armandi A
PROVIDER: S-EPMC8226973 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Although the 'Low-Fat' diet was the predominant public health recommendation for weight loss and weight control for the past several decades, the obesity epidemic continued to grow during this time period. An alternative 'low-carbohydrate' (Low-Carb) approach, although originally dismissed and even vilified, was comparatively tested in a series of studies over the past decade, and has been found in general to be as effective, if not more, as the Low-Fat approach for weight loss and for several related metabolic health measures. From a glass half full perspective, this suggests that there is more than one choice for a dietary approach to lose weight, and that Low-Fat and Low-Carb diets may be equally effective. From a glass half empty perspective, the average amount of weight lost on either of these two dietary approaches under the conditions studied, particularly when followed beyond 1 year, has been modest at best and negligible at worst, suggesting that the two approaches may be equally ineffective. One could resign themselves at this point to focusing on calories and energy intake restriction, regardless of macronutrient distributions. However, before throwing out the half-glass of water, it is worthwhile to consider that focusing on average results may mask important subgroup successes and failures. In all weight-loss studies, without exception, the range of individual differences in weight change within any particular diet groups is orders of magnitude greater than the average group differences between diet groups. Several studies have now reported that adults with greater insulin resistance are more successful with weight loss on a lower-carbohydrate diet compared with a lower-fat diet, whereas adults with greater insulin sensitivity are equally or more successful with weight loss on a lower-fat diet compared with a lower-carbohydrate diet. Other preliminary findings suggest that there may be some promise with matching individuals with certain genotypes to one type of diet over another for increasing weight-loss success. Future research to address the macronutrient intake component of the obesity epidemic should build on these recent insights and be directed toward effectively classifying individuals who can be differentially matched to alternate types of weight-loss diets that maximize weight-loss and weight-control success.
| S-EPMC4109087 | biostudies-other
Project description:Non-alcoholic fatty liver disease (NAFLD) is the first cause of chronic liver disease and is also associated with other harmful entities such as obesity, metabolic syndrome, dyslipidemia, and diabetes. NAFLD is a significant public health concern worldwide, impacting individuals of all ages, and its prevalence is projected to increase in the near future due to its connection with obesity. Intrinsic (genetics) and external (lifestyle) factors may also modulate NAFLD, and, in turn, may partly explain the observed relationship between NAFLD and cardiovascular disease (CVD). Although many drugs are been tested to treat NAFLD, to date, no drug has indication to specifically treat this disorder. Thus, the current management of NAFLD relies on lifestyle modifications and specifically on weight loss, physical activity, and the intake of a healthy diet. In the present narrative review, we will discuss the effects of certain dietary patterns on NAFLD incidence and progression.
| S-EPMC10058124 | biostudies-literature
Project description:Lifestyle interventions, namely optimizing nutrition and increasing physical activity, remain the cornerstone of therapy for non-alcoholic fatty liver disease (NAFLD), as this can lead to the significant improvement or resolution of disease. The optimal nutritional approach to treat NAFLD remains unclear. The aim of this systematic review is to evaluate the effectiveness of different nutritional patterns on hepatic, metabolic, and weight-loss endpoints. MEDLINE via PubMed, Embase, Scopus, and Google Scholar were searched. Randomized trials of dietary interventions alone for adults with NAFLD were selected. Two authors independently reviewed articles, to select eligible studies, and performed data abstraction. Six studies, representing 317 patients, were included. The participants had a median age of 46, mean body mass index (BMI) 31.5 and were 64.3% male. The mean study duration was 16.33 ± 8.62 weeks. Reduction in hepatic steatosis (HS) was statistically significant in 3/5 Mediterranean Diet (MD), one low-carbohydrate, one intermittent fasting (IF) and 1/2 low fat (LF) diet interventions. A total of 3/5 studies using MD, 1/2 LF interventions, and the one IF intervention demonstrated significant reductions in weight. In conclusion, there appears to be most data in support of MD-based interventions, though further randomized trials are needed to assess comparative effectiveness for NAFLD.
| S-EPMC6950283 | biostudies-literature
Project description:ObjectiveObesity, often associated with non-alcoholic fatty liver disease (NAFLD), is characterized by an imbalance between energy expenditure and food intake, which is also reflected by desensitization of fibroblast growth factor 21 (FGF21). FGF21 is strongly influenced, among others, by TNFα, which is known to be upregulated in obesity-induced inflammation. Successful long-term treatments of NAFLD might be dietary modification, exercise, or fasting.Materials and methodsWhether succeeded NAFLD recovery is linked with improved FGF21 sensitivity and finally reverted FGF21 resistance was the focus of the present study. For this purpose, mice received a high-fat diet (HFD) for 6 months to establish obesity. Afterward, the mice were subjected to three different weight loss interventions, namely, dietary change to low-fat diet (LFD), treadmill training, and/or time-restricted feeding for additional 6 months, whereas one group remained on HFD.ResultsIn addition to the expected decrease in NAFLD activity with dietary change, this was also observed in the HFD group with additional time-restricted feeding. There was also an associated decrease in hepatic TNFα and FGF21 expression and an increase in ß-klotho expression, demonstrated mainly by using principal component analysis. Pearson correlation analysis shows that independent of any intervention, TNFα expression decreased with improved NAFLD recovery. This was accompanied with higher FGF21 sensitivity, as expressed by an increase in β-klotho and FGFR1c expression and concomitantly decreased FGF21 levels.ConclusionIn summary, we conclude that successful NAFLD therapy is associated with a reversion of the TNFα-triggered FGF21-resistant state or desensitization.
| S-EPMC9399780 | biostudies-literature
Project description:Non-alcoholic fatty liver disease (NAFLD) is a multifaceted metabolic disorder, whose spectrum covers clinical, histological and pathophysiological developments ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and liver fibrosis, potentially evolving into cirrhosis, hepatocellular carcinoma and liver failure. Liver biopsy remains the gold standard for diagnosing NAFLD, while there are no specific treatments. An ever-increasing number of high-throughput Omics investigations on the molecular pathobiology of NAFLD at the cellular, tissue and system levels produce comprehensive biochemical patient snapshots. In the clinical setting, these applications are considerably enhancing our efforts towards obtaining a holistic insight on NAFLD pathophysiology. Omics are also generating non-invasive diagnostic modalities for the distinct stages of NAFLD, that remain though to be validated in multiple, large, heterogenous and independent cohorts, both cross-sectionally as well as prospectively. Finally, they aid in developing novel therapies. By tracing the flow of information from genomics to epigenomics, transcriptomics, proteomics, metabolomics, lipidomics and glycomics, the chief contributions of these techniques in understanding, diagnosing and treating NAFLD are summarized herein.
| S-EPMC7377759 | biostudies-literature
Project description:Background: Evidence on the association of non-alcoholic fatty liver disease (NAFLD), a public health concern, with dietary fiber intake is inconsistent. Objective: To investigate the relationship between dietary fiber intake from different sources and NAFLD risk in US adults. Methods: Data were collected from the 2007-2014 National Health and Nutrition Examination Survey. NAFLD was defined as a United States Fatty Liver Index ≥30, and dietary fiber intake was assessed through two 24-h dietary recall interviews. Logistic regression and restricted cubic spline models were used to explore the relationship of dietary intakes of total, cereal, fruit, and vegetable fiber with NAFLD risk. Results: A total of 6,613 participants, aged more than 20 years, were included in this study. After adjusting for multiple confounding factors, the odds ratios and 95% confidence intervals of NAFLD for the highest quartile vs. lowest quartile intakes of total, cereal, fruit, and vegetable fiber were 0.12 (0.08-0.16), 0.25 (0.19-0.33), 0.41 (0.33-0.52), and 0.42 (0.32-0.56), respectively. In stratified analyses by sex and age, statistically significant negative associations of dietary intakes of total, cereal, fruit, and vegetable fiber with NAFLD risk were observed in all participants. Dose-response analysis indicated a non-linear correlation between NAFLD risk and dietary intake of total fiber, whereas the relationship was linear for cereal, fruit, and vegetable fiber intakes. Conclusion: Total, cereal, fruit, and vegetable fiber intakes exhibit negative correlations with NAFLD risk in the general adult population in the United States.
| S-EPMC7710900 | biostudies-literature
Project description:Background and Aims: Previous studies have explored the associations between nutrition (food groups, nutrients, and dietary patterns) and the prevalence of non-alcoholic fatty liver disease. However, it remains unclear whether how foods are consumed together is associated with non-alcoholic fatty liver disease. The present study aims to construct dietary networks from network science and to explore the associations between complex dietary networks and non-alcoholic fatty liver disease. Methods: The present case-control study generated 2,043 multivariate matched controls for 2,043 newly diagnosed non-alcoholic fatty liver disease cases. Mutual information, which represents both linear and non-linear dependencies among food groups, was used to construct the network topologies. Results: The dietary topologies in the studied case and control groups were different despite the fact that only few food groups show differences in absolute intake. The dietary structure of the case group focused on two major components with more cohesion among food groups, while contrarily the control group had one major component with higher diversity of food groups. The dietary topology of the case group showed equality in connections among beneficial and detrimental food groups, whereas the control group focused more on healthier food choices. Conclusions: This study suggests how foods are consumed, besides the absolute intake, could be an important determinant of the occurrence of non-alcoholic fatty liver disease. A diverse diet that focuses on whole grain, tubers, and vegetables could yield beneficial effects regarding non-alcoholic fatty liver disease. Network science could offer a complementary tool in nutritional epidemiology.
| S-EPMC7557363 | biostudies-literature
Project description:Protective effects of granulocyte colony stimulating factor (G-CSF) in acute liver injury via marrow cell mobilization have been reported in several studies. But exact mode of action and optimal protocol of G-CSF has been still doubt in chronic disease. Here we investigated mode of action and optimization of G-CSF as a treatment for non-alcoholic fatty liver disease (NAFLD). Various doses of conventional G-CSF (30 ?g/kg once weekly, once daily for 5 days, twice weekly) and long acting G-CSF (30 ?g/kg once a month) were evaluated in two kinds of NAFLD animal models to optimize the G-CSF protocol. G-CSF receptor expression highest increased in NAFLD model among various liver diseases compare to control (NAFLD: 14.7 times, alcohol hepatitis: 7.1 times, cirrhosis: 2.4 times, and ischemia reperfusion: 6.8 times). G-CSF treatment reduced intrahepatic fat accumulation, and inflammation in two kinds of NAFLD animal models. G-CSF increased PI3K/Akt expression in hepatocyte as well as decreased apoptotic drive (increased Bcl-2 expression and decreased Bax expression) in animal model. Five day consecutive G-CSF treatment and once a month long acting G-CSF increased marrow derived stem cell marker in peripheral blood. But twice a week conventional G-CSF treatment did not increased CD34+ cell in peripheral blood and liver neither. Not only high dose G-CSF (once daily for 5 days) but also hepatotropic dose G-CSF (twice a week) significantly reduced hepatocyte apoptosis via PI3K and Akt pathway activation without marrow cell mobilization in NAFLD animal model.
| S-EPMC5716706 | biostudies-literature
Project description:The prevalence of non-alcoholic fatty liver disease (NAFLD) in heart failure (HF) preserved left ventricular ejection fraction (HFpEF) patients could reach 50%. Therefore, NAFLD is considered an emerging risk factor. In 20% of NAFLD patients, the condition progresses to non-alcoholic steatohepatitis (NASH), the aggressive form of NAFLD characterized by the development of fibrosis in the liver, leading to cirrhosis. The purpose of this review is to provide an overview of the relationships between NAFLD and HFpEF and to discuss its impact in clinical setting. Based on international reports published during the past decade, there is growing evidence that NAFLD is associated with an increased incidence of cardiovascular diseases, including impaired cardiac structure and function, arterial hypertension, endothelial dysfunction, and early carotid atherosclerosis. NAFLD and HFpEF share common risk factors, co-morbidities, and cardiac outcomes, in favour of a pathophysiological continuum. Currently, NAFLD and NASH are principally managed with non-specific therapies targeting insulin resistance like sodium-glucose co-transporter-2 inhibitors and liraglutide, which can effectively treat hepatic and cardiac issues. Studies including HFpEF patients are ongoing. Several specific NAFLD-oriented therapies are currently being developed either alone or as combinations. NAFLD diagnosis is based on a chronic elevation of liver enzymes in a context of metabolic syndrome and insulin resistance, with fibrosis scores being available for clinical practice. In conclusion, identifying HF patients at risk of NAFLD is a critically important issue. As soon as NAFLD is confirmed and its severity determined, patients should be proposed a management focused on symptoms and co-morbidities.
| S-EPMC8006705 | biostudies-literature
Project description:Background & aimHepatic fat excess in non-alcoholic fatty liver disease (NAFLD) reflects an imbalance between fat accumulation and disposal. Conflicting data exist for the role of fatty acid oxidation (FAO), one of the disposal pathways, and have mostly come from the studies delivering fatty acids (FAs) intravenously. Whether FAO of orally provided FAs is affected in NAFLD is unknown.MethodsWe performed a breath test study to measure FAO in subjects with NAFLD and healthy controls. Subjects ingested [1-13 C] palmitic acid (PA, 10 mg/kg) in a liquid meal and the rate of 13 CO2 appearance in expired air was measured over 6 hours by a BreathID device (Exalenz) to obtain the cumulative percent dose recovered (CPDR), the total amount of ingested 13 C recovered. CPDR was corrected by the results of a [1-13 C] acetate breath test, performed 1-4 weeks later, to calculate the rate of PA ?-oxidation.ResultsPalmitic acid oxidation was 27% lower in 43 subjects with NAFLD compared to 11 controls (CPDR 9.5 ± 2.4% vs 13.1 ± 3.7%, P = .0001) and this persisted after correcting for acetate (29.3 ± 10.5 vs 36.6 ± 13.9, P = .03). The decrease in FAO was not because of the delayed transit as the time to peak 13 C detection did not differ between groups (4.9 ± 1.2 hours vs 4.7 ± 0.8 hours, P = .7). Rates of PA oxidation were not correlated with obesity, hepatic or adipose insulin resistance, alanine aminotransferase, liver fat content and NAFLD histology.ConclusionFatty acid oxidation of orally delivered FA is decreased in NAFLD compared to healthy controls, likely reflecting decreased ?-oxidation. The use of a breath test offers non-invasive dynamic assessment of FAO.
| S-EPMC7056545 | biostudies-literature