scholarly journals Beyond Body Weight-Loss: Dietary Strategies Targeting Intrahepatic Fat in NAFLD

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1316 ◽  
Author(s):  
Nicolai Worm
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Body Weight ◽  
Liver Disease ◽  
Glycogen Synthesis ◽  
Liver Fat ◽  
Meal Replacement ◽  
Alcoholic Fatty Liver ◽  
Therapeutic Concept ◽  
The Metabolic Syndrome

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent liver disease in industrialized countries. It is regarded as the hepatic manifestation of the metabolic syndrome (MetS) resulting from insulin resistance. Moreover, insulin resistance impairs glycogen synthesis, postprandially diverting a substantial amount of carbohydrates to the liver and storing them there as fat. NAFLD has far-reaching metabolic consequences involving glucose and lipoprotein metabolism disorders and risk of cardiovascular disease, the leading cause of death worldwide. No pharmaceutical options are currently approved for the treatment of NAFLD. Exercise training and dietary interventions remain the cornerstone of NAFLD treatment. Current international guidelines state that the primary goal of nutritional therapy is to reduce energy intake to achieve a 7%–10% reduction in body weight. Meal replacement therapy (formula diets) results in more pronounced weight loss compared to conventional calorie-restricted diets. However, studies have shown that body mass index (BMI) or weight reduction is not obligatory for decreasing hepatic fat content or to restore normal liver function. Recent studies have achieved significant reductions in liver fat with eucaloric diets and without weight loss through macronutrient modifications. Based on this evidence, an integrative nutritional therapeutic concept was formulated that combines the most effective nutrition approaches termed “liver-fasting.” It involves the temporary use of a low calorie diet (total meal replacement with a specific high-protein, high-soluble fiber, lower-carbohydrate formula), followed by stepwise food reintroduction that implements a Mediterranean style low-carb diet as basic nutrition.

Healthy PNPLA3 Risk Allele Carriers Present with Unexpected Body Fat Composition. A Study of One ousand Subjects

2014 ◽  
Vol 23 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Agnieszka Kempinska-Podhorodecka ◽  
Marcin Krawczyk ◽  
Marta Klak ◽  
Malgorzata Blatkiewicz ◽  
Frank Lammert ◽  
...  
Keyword(s):  
Body Weight ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Anthropometric Characteristics ◽  
The Common ◽  
Total Fat ◽  
Alcoholic Fatty Liver Disease

Introduction: The common PNPLA3 (adiponutrin) variant p.I148M represents a major genetic driver of progression in non-alcoholic fatty liver disease (NAFLD). NAFLD is commonly associated with traits of the metabolic syndrome, therefore it is mostly suspected in obese individuals. Here, we investigate the association between the PNPLA3 variant and anthropometric traits in a cohort of healthy individuals.Patients and methods: We recruited 1,000 (500 females; age 18 - 66 years) healthy blood donors. The PNPLA3 variant was genotyped using TaqMan assays. All individuals were phenotyped with respect to anthropometric characteristics. We also determined the percentage of total fat (F%) and active tissue (TA%) of body weight.Results: Healthy carriers of the PNPLA3 [IM] and [MM] genotypes, although not differing in height from individuals with the genotype [II], displayed significantly lower body weight and lower BMI (both P = 0.005), higher TA% (P = 0.03) but lower F% (P = 0.03) and smaller waist, chest and shin circumferences (all P < 0.05). Separate analysis for males and females demonstrated an association between the [IM] and [MM] genotypes and higher TA% but lower F% (P = 0.04) in females. In males, BMI and total weight were significantly (P = 0.04) lower among carriers of the [M] allele.Discussion: Healthy individuals carrying the prosteatotic PNPLA3 allele p.I48M may be leaner as compared to the carriers of the common allele. Hence in clinical practice they might be overlooked since they do not necessarily present with the anthropometric characteristics commonly associated with severe hepatic steatosis.Abbreviations: ATX - autotaxin; BMI - body mass index; F% - total fat of body weight in %; Fkg - total fat of body weight in kilograms; GWAS - genome-wide association study; LPA - lysophosphatidic acid; NAFLD, non-alcoholic fatty liver disease; NASH - non-alcoholic steatohepatitis; PA - phosphatidic acid; PNPLA3-patatin-like phospholipase domain containing 3 (adiponutrin); TA% - active tissue of body weight in %; TAkg - active tissue of body weight in kilograms; WHR - waist-to-hip ratio.

scholarly journals Comparison of High Fructose Corn Syrup Versus Sucrose Consumption on Non-Alcoholic Fatty Liver Disease in Juvenile Iberian Pigs

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 691-691 ◽  
Author(s):  
Catherine Johnson ◽  
Brooke Harbottle ◽  
Gabriella Hernandez ◽  
Victoria Smith ◽  
Morgan Coffin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Liver Disease ◽  
Lean Mass ◽  
Fatty Liver Disease ◽  
High Fructose Corn Syrup ◽  
Alcoholic Fatty Liver ◽  
Corn Syrup ◽  
High Fructose ◽  
Alcoholic Fatty Liver Disease

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) is a chronic metabolic disorder and the most common liver disease in pediatric populations. Epidemiological studies have observed a parallel increase in fructose consumption and incidence of NAFLD among children. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of high fructose corn syrup (66.5% fructose, 33.5% glucose) versus sucrose (50% fructose, 50% glucose) in the diet for 16 weeks on endpoints of NAFLD and insulin resistance. Methods 30-d-old Iberian pigs were housed in pairs and randomly assigned to receive solid diets (g/kg body weight × d) of 1) control (CON; n = 6): 0 g HFCS, 0 g SUC, and 174.03 kcal metabolizable energy (ME), 2) high-fructose corn syrup (HFCS; n = 8): 31.20 g high-fructose corn syrup, 0 g sucrose and 261 kcal ME, and 3) Sucrose (SUC; n = 6): 0 g high-fructose corn syrup, 24.04 g sucrose and 261 kcal ME for 16 consecutive weeks. Results Compared to CON, both HFCS and SUC diets increased body weight gain (P ≤ 0.001), relative liver weight (P ≤ 0.01) and leptin levels (P ≤ 0.01), and decreased percentage of lean mass composition in the animals (P ≤ 0.001). In addition, HFCS increased fasting insulin levels compared to CON (P ≤ 0.05), and decreased percentage lean mass compared to SUC (P ≤ 0.05). 75% of HFCS and 66.6% of SUC pigs showed histopathological lesions consistent with microvesicular steatosis with periportal or diffuse distribution. Serum markers of liver injury did not differ between diets, and none of the animals developed inflammation, hepatocellular ballooning, Mallory hyaline or necrosis in the liver. Metabolomics analysis revealed liver sorbitol and monosaccharide concentrations were higher in both the HFCS and SUC groups versus CON (P ≤ 0.05), while adenosine monophosphate (AMP) were higher and adenosine diphosphate levels lower in the HFCS and SUC in comparison to CON (P ≤ 0.05). Numerous phosphatidylcholines and sphingomyelins were differentially changed in the HFCS group versus CON (P ≤ 0.05). Conclusions Feeding diets high in either sucrose or high fructose corn syrup promoted obesity and steatosis in the animals. Further research is needed to investigate the mechanisms leading to increased insulin resistance in the HFCS group. Funding Sources ARI #58,873, AcornSeekers, STRIDE.

scholarly journals Metabolic Syndrome and Nonalcoholic Fatty Liver Disease

2019 ◽  
Vol 16 (1) ◽  
pp. 51-58
Author(s):  
Oana Irina Gavril ◽  
Lidia Iuliana Arhire ◽  
Ovidiu Mitu ◽  
Radu Sebastian Gavril ◽  
Alexandra Mastaleru ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Normal Liver ◽  
Liver Fat ◽  
Equal Distribution ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
The Metabolic Syndrome

AbstractIntroduction. Non-alcoholic fatty liver disease (NAFLD) is regarded as the hepatic expression of the metabolic syndrome, both conditions presenting similar clinical features.Aim. The aim of this study was to evaluate, among diabetic subjects, the relationship between fatty liver load and the presence of metabolic syndrome criteria.Methods. An observational study was conducted on 92 subjects with type 2 diabetes. We followed anthropometric measurments, lipid profile, blood pressure and the degree of hepatic steatosis using ultrasonography.Results. The average age of the study group was 60,38 ± 10,37 years, with an approximately equal distribution by gender (48% male and 52% female). More than half of the subjects presented hypercholesterolemia, hypertriglyceridemia, and low HDL cholesterol level. Most of the patients included in the study had varying degrees of liver fat load (only 9,89% of cases of apparently normal liver on ultrasound), and met the criteria for metabolic syndrome (81,31%). It was found that the frequency of the cases with fatty liver impairment was significantly higher in subjects with metabolic syndrome (32,43% compared to 5,88% for those without metabolic syndrome, p = 0,01) and the frequency of the cases with normal liver were significantly higher in subjects without metabolic syndrome (23,53% to 6,76%, p=0,02).Conclusion. We can say that NAFLD is a risk factor for the presence of metabolic syndrome and it can be considered the hepatic expression of this syndrome.

scholarly journals Response of Inflammatory Biomarkers to 10 Weeks of Aerobic Resistance Training in Inactive Postmenopausal Women with Non-alcoholic Fatty Liver

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Masumeh Norouzpour ◽  
Sayed Mohammad Marandi ◽  
Mohsen Ghanbarzadeh ◽  
Abbasali Zare Maivan
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Resistance Training ◽  
Fatty Liver ◽  
Postmenopausal Women ◽  
Fatty Liver Disease ◽  
Negative Relationship ◽  
Inflammatory Biomarkers ◽  
Liver Fat ◽  
Alcoholic Fatty Liver

Background: Research evidence shows that non-alcoholic fatty liver disease (NAFLD) is closely related to inflammation. Objectives: This study aimed to evaluate the response of inflammatory biomarkers to 10 weeks of aerobic resistance exercise in inactive postmenopausal women with NAFLD. Methods: In this purposeful quasi-experimental study, conducted in Mahshahr, Iran, in 2019, 24 inactive women aged 50 - 68 years who were diagnosed with fatty liver disease by ultrasound were randomly divided into training or control groups. The training group performed aerobic resistance training for 10 weeks using treadmills and bodybuilding machines. At the beginning and end of the study, serum interleukin 18 (IL18), interleukin 10 (IL10), and other blood parameters were measured, and the subjects underwent liver ultrasound and anthropometric evaluations. Results: The results of intergroup ANCOVA, intragroup paired t-test, and Wilcoxon showed that in response to 10 weeks of training, IL18 levels, anthropometric parameters, insulin resistance (HOMA-IR), liver enzymes, fasting glucose, triglyceride (TG), and liver fat were significantly decreased and plasma IL10 was significantly increased when compared to baseline results (P < 0.05). Also, the results of the Spearman correlation test showed a significant positive relationship between IL18 and waist circumference (WC), alanine aminotransferase (ALT), and HOMA-IR and a significant negative relationship between IL10 and weight, WC, TG, HOMA-IR, and liver fat (P < 0.05). Conclusions: Ten weeks of aerobic resistance training has a significant effect on reducing serum IL18 and increasing IL10 levels in postmenopausal women with fatty liver and can be effective in improving NAFLD by losing weight, improving body composition, and reducing insulin resistance.

scholarly journals Homeostasis of Glucose and Lipid in Non-Alcoholic Fatty Liver Disease

2019 ◽  
Vol 20 (2) ◽  
pp. 298 ◽  
Author(s):  
Hsu-Wen Chao ◽  
Shi-Wei Chao ◽  
Heng Lin ◽  
Hui-Chen Ku ◽  
Ching-Feng Cheng
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Dietary Intake ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Underlying Causes ◽  
Alcoholic Fatty Liver Disease

Industrialized society-caused dysregular human behaviors and activities such as overworking, excessive dietary intake, and sleep deprivation lead to perturbations in the metabolism and the development of metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease worldwide, affects around 30% and 25% of people in Western and Asian countries, respectively, which leads to numerous medical costs annually. Insulin resistance is the major hallmark of NAFLD and is crucial in the pathogenesis and for the progression from NAFLD to non-alcoholic steatohepatitis (NASH). Excessive dietary intake of saturated fats and carbohydrate-enriched foods contributes to both insulin resistance and NAFLD. Once NAFLD is established, insulin resistance can promote the progression to the more severe state of liver endangerment like NASH. Here, we review current and potential studies for understanding the complexity between insulin-regulated glycolytic and lipogenic homeostasis and the underlying causes of NAFLD. We discuss how disruption of the insulin signal is associated with various metabolic disorders of glucoses and lipids that constitute both the metabolic syndrome and NAFLD.

scholarly journals Molecular pathways involved in the improvement of non-alcoholic fatty liver disease

2013 ◽  
Vol 51 (1) ◽  
pp. 167-179 ◽  
Author(s):  
Gilberto Paz-Filho ◽  
Claudio Alberto Mastronardi ◽  
Brian J Parker ◽  
Ainy Khan ◽  
Antonio Inserra ◽  
...  
Keyword(s):  
Body Weight ◽  
Liver Disease ◽  
Liver Injury ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Glutathione Metabolism ◽  
Wild Type ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis are components of the metabolic syndrome. Serum leptin levels are elevated in obesity, but the role of leptin in the pathophysiology of the liver involvement is still unclear. To identify the effects and mechanisms by which leptin influences the pathogenesis of NAFLD, we performed epididymal white adipose tissue (eWAT) transplantation from congenic wild-type mice into the subcutaneous dorsal area ofLepob/obrecipient mice and compared the results with those of theLepob/obsham-operated mice. The mice were followed for 102–216 days. During killing, the transplanted mice had significantly lost body weight and exhibited significantly higher leptin levels, improved glucose tolerance, and lower liver injury scores than the sham-operated mice. Liver microarray analysis showed that novel pathways related to GA-binding protein (GABP) transcription factor targets, pheromone binding, and olfactory signaling were differentially expressed in the transplanted mice. Our data also replicate pathways known to be involved in NAFLD, such as those involved in the regulation of microRNAs, lipid, glucose, and glutathione metabolism, peroxisome proliferator-activated receptor signaling, cellular regulation, carboxylic acid processes, iron, heme, and tetrapyrrole binding, immunity and inflammation, insulin signaling, cytochrome P450 function, and cancer. Conclusion: wild-type eWAT transplantation intoLepob/obmice led to improvements in metabolism, body weight, and liver injury, possibly attributed to the production of leptin by the transplanted eWAT. These improvements were accompanied by the differential expression of novel pathways. The causal relationship between GABP downregulation and NAFLD improvement remains to be determined.

scholarly journals Amylin and Calcitonin: Potential Therapeutic Strategies to Reduce Body Weight and Liver Fat

2021 ◽  
Vol 11 ◽  
Author(s):  
David S. Mathiesen ◽  
Asger Lund ◽  
Tina Vilsbøll ◽  
Filip K. Knop ◽  
Jonatan I. Bagger
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Gastric Emptying ◽  
Pancreatic Beta Cells ◽  
Metabolic Diseases ◽  
Body Weight Loss ◽  
Liver Fat ◽  
Metabolic Effects ◽  
Human Organism ◽  
Alcoholic Fatty Liver

The hormones amylin and calcitonin interact with receptors within the same family to exert their effects on the human organism. Calcitonin, derived from thyroid C cells, is known for its inhibitory effect on osteoclasts. Calcitonin of mammalian origin promotes insulin sensitivity, while the more potent calcitonin extracted from salmon additionally inhibits gastric emptying, promotes gallbladder relaxation, increases energy expenditure and induces satiety as well as weight loss. Amylin, derived from pancreatic beta cells, regulates plasma glucose by delaying gastric emptying after meal ingestion, and modulates glucagon secretion and central satiety signals in the brain. Thus, both hormones seem to have metabolic effects of relevance in the context of non-alcoholic fatty liver disease (NAFLD) and other metabolic diseases. In rats, studies with dual amylin and calcitonin receptor agonists have demonstrated robust body weight loss, improved glucose tolerance and a decreased deposition of fat in liver tissue beyond what is observed after a body weight loss. The translational aspects of these preclinical data currently remain unknown. Here, we describe the physiology, pathophysiology, and pharmacological effects of amylin and calcitonin and review preclinical and clinical findings alluding to the future potential of amylin and calcitonin-based drugs for the treatment of obesity and NAFLD.

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