scholarly journals Reversion to regular diet with alternate day fasting can cure grade-I non-alcoholic fatty liver disease (NAFLD) in high-fructose-intake-associated metabolic syndrome

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nehal Mohamed Bahgat Gamil ◽  
Sahar Mohamed El Agaty ◽  
Gehan Khalaf Megahed ◽  
Rania Salah Mansour ◽  
Marwa Saad Abdel-Latif
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver Disease ◽  
Male Rats ◽  
Alcoholic Fatty Liver ◽  
Liver Histopathology ◽  
Fructose Intake ◽  
High Fructose ◽  
Alternate Day Fasting ◽  
Alcoholic Fatty Liver Disease

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is an emerging global health problem that accompanied the obesity epidemic and is considered as the hepatic component of metabolic syndrome (MetS). Modification of lifestyle of MetS patients remains the focus to reverse and prevent progression of hepatic steatosis to NAFLD and its worsening to severe forms. The present study investigates the possible curability of metabolic syndrome -associated grade-1 NAFLD merely by alternate day fasting with or without reversion to regular diet in adult male rats. The present study was performed on 66 local strain male rats aged (6–10 m.) distributed randomly into C group (n = 12), on regular rat diet; and M group (n = 54) on high fructose- intake. On the 8th week, then rats were subjected to measurement of BW, BMI, WC, FBG, IPGTT, HDL-C, TGs, and liver histopathology, to include MetS rats randomly into four experimental groups for 4 weeks as follows: MS (n = 14); MSRD (n = 12); MSF (n = 13); and MSRDF (n = 12). On the 12th week, all rats were subjected to measurements of BW, BMI, WC, LW, LW/BW, VFW, VFW/BW, FBG, IPGTT, Ins., HOMA-IR, HbA1C, TGs, TC, LDL-C, HDL-C, CRP, Alb., bilirubin, ALT, L-MDA, and liver histopathology. Results On the 8th week, M group developed MerS and grade-I NAFLD with score-4 hepatosteatosis (69%). On the 12th week, MS group had grade-1 NAFLD with score-4 hepatosteatosis (82%) with significantly increased Ins., HOMA-IR, HDL-C, LW, LW/BW, L-MDA, ALT, CRP, and significantly decreased Alb. than C rats. Both MSRD and MSF groups had grade-1 NAFLD with score-3 hepatosteatosis (42%) with significantly decreased Ins., HOMA-IR, TC, LDL-C, LW, LW/BW, L-MDA, ALT, CRP, and significantly increased HDL-C and Alb. than MS group. MSRDF rats showed cure of grade-1 NAFLD and significantly decreased LW than other groups and normalized HOMA-IR, HbA1C TC, LDL-C, ALT, and CRP. Conclusion One month of alternate-day fasting and regular rat diet could cure grade-I NAFLD associated with Mets due to high fructose intake possibly by attenuating metabolic disorders. These two interventions might be recommended in the management of MetS patients with grade 1-NAFLD disease.

scholarly journals Mechanisms of Non-Alcoholic Fatty Liver Disease in the Metabolic Syndrome. A Narrative Review

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 270
Author(s):  
Luca Rinaldi ◽  
Pia Clara Pafundi ◽  
Raffaele Galiero ◽  
Alfredo Caturano ◽  
Maria Vittoria Morone ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Risk Factor ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Smoking Habit ◽  
Lifestyle Modifications ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are two different entities sharing common clinical and physio-pathological features, with insulin resistance (IR) as the most relevant. Large evidence leads to consider it as a risk factor for cardiovascular disease, regardless of age, sex, smoking habit, cholesterolemia, and other elements of MS. Therapeutic strategies remain still unclear, but lifestyle modifications (diet, physical exercise, and weight loss) determine an improvement in IR, MS, and both clinical and histologic liver picture. NAFLD and IR are bidirectionally correlated and, consequently, the development of pre-diabetes and diabetes is the most direct consequence at the extrahepatic level. In turn, type 2 diabetes is a well-known risk factor for multiorgan damage, including an involvement of cardiovascular system, kidney and peripheral nervous system. The increased MS incidence worldwide, above all due to changes in diet and lifestyle, is associated with an equally significant increase in NAFLD, with a subsequent rise in both morbidity and mortality due to both metabolic, hepatic and cardiovascular diseases. Therefore, the slowdown in the increase of the “bad company” constituted by MS and NAFLD, with all the consequent direct and indirect costs, represents one of the main challenges for the National Health Systems.

scholarly journals High-fructose feeding does not induce steatosis or non-alcoholic fatty liver disease in pigs

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nikolaj H. Schmidt ◽  
Pia Svendsen ◽  
Julián Albarrán-Juárez ◽  
Søren K. Moestrup ◽  
Jacob Fog Bentzon
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Histopathological Examination ◽  
De Novo Lipogenesis ◽  
Large Animal ◽  
Alcoholic Fatty Liver ◽  
High Fructose ◽  
Alcoholic Fatty Liver Disease

AbstractNon-alcoholic fatty liver disease (NAFLD) is an increasingly prevalent condition that has been linked to high-fructose corn syrup consumption with induction of hepatic de novo lipogenesis (DNL) as the suggested central mechanism. Feeding diets very high in fructose (> 60%) rapidly induce several features of NAFLD in rodents, but similar diets have not yet been applied in larger animals, such as pigs. With the aim to develop a large animal NAFLD model, we analysed the effects of feeding a high-fructose (HF, 60% w/w) diet for four weeks to castrated male Danish Landrace-York-Duroc pigs. HF feeding upregulated expression of hepatic DNL proteins, but levels were low compared with adipose tissue. No steatosis or hepatocellular ballooning was seen on histopathological examination, and plasma levels of transaminases were similar between groups. Inflammatory infiltrates and the amount of connective tissue was slightly elevated in liver sections from fructose-fed pigs, which was corroborated by up-regulation of macrophage marker expression in liver homogenates. Supported by RNA-profiling, quantitative protein analysis, histopathological examination, and biochemistry, our data suggest that pigs, contrary to rodents and humans, are protected against fructose-induced steatosis by relying on adipose tissue rather than liver for DNL.

scholarly journals Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome

2010 ◽  
Vol 69 (2) ◽  
pp. 211-220 ◽  
Author(s):  
J. Bernadette Moore
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Response To Treatment ◽  
Health Concern ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease in both adults and children worldwide. As a disease spectrum, NAFLD may progress from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. An estimated 20–35% of the general population has steatosis, 10% of whom will develop the more progressive non-alcoholic steatohepatitis associated with markedly increased risk of cardiovascular- and liver-related mortality. Development of NAFLD is strongly linked to components of the metabolic syndrome including obesity, insulin resistance, dyslipidaemia and type 2 diabetes. The recognition that NAFLD is an independent risk factor for CVD is a major public health concern. There is a great need for a sensitive non-invasive test for the early detection and assessment of the stage of NAFLD that could also be used to monitor response to treatment. The cellular and molecular aetiology of NAFLD is multi-factorial; genetic polymorphisms influencing NAFLD have been identified and nutrition is a modifiable environmental factor influencing NAFLD progression. Weight loss through diet and exercise is the primary recommendation in the clinical management of NAFLD. The application of systems biology to the identification of NAFLD biomarkers and factors involved in NAFLD progression is an area of promising research.

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