Nutrition and Non-alcoholic fatty liver disease Carlton Li QEH - - PowerPoint PPT Presentation

nutrition and non alcoholic fatty liver disease
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Nutrition and Non-alcoholic fatty liver disease Carlton Li QEH - - PowerPoint PPT Presentation

Nutrition and Non-alcoholic fatty liver disease Carlton Li QEH Definition 1) Evidence of hepatic steatosis, either by imaging or histology 2) Lack of secondary causes of hepatic fat accumulation NAFL presence of >=5% hepatic steatosis


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Nutrition and Non-alcoholic fatty liver disease

Carlton Li QEH

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Definition

1) Evidence of hepatic steatosis, either by imaging or histology 2) Lack of secondary causes of hepatic fat accumulation

NAFL – presence of >=5% hepatic steatosis without evidence of hepatocellular injury in the form of hepatocyte ballooning NASH – presence of >=5% hepatic steatosis and inflammation with hepatocyte injury, with or without any fibrosis

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Weight loss Works

Vilar-Gomez et al. Gastroenterology 2015

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Atherosclerosis 2015 Apr;239(2):483-95

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Hypothesis

u IRS hypothesis u ER stress hypothesis u mTORC1 hypothesis

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Biochemical changes in liver cells

u Overexpress SREBP-1c u Increase in expression of genes encoding fatty acid synthase and acetyl-coA

carboxylase (lipogenic enzymes)

Clin Sci (Lond) 120(6):239-250 Hepatol Res 38(11):1122-1129

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Both carbohydrates and fat contribute to fatty liver

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Nutritional induction of NAFLD

Overnutrition is the primary driver

  • Increased energy uptake supports hepatic fat accumulation by delivery of

excess fat and carbohydrates-> de-novo-lipogenesis

  • Expansion of adipose tissue, if compounded with inflammation-> increase in

nonesterified fatty acids pool in the serum

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A calorie is a calorie

u Law of conservation of energy –

energy can neither be created nor destroyed

u Prevention of obesity = Eat less

and exercise more?

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Theories behind manipulation of macronutrients

u alter overall calorie intake and expenditure u corresponding change in energy stores of the body u Alter endocrine factors that influence the propensity to accumulate body fat

  • r direct the storage of fat to particular locations
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u Dietary interventional

study for 2 years

u 750kcal calorie deficit u 4 groups with different

composition of carbohydrate/protein/fat (HLL, MLH, MHL, LHH)

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Key factors

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Macronutrient composition is not a key determinant in weight loss success Adherence to the dietary protocol is more important

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EASL 2016 guideline

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AASLD 2018 guideline

  • 20. Weight loss generally reduces Hepatic Steatosis, achieved either by

hypocaloric diet alone or in conjunction with increased physical activity. A combination of a hypocaloric diet (daily reduction by 500-1,000 kcal) and moderate-intensity exercise is likely to provide the best likelihood of sustaining weight loss over time.

CHALASANI ET AL. HEPATOLOGY , January 2018

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Fructose

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Fructose

u Potent stimulator of de-novo-lipogenesis u Bypass the regulatory enzymes of the glycolytic pathway u Provide lipogenic precursors for lipogenesis (acetyl coA)

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Mediterranean Diet

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Recommendations

u Intense nutritional education u Hypocaloric diet is helpful to induce

weight loss

u A diet with reduced simple sugar intake,

especially fructose, to less than 10% of caloric intake

u Mediterranean diet maybe protective

against NAFLD (high intakes of fruits, nuts, vegetables, whole grain cereals,

  • live oil, and moderate consumption of

fish, poultry, wine, and low intake of dairy, red meats, and sweets)

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