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Nutritional Modulation of Non-Alcoholic Fatty Liver Disease and Insulin Resistance.

Yki-Järvinen H - Nutrients (2015)

Bottom Line: However, any type of caloric restriction seems effective long-term.Overfeeding either saturated fat or carbohydrate increases liver fat content.Vitamin E supplementation decreases liver fat content as well as fibrosis but has no effect on features of insulin resistance.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, University of Helsinki, and Minerva Foundation Institute for Medical Research, Haartmaninkatu 8, 00290 Helsinki, Finland. Hannele.Yki-Jarvinen@helsinki.fi.

ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) covers a spectrum of disorders ranging from simple steatosis (non-alcoholic fatty liver, NAFL) to non-alcoholic steatohepatitis (NASH) and cirrhosis. NAFL increases the risk of liver fibrosis. If the liver is fatty due to causes of insulin resistance such as obesity and physical inactivity, it overproduces glucose and triglycerides leading to hyperinsulinemia and a low high-density lipoprotein (HDL) cholesterol concentration. The latter features predispose to type 2 diabetes and cardiovascular disease (CVD). Understanding the impact of nutritional modulation of liver fat content and insulin resistance is therefore of interest for prevention and treatment of NAFLD. Hypocaloric, especially low carbohydrate ketogenic diets rapidly decrease liver fat content and associated metabolic abnormalities. However, any type of caloric restriction seems effective long-term. Isocaloric diets containing 16%-23% fat and 57%-65% carbohydrate lower liver fat compared to diets with 43%-55% fat and 27%-38% carbohydrate. Diets rich in saturated (SFA) as compared to monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids appear particularly harmful as they increase both liver fat and insulin resistance. Overfeeding either saturated fat or carbohydrate increases liver fat content. Vitamin E supplementation decreases liver fat content as well as fibrosis but has no effect on features of insulin resistance.

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Effect of dietary composition on liver fat content, expressed as relative change from baseline measured by proton magnetic resonance spectroscopy (1H-MRS). Diets comparing isocaloric low fat/high carbohydrate (Low Fat High Carb) to high fat/low-carbohydrate (High Fat Low Carb) diets (upper panel on the left, 1 = [25], 2 = [26], 3 = [29]), isocaloric low saturated fat/high polyunsaturated fat (Low SFA High PUFA) to high saturated/low polyunsaturated fat (High SFA Low PUFA) or isocaloric high monounsaturated (High MUFA) to low monounsaturated fat (Low MUFA) (upper panel on the right, 4 = [27], 5 = [28], 6 = [30]) diets. The bottom panels depict effects of hypocaloric Low Fat High Carb compared to High Fat Low Carb diets (panel on the left, 7 = [31], 8 = [32], 9 = [33]) and hypercaloric Low Fat High Carb vs. High Fat Low Carb (10 = [34]) and High PUFA Low SFA vs. Low PUFA High SFA (11 = [35]) diets on liver fat content.
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nutrients-07-05454-f002: Effect of dietary composition on liver fat content, expressed as relative change from baseline measured by proton magnetic resonance spectroscopy (1H-MRS). Diets comparing isocaloric low fat/high carbohydrate (Low Fat High Carb) to high fat/low-carbohydrate (High Fat Low Carb) diets (upper panel on the left, 1 = [25], 2 = [26], 3 = [29]), isocaloric low saturated fat/high polyunsaturated fat (Low SFA High PUFA) to high saturated/low polyunsaturated fat (High SFA Low PUFA) or isocaloric high monounsaturated (High MUFA) to low monounsaturated fat (Low MUFA) (upper panel on the right, 4 = [27], 5 = [28], 6 = [30]) diets. The bottom panels depict effects of hypocaloric Low Fat High Carb compared to High Fat Low Carb diets (panel on the left, 7 = [31], 8 = [32], 9 = [33]) and hypercaloric Low Fat High Carb vs. High Fat Low Carb (10 = [34]) and High PUFA Low SFA vs. Low PUFA High SFA (11 = [35]) diets on liver fat content.

Mentions: Overall, as shown by Figure 2, the energy content of the diet is the most important factor influencing liver fat content, which is why weight loss is recommended to all overweight or obese patients with NAFLD [2] Given that conventional hypocaloric diets are unable to achieve persistent weight loss in morbidly obese patients, bariatric surgery is becoming increasingly important in the management of NAFLD. Weight loss following bariatric surgery induces improvements in steatosis, necroinflammation and fibrosis and insulin resistance. NASH is not a contraindication for surgery unless complicated by cirrhosis or portal hypertension (see [42,43,44,45] for reviews).


Nutritional Modulation of Non-Alcoholic Fatty Liver Disease and Insulin Resistance.

Yki-Järvinen H - Nutrients (2015)

Effect of dietary composition on liver fat content, expressed as relative change from baseline measured by proton magnetic resonance spectroscopy (1H-MRS). Diets comparing isocaloric low fat/high carbohydrate (Low Fat High Carb) to high fat/low-carbohydrate (High Fat Low Carb) diets (upper panel on the left, 1 = [25], 2 = [26], 3 = [29]), isocaloric low saturated fat/high polyunsaturated fat (Low SFA High PUFA) to high saturated/low polyunsaturated fat (High SFA Low PUFA) or isocaloric high monounsaturated (High MUFA) to low monounsaturated fat (Low MUFA) (upper panel on the right, 4 = [27], 5 = [28], 6 = [30]) diets. The bottom panels depict effects of hypocaloric Low Fat High Carb compared to High Fat Low Carb diets (panel on the left, 7 = [31], 8 = [32], 9 = [33]) and hypercaloric Low Fat High Carb vs. High Fat Low Carb (10 = [34]) and High PUFA Low SFA vs. Low PUFA High SFA (11 = [35]) diets on liver fat content.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663582&req=5

nutrients-07-05454-f002: Effect of dietary composition on liver fat content, expressed as relative change from baseline measured by proton magnetic resonance spectroscopy (1H-MRS). Diets comparing isocaloric low fat/high carbohydrate (Low Fat High Carb) to high fat/low-carbohydrate (High Fat Low Carb) diets (upper panel on the left, 1 = [25], 2 = [26], 3 = [29]), isocaloric low saturated fat/high polyunsaturated fat (Low SFA High PUFA) to high saturated/low polyunsaturated fat (High SFA Low PUFA) or isocaloric high monounsaturated (High MUFA) to low monounsaturated fat (Low MUFA) (upper panel on the right, 4 = [27], 5 = [28], 6 = [30]) diets. The bottom panels depict effects of hypocaloric Low Fat High Carb compared to High Fat Low Carb diets (panel on the left, 7 = [31], 8 = [32], 9 = [33]) and hypercaloric Low Fat High Carb vs. High Fat Low Carb (10 = [34]) and High PUFA Low SFA vs. Low PUFA High SFA (11 = [35]) diets on liver fat content.
Mentions: Overall, as shown by Figure 2, the energy content of the diet is the most important factor influencing liver fat content, which is why weight loss is recommended to all overweight or obese patients with NAFLD [2] Given that conventional hypocaloric diets are unable to achieve persistent weight loss in morbidly obese patients, bariatric surgery is becoming increasingly important in the management of NAFLD. Weight loss following bariatric surgery induces improvements in steatosis, necroinflammation and fibrosis and insulin resistance. NASH is not a contraindication for surgery unless complicated by cirrhosis or portal hypertension (see [42,43,44,45] for reviews).

Bottom Line: However, any type of caloric restriction seems effective long-term.Overfeeding either saturated fat or carbohydrate increases liver fat content.Vitamin E supplementation decreases liver fat content as well as fibrosis but has no effect on features of insulin resistance.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, University of Helsinki, and Minerva Foundation Institute for Medical Research, Haartmaninkatu 8, 00290 Helsinki, Finland. Hannele.Yki-Jarvinen@helsinki.fi.

ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) covers a spectrum of disorders ranging from simple steatosis (non-alcoholic fatty liver, NAFL) to non-alcoholic steatohepatitis (NASH) and cirrhosis. NAFL increases the risk of liver fibrosis. If the liver is fatty due to causes of insulin resistance such as obesity and physical inactivity, it overproduces glucose and triglycerides leading to hyperinsulinemia and a low high-density lipoprotein (HDL) cholesterol concentration. The latter features predispose to type 2 diabetes and cardiovascular disease (CVD). Understanding the impact of nutritional modulation of liver fat content and insulin resistance is therefore of interest for prevention and treatment of NAFLD. Hypocaloric, especially low carbohydrate ketogenic diets rapidly decrease liver fat content and associated metabolic abnormalities. However, any type of caloric restriction seems effective long-term. Isocaloric diets containing 16%-23% fat and 57%-65% carbohydrate lower liver fat compared to diets with 43%-55% fat and 27%-38% carbohydrate. Diets rich in saturated (SFA) as compared to monounsaturated (MUFA) or polyunsaturated (PUFA) fatty acids appear particularly harmful as they increase both liver fat and insulin resistance. Overfeeding either saturated fat or carbohydrate increases liver fat content. Vitamin E supplementation decreases liver fat content as well as fibrosis but has no effect on features of insulin resistance.

Show MeSH
Related in: MedlinePlus