Beneficial effect of a weight-stable, low-fat/low-saturated fat/low-glycaemic index diet to reduce liver fat in older subjects

Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quan...

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Published inBritish journal of nutrition Vol. 109; no. 6; pp. 1096 - 1104
Main Authors Utzschneider, Kristina M., Bayer-Carter, Jennifer L., Arbuckle, Matthew D., Tidwell, Jaime M., Richards, Todd L., Craft, Suzanne
Format Journal Article
LanguageEnglish
Published Cambridge, UK Cambridge University Press 28.03.2013
Subjects
Addictive behaviors
Adult and adolescent clinical studies
Aged
Alcoholism
Alcoholism and acute alcohol poisoning
Biological and medical sciences
Body Fat Distribution
Body Mass Index
Body Weight
Cholesterol
Diet
Diet, Fat-Restricted
Diet, High-Fat
dietary fat
Double-Blind Method
Energy Intake
fasting
fatty liver
Fatty Liver - diet therapy
Fatty Liver - pathology
Feeding. Feeding behavior
Female
females
Fundamental and applied biological sciences. Psychology
Gastroenterology. Liver. Pancreas. Abdomen
glucose
Glycemic Index
high density lipoprotein cholesterol
homeostasis
Human and Clinical Nutrition
Humans
hyperlipidemia
insulin
Insulin Resistance
lipid content
Lipids - blood
Liver
Liver diseases
Liver. Biliary tract. Portal circulation. Exocrine pancreas
low density lipoprotein cholesterol
Magnetic Resonance Spectroscopy
Male
males
Medical sciences
Older people
Other diseases. Semiology
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
saturated fats
spectroscopy
Toxicology
Vertebrates: anatomy and physiology, studies on body, several organs or systems
United States > US
Dietary fat
Non-alcoholic fatty liver
Saturated fat
Glycaemic index
Human
Nutrition
Digestive system
Alcoholism
Liver
Lipids
Hepatic disease
Index
Weight
Fatty liver
Saturated fatty acid
Low fat diet
Fat
Digestive diseases
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Abstract Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0·05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
AbstractList Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 ( sem 1·6) years, BMI 26·9 ( sem 0·8) kg/m 2 ) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 ( sem 1·8) years, BMI 28·1 ( sem 0·9) kg/m 2 ) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P = 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG ( P < 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol ( P < 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet ( P < 0·05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69.3 (SEM 1.6) years, BMI 26.9 (SEM 0.8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68.6 (SEM 1.8) years, BMI 28.1 (SEM 0.9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2.2 (interquartile range (IQR) 3.1) to 1.7 (IQR 1.8) %, P= 0.002) but did not change on the HSAT diet (median 1.2 (IQR 4.1) to 1.6 (IQR 3.9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0.05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0.05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0.05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69.3 (SEM 1.6) years, BMI 26.9 (SEM 0.8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68.6 (SEM 1.8) years, BMI 28.1 (SEM 0.9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2.2 (interquartile range (IQR) 3.1) to 1.7 (IQR 1.8) %, P= 0.002) but did not change on the HSAT diet (median 1.2 (IQR 4.1) to 1.6 (IQR 3.9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0.05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0.05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0.05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m²) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m²) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0·05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69.3 (SEM 1.6) years, BMI 26.9 (SEM 0.8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68.6 (SEM 1.8) years, BMI 28.1 (SEM 0.9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2.2 (interquartile range (IQR) 3.1) to 1.7 (IQR 1.8) %, P= 0.002) but did not change on the HSAT diet (median 1.2 (IQR 4.1) to 1.6 (IQR 3.9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0.05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0.05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0.05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23% fat/7% saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43% fat/24% saturated fat/GI > 70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 ( sem 1·6) years, BMI 26·9 ( sem 0·8) kg/m 2 ) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 ( sem 1·8) years, BMI 28·1 ( sem 0·9) kg/m 2 ) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P =0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG ( P <0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol ( P <0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet ( P <0·05). Assignment to the LSAT ν. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycemic index (LGI) (LAST: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m2) were randomized to the LAST diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LAST diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LAST diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LAST diet (P< 0·05). Assignment to the LAST v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial. 55 references
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycaemic index (LGI) (LSAT: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m2) were randomised to the LSAT diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LSAT diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LSAT diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LSAT diet (P< 0·05). Assignment to the LSAT v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial.
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidemia and can progress to steatohepatitis and cirrhosis. We sought to determine whether dietary fat and saturated fat content alter liver fat in the absence of weight change in an older population. Liver fat was quantified by magnetic resonance spectroscopy before and after 4 weeks on an isoenergetic low-fat/low-saturated fat/low-glycemic index (LGI) (LAST: 23 % fat/7 % saturated fat/GI < 55) or a high-fat/high-saturated fat/high-GI (HSAT: 43 % fat/24 % saturated fat/GI>70) diet in older subjects. In the present study, twenty subjects (seven males/thirteen females; age 69·3 (sem 1·6) years, BMI 26·9 (sem 0·8) kg/m2) were randomized to the LAST diet and fifteen subjects (six males/nine females; age 68·6 (sem 1·8) years, BMI 28·1 (sem 0·9) kg/m2) to the HSAT diet. Weight remained stable. Liver fat decreased significantly on the LAST diet (median 2·2 (interquartile range (IQR) 3·1) to 1·7 (IQR 1·8) %, P= 0·002) but did not change on the HSAT diet (median 1·2 (IQR 4·1) to 1·6 (IQR 3·9) %). The LAST diet lowered fasting glucose and total cholesterol, HDL-cholesterol and LDL-cholesterol and raised TAG (P< 0·05), while the HSAT diet had no effect on glucose or HDL-cholesterol but increased total cholesterol and LDL-cholesterol (P< 0·05). Fasting insulin and homeostasis model of insulin resistance did not change significantly on either diet, but the Matsuda index of insulin sensitivity improved on the LAST diet (P< 0·05). Assignment to the LAST v. HSAT diet was a predictor of changes in lipid parameters but not liver fat. We conclude that diet composition may be an important factor in the accumulation of liver fat, with a low-fat/low-saturated fat/LGI diet being beneficial. [PUBLICATION ABSTRACT]
Author Bayer-Carter, Jennifer L.
Tidwell, Jaime M.
Arbuckle, Matthew D.
Utzschneider, Kristina M.
Richards, Todd L.
Craft, Suzanne
AuthorAffiliation 4 Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98195, USA
2 Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA 98195, USA
5 Department of Radiology, University of Washington, Seattle, WA 98195, USA
1 Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA
3 Geriatric Research Education and Clinical Center (GRECC), VA Puget Sound Health Care System, Seattle, WA 98108, USA
AuthorAffiliation_xml – name: 2 Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA 98195, USA
– name: 4 Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA 98195, USA
– name: 3 Geriatric Research Education and Clinical Center (GRECC), VA Puget Sound Health Care System, Seattle, WA 98108, USA
– name: 5 Department of Radiology, University of Washington, Seattle, WA 98195, USA
– name: 1 Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA 98108, USA
Author_xml – sequence: 1
  givenname: Kristina M.
  surname: Utzschneider
  fullname: Utzschneider, Kristina M.
  email: kutzschn@u.washington.edu
  organization: 1Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, 1660 South Columbian Way, Seattle, WA98108, USA
– sequence: 2
  givenname: Jennifer L.
  surname: Bayer-Carter
  fullname: Bayer-Carter, Jennifer L.
  organization: 3Geriatric Research Education and Clinical Center (GRECC), VA Puget Sound Health Care System, Seattle, WA98108, USA
– sequence: 3
  givenname: Matthew D.
  surname: Arbuckle
  fullname: Arbuckle, Matthew D.
  organization: 3Geriatric Research Education and Clinical Center (GRECC), VA Puget Sound Health Care System, Seattle, WA98108, USA
– sequence: 4
  givenname: Jaime M.
  surname: Tidwell
  fullname: Tidwell, Jaime M.
  organization: 3Geriatric Research Education and Clinical Center (GRECC), VA Puget Sound Health Care System, Seattle, WA98108, USA
– sequence: 5
  givenname: Todd L.
  surname: Richards
  fullname: Richards, Todd L.
  organization: 5Department of Radiology, University of Washington, Seattle, WA98195, USA
– sequence: 6
  givenname: Suzanne
  surname: Craft
  fullname: Craft, Suzanne
  organization: 3Geriatric Research Education and Clinical Center (GRECC), VA Puget Sound Health Care System, Seattle, WA98108, USA
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Issue 6
Keywords Dietary fat
Non-alcoholic fatty liver
Saturated fat
Glycaemic index
Human
Nutrition
Digestive system
Alcoholism
Liver
Lipids
Hepatic disease
Index
Weight
Fatty liver
Saturated fatty acid
Low fat diet
Fat
Digestive diseases
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Snippet Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidaemia and can progress to steatohepatitis and cirrhosis. We sought to...
Non-alcoholic fatty liver disease is associated with insulin resistance and dyslipidemia and can progress to steatohepatitis and cirrhosis. We sought to...
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pubmed
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cambridge
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StartPage 1096
SubjectTerms Addictive behaviors
Adult and adolescent clinical studies
Aged
Alcoholism
Alcoholism and acute alcohol poisoning
Biological and medical sciences
Body Fat Distribution
Body Mass Index
Body Weight
Cholesterol
Diet
Diet, Fat-Restricted
Diet, High-Fat
dietary fat
Double-Blind Method
Energy Intake
fasting
fatty liver
Fatty Liver - diet therapy
Fatty Liver - pathology
Feeding. Feeding behavior
Female
females
Fundamental and applied biological sciences. Psychology
Gastroenterology. Liver. Pancreas. Abdomen
glucose
Glycemic Index
high density lipoprotein cholesterol
homeostasis
Human and Clinical Nutrition
Humans
hyperlipidemia
insulin
Insulin Resistance
lipid content
Lipids - blood
Liver
Liver diseases
Liver. Biliary tract. Portal circulation. Exocrine pancreas
low density lipoprotein cholesterol
Magnetic Resonance Spectroscopy
Male
males
Medical sciences
Older people
Other diseases. Semiology
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
saturated fats
spectroscopy
Toxicology
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Title Beneficial effect of a weight-stable, low-fat/low-saturated fat/low-glycaemic index diet to reduce liver fat in older subjects
URI https://www.cambridge.org/core/product/identifier/S0007114512002966/type/journal_article
https://www.ncbi.nlm.nih.gov/pubmed/22849970
https://www.proquest.com/docview/1316243398
https://www.proquest.com/docview/1317405194
https://www.proquest.com/docview/1523398948
https://www.proquest.com/docview/1825423730
https://pubmed.ncbi.nlm.nih.gov/PMC3909493
Volume 109
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