Metabolic Syndrome Associated With More Severe NFLD
Metabolic Syndrome Associated With More Severe NFLD
Nov. 15, 2005 (San Francisco) - In a prospective study comparing diet, physical activity, and histological severity of nonalcoholic fatty acid liver disease (NAFLD) in patients with and without metabolic syndrome, researchers found that patients with metabolic syndrome had more severe NAFLD and ate more carbohydrates and less fat.
Although metabolic syndrome and insulin resistance are thought to be the underlying causes of NAFLD, few studies have looked at the relationship between diet composition and NAFLD severity. To begin to learn how the two disorders are related, Hellan Kang, MD, and colleagues, from the Division of Gastroenterology at the University of Michigan in Ann Arbor, enrolled 101 patients suspected of having NAFLD in a prospective study. Dr. Kang presented the results of the study here at the 56th annual meeting of the American Association for the Study of Liver Diseases.
Each participant filled out the validated Paffenbarger physical activity questionnaire, which measures both daily lifestyle activity and recreational exercise, and the Food Frequency Questionnaire (Block 98 FFQ). The scientists also assessed insulin resistance, using the homeostasis model assessment (HOMA), and the degree of NAFLD histology through liver biopsies.
A total of 97 biopsies have been reviewed and 91 patients were found to have NAFLD. Of those, 31 patients (34%) had metabolic syndrome and 75 patients (82%) had evidence of insulin resistance, with a HOMA index above two.
NAFLD patients with metabolic syndrome consumed significantly more carbohydrates (accounting for 51% of their dietary macronutrients) than did patients without metabolic syndrome (45% of dietary macronutrients); P = .03. Fat consumption was lower in the metabolic syndrome group at 34% of macronutrients compared with 40% in the non-metabolic syndrome group ( P = .006). There was no statistically significant difference in protein consumption, total calories consumed, or daily activity between the two groups.
Patients with metabolic syndrome had a higher global nonalcoholic steatohepatitis (NASH) score based on liver histology than did patients without metabolic syndrome (5.9 +177; 1.7 vs 4.4 +177; 2.3, using the NASH clinical network scoring system; P = .0006). They also had more severe steatosis (2.0 +177; 0.8 vs 1.4 +177; 1.0; P = .002), hepatocytic ballooning (0.6 +177; 0.5 vs 0.4 +177; 0.5; P = .008), and a higher NASH activity score (4.1 +177; 1.4 vs 3.1 +177; 1.7; P = .004). There was no difference between the two patient groups in terms of fibrosis score or lobular inflammation.
When the team categorized the patients into those with high (6-12) and low (0-5) global NASH scores, irrespective of metabolic syndrome status, they found that patients with more severe disease had a higher percentage of body fat based on a body impedance assay (42% +177; 12% vs 35% +177; 13%; P = .01), a higher HOMA index (7 +177; 4 vs 4.26 +177; 3.11; P = .003), and higher AST levels (66 +177; 47 vs 46 +177; 24; P = .03). The patients with higher NASH scores also were significantly less active than those in the low-score group ( P = .01).
"It is too early to counsel patients to change their diet," Dr. Kang told Medscape. However, the data is important to direct future studies. "We need to do a larger dietary study to look at the impact of different types of fats and whether high glycemic index carbohydrates are a driving force in the disease."
The authors reported no financial conflicts of interest.
AASLD 56th Annual Meeting: Abstract 1056. PresentedNov. 14, 2005.
Reviewed by Maria L. Gaiso, PhD
Nov. 15, 2005 (San Francisco) - In a prospective study comparing diet, physical activity, and histological severity of nonalcoholic fatty acid liver disease (NAFLD) in patients with and without metabolic syndrome, researchers found that patients with metabolic syndrome had more severe NAFLD and ate more carbohydrates and less fat.
Although metabolic syndrome and insulin resistance are thought to be the underlying causes of NAFLD, few studies have looked at the relationship between diet composition and NAFLD severity. To begin to learn how the two disorders are related, Hellan Kang, MD, and colleagues, from the Division of Gastroenterology at the University of Michigan in Ann Arbor, enrolled 101 patients suspected of having NAFLD in a prospective study. Dr. Kang presented the results of the study here at the 56th annual meeting of the American Association for the Study of Liver Diseases.
Each participant filled out the validated Paffenbarger physical activity questionnaire, which measures both daily lifestyle activity and recreational exercise, and the Food Frequency Questionnaire (Block 98 FFQ). The scientists also assessed insulin resistance, using the homeostasis model assessment (HOMA), and the degree of NAFLD histology through liver biopsies.
A total of 97 biopsies have been reviewed and 91 patients were found to have NAFLD. Of those, 31 patients (34%) had metabolic syndrome and 75 patients (82%) had evidence of insulin resistance, with a HOMA index above two.
NAFLD patients with metabolic syndrome consumed significantly more carbohydrates (accounting for 51% of their dietary macronutrients) than did patients without metabolic syndrome (45% of dietary macronutrients); P = .03. Fat consumption was lower in the metabolic syndrome group at 34% of macronutrients compared with 40% in the non-metabolic syndrome group ( P = .006). There was no statistically significant difference in protein consumption, total calories consumed, or daily activity between the two groups.
Patients with metabolic syndrome had a higher global nonalcoholic steatohepatitis (NASH) score based on liver histology than did patients without metabolic syndrome (5.9 +177; 1.7 vs 4.4 +177; 2.3, using the NASH clinical network scoring system; P = .0006). They also had more severe steatosis (2.0 +177; 0.8 vs 1.4 +177; 1.0; P = .002), hepatocytic ballooning (0.6 +177; 0.5 vs 0.4 +177; 0.5; P = .008), and a higher NASH activity score (4.1 +177; 1.4 vs 3.1 +177; 1.7; P = .004). There was no difference between the two patient groups in terms of fibrosis score or lobular inflammation.
When the team categorized the patients into those with high (6-12) and low (0-5) global NASH scores, irrespective of metabolic syndrome status, they found that patients with more severe disease had a higher percentage of body fat based on a body impedance assay (42% +177; 12% vs 35% +177; 13%; P = .01), a higher HOMA index (7 +177; 4 vs 4.26 +177; 3.11; P = .003), and higher AST levels (66 +177; 47 vs 46 +177; 24; P = .03). The patients with higher NASH scores also were significantly less active than those in the low-score group ( P = .01).
"It is too early to counsel patients to change their diet," Dr. Kang told Medscape. However, the data is important to direct future studies. "We need to do a larger dietary study to look at the impact of different types of fats and whether high glycemic index carbohydrates are a driving force in the disease."
The authors reported no financial conflicts of interest.
AASLD 56th Annual Meeting: Abstract 1056. PresentedNov. 14, 2005.
Reviewed by Maria L. Gaiso, PhD
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