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Liver Fat Is Increased in Type 2 Diabetic Patients and Underestimated by Serum Alanine Aminotransferase Compared With Equally Obese Nondiabetic Subjects
Author(s) -
Anna Kotronen,
Leena Juurinen,
Antti Hakkarainen,
Jukka Westerbacka,
A. H. Corner,
Robert Bergholm,
Hannele YkiJärvinen
Publication year - 2007
Publication title -
diabetes care
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.636
H-Index - 363
eISSN - 1935-5548
pISSN - 0149-5992
DOI - 10.2337/dc07-1463
Subject(s) - medicine , endocrinology , insulin resistance , type 2 diabetes , liver function , diabetes mellitus , fatty liver , waist , insulin , obesity , disease
OBJECTIVE—The purpose of this study was to determine whether type 2 diabetic patients have more liver fat than age-, sex-, and BMI-matched nondiabetic subjects and whether liver enzymes (serum alanine aminotransferase [S-ALT] and serum aspartate aminotransferase) are similarly related to liver fat in type 2 diabetic patients and normal subjects. RESEARCH DESIGN AND METHODS—Seventy type 2 diabetic patients and 70 nondiabetic subjects matched for BMI, age, and sex were studied. Liver fat (1H-magnetic resonance spectroscopy), body composition (magnetic resonance imaging), and biochemical markers of insulin resistance were measured. RESULTS—The type 2 diabetic patients had, on average, 80% more liver fat and 16% more intra-abdominal fat than the nondiabetic subjects. The difference in liver fat between the two groups remained statistically significant when adjusted for intra-abdominal fat (P < 0.05). At any given BMI or waist circumference, the type 2 diabetic patients had more liver fat than the nondiabetic subjects. The difference in liver fat between the groups rose as a function of BMI and waist circumference. Fasting serum insulin (r = 0.55, P < 0.0001), fasting plasma glucose (r = 0.29, P = 0.0006), A1C (r = 0.34, P < 0.0001), fasting serum triglycerides (r = 0.36, P < 0.0001), and fasting serum HDL cholesterol (r = −0.31, P = 0.0002) correlated with liver fat similarly in both groups. The slopes of the relationships between S-ALT and liver fat were significantly different (P = 0.004). Liver fat content did not differ between the groups at low S-ALT concentrations (10–20 units/l) but was 70–200% higher in type 2 diabetic patients compared with control subjects at S-ALT concentrations of 50–200 units/l. CONCLUSIONS—Type 2 diabetic patients have 80% more liver fat than age-, weight-, and sex-matched nondiabetic subjects. S-ALT underestimates liver fat in type 2 diabetic patients.

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