THE RELATIONSHIPS AMONG INADEQUATE NUTRIENT INTAKES, INSULIN RESISTANCE AND LIVER DYSFUNCTION IN OBESE SUBJECTS

Background and aim: Non-normal serum alanine aminotransferase (ALT) levels and elevation of homeostasis model assessment of insulin resistance (HOMA-IR) are widely considered as the hallmarks of liver and metabolic derangement in obese subjects. On the other hand, few reports have so far focused on the influence of inadequate nutrient intakes on obesity with liver disease. The relationships between the inadequate nutrient intakes and the markers of metabolic and liver dysfunction were investigated in obese subjects. Material and methods: A total of 111 obese and severely obese subjects (32M/79F; age 18–66 yr; BMI 30-73 kg/m2) were admitted, under informed consent, to the study. HBV(+), HCV(+), alcohol consumption >30g/day, and steatogenic drugs were exclusion criteria. Anthropometric and laboratory data were collected at the admission; HOMA-IR values >2.5 indicate an IR state and serum ALT values >35 U/l a liver dysfunction, as previously reported. Dietary habits were recorded by detailed questioning and a computed database determined the nutrient intakes. The recommended dietary allowances (RDA) for the Italian population were used for reference range, set at the highest limit. The median value of each nutrient was used as the cut-off value for highlighting the inadequate (at most excessive) intakes. The statistical analysis was performed with PASW 18.0 software. Results: ALT (35±28 U/l) was >35 U/l in 34%. HOMA-IR (4.4±3.5) was >2.5 in 70%. 33% showed both non-normal ALT and IR. Intakes were at most higher than RDA, except for the significantly lower polyunsaturated fatty acid (PUFA) intake. Logistic regression showed that IR was not associated with excessive total carbohydrate intake, also as simple carbohydrates (>108g; OR 1.2; 95%CI=0.4-3.4). The cases with non-normal ALT and IR were associated with inadequate intakes of animal protein (>72g; OR 2.65; 95%CI=0.7-11), fat (>140g; OR 2.9; 95%CI=0.9-9), and low PUFA intake (