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Fatty Liver Disease : Nash and Related Disorders - part 3

Các mô hình của sự đề kháng insulin cho đến nay được mô tả trong các bệnh nhân NAFLD là giống như quan sát thấy ở những bệnh nhân với bệnh tiểu đường type 2 hoặc thân nhân của họ, hơn là ở những bệnh nhân bị xơ gan. | NASH AS PART OF THE METABOLIC SYNDROME Table 5.3 Metabolic features of insulin resistance in various clinical disorders. NAFLD Cirrhosis Obesity Type 2 diabetes Total glucose disposal ị ị ị ị Glucose oxidation ị o ị ị Non-oxidative glucose disposal ị ị ị ị Suppression of hepatic glucose output ị o ị ị Suppression of lipolysis ị o ị ị Insulin secretion T T T ịT The pattern of insulin resistance so far described in NAFLD patients is more like that observed in patients with type 2 diabetes or in their relatives than in patients with cirrhosis. Non-diabetic patients with cirrhosis are characterized by hyperinsulinaemia both in the fasting state and following glucose load but basal endogenous glucose production is normal and is normally suppressed by insulin. In contrast both diabetic and NAFLD patients have a blunted insulin-mediated suppression of hepatic glucose production and decreased rates of both oxidative and non-oxidative glycogen synthesis glucose metabolism. The derangement in lipid metabolism so far described is to be expected in NAFLD patients with obesity or hypertriglyceridaemia but it is still present when these confounding factors are absent. In a selected population of lean NAFLD patients with normal glucose tolerance and lipid levels lipolysis was increased by approximately 40 in the basal state and less efficiently inhibited after insulin administration. Although the percentage decrease of glycerol turnover was comparable to controls after insulin administration -62 its absolute value remained higher in NAFLD patients Bugianesi et al. personal communication . Likewise lipid oxidation was higher in the basal state and less efficiently inhibited by insulin. The pattern of metabolic defects in non-obese non-diabetic NAFLD patients is thus consistent with accelerated lipolysis the immediate result of insulin resistance in adipose tissue being responsible for the increased FFA supply and their oxidative use at the whole body level. The finding of a tight